REVIEW ARTICLE

EXERCISE UNDER HEAT STRESS:

THERMOREGULATION, HYDRATION,
PERFORMANCE IMPLICATIONS, AND
MITIGATION STRATEGIES
AUTHORS

riard, Thijs M. H. Eijsvogels,
Julien D. Pe
Hein A. M. Daanen

CORRESPONDENCE
[email protected]

KEY WORDS
cooling; exercise capacity; fatigue; fluid balance;
heat acclimation

CLINICAL HIGHLIGHTS
This review examines historical perspectives and recent advances in understanding of the impact of heat stress on
human physiological function. Endurance exercise capacity and performance are impaired with a rise in thermal strain,
which is determined by the thermal environment. The impairment is primarily mediated by hyperthermia-induced adjust-
ments in cardiovascular, central nervous system, and skeletal muscle function. Failure to replenish excessive body water
losses incurred via sweating compromises thermoregulatory capacity and further exacerbates the rise in physiological
strain, precipitating fatigue development. The decision to reduce work rate or discontinue exercise in the heat, with or
without hypohydration, occurs across a spectrum of physiological and perceptual responses that are task specific. Heat
acclimation, along with cooling and hydration strategies, mitigate the deleterious influence of heat stress on exercise per-
formance; however, several aspects of these strategies remain to be elucidated. Along with influencing performance,
exercise under heat stress can disrupt homeostatic processes and lead to the development of clinically relevant disorders
such as exertional heat-related illness (i.e., muscle cramps, heat syncope, heat exhaustion, and heat stroke) and fluid and
electrolyte disturbances (e.g., hypovolemia, hypernatremia, and hyponatremia).

PÉRIARD ET AL., 2021, Physiol Rev 101: 1873–1979

April 8, 2021; Copyright © 2021 The Authors. Licensed under Creative Commons Attribution CC-BY 4.0. Published by the American Physiological Society.
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 Physiol Rev 101: 1873–1979, 2021
First published April 8, 2021; doi:10.1152/physrev.00038.2020

REVIEW ARTICLE

EXERCISE UNDER HEAT STRESS:

THERMOREGULATION, HYDRATION,
PERFORMANCE IMPLICATIONS, AND
MITIGATION STRATEGIES

riard,1
Julien D. Pe Thijs M. H. Eijsvogels2, and Hein A. M. Daanen3
1
University of Canberra Research Institute for Sport and Exercise, Bruce, Australia; 2Department of Physiology, Radboud Institute for
Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands; and 3Department of Human Movement Sciences,
Faculty of Behavioural and Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands

Abstract
A rise in body core temperature and loss of body water via sweating are natural consequences of prolonged
exercise in the heat. This review provides a comprehensive and integrative overview of how the human body
responds to exercise under heat stress and the countermeasures that can be adopted to enhance aerobic per-
formance under such environmental conditions. The fundamental concepts and physiological processes associ-
ated with thermoregulation and fluid balance are initially described, followed by a summary of methods to
determine thermal strain and hydration status. An outline is provided on how exercise-heat stress disrupts these
homeostatic processes, leading to hyperthermia, hypohydration, sodium disturbances, and in some cases exer-
tional heat illness. The impact of heat stress on human performance is also examined, including the underlying
physiological mechanisms that mediate the impairment of exercise performance. Similarly, the influence of
hydration status on performance in the heat and how systemic and peripheral hemodynamic adjustments con-
tribute to fatigue development is elucidated. This review also discusses strategies to mitigate the effects of
hyperthermia and hypohydration on exercise performance in the heat by examining the benefits of heat accli-
mation, cooling strategies, and hyperhydration. Finally, contemporary controversies are summarized and future
research directions are provided.
cooling; exercise capacity; fatigue; fluid balance; heat acclimation

1. INTRODUCTION 1873
2. HUMAN THERMOREGULATION AND HEAT... 1874
CLINICAL HIGHLIGHTS
3. BODY FLUID BALANCE 1882
4. HEAT STRESS AND AEROBIC EXERCISE... 1886
This review examines historical perspectives and recent advances in
5. HEAT STRESS, HYDRATION STATUS,... 1900
understanding of the impact of heat stress on human physiological
6. MITIGATING THE IMPACT... 1917 function. Endurance exercise capacity and performance are impaired
7. CONCLUSIONS 1939 with a rise in thermal strain, which is determined by the thermal envi-
ronment. The impairment is primarily mediated by hyperthermia-
induced adjustments in cardiovascular, central nervous system, and
skeletal muscle function. Failure to replenish excessive body water
1. INTRODUCTION losses incurred via sweating compromises thermoregulatory capacity
and further exacerbates the rise in physiological strain, precipitating fa-
tigue development. The decision to reduce work rate or discontinue
Our early ancestors evolved to travel long distances by exercise in the heat, with or without hypohydration, occurs across a
walking and eventually running in semi-arid environ- spectrum of physiological and perceptual responses that are task spe-
cific. Heat acclimation, along with cooling and hydration strategies,
ments to scavenge and possibly hunt for protein-rich mitigate the deleterious influence of heat stress on exercise perform-
food sources (1). After leaving the African savannah ance; however, several aspects of these strategies remain to be eluci-
100,000 yr ago, minor physiological adaptations to dated. Along with influencing performance, exercise under heat stress
can disrupt homeostatic processes and lead to the development of
cold occurred (2); however, humans remain predomi-
clinically relevant disorders such as exertional heat-related illness (i.e.,
nantly tropical animals (3). The ability of humans to main- muscle cramps, heat syncope, heat exhaustion, and heat stroke) and
tain a stable body core temperature stems from the fluid and electrolyte disturbances (e.g., hypovolemia, hypernatremia,
evolution of several features commensurate with heat and hyponatremia).
dissipation. These features include the multiplication of

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 PÉRIARD ET AL.

eccrine sweat glands, an elongated body form and exercising in the heat also continues to draw discussion
reduced body hair favoring convective heat loss, as well and examination. These issues, along with strategies to
as changing from nasal to oronasal breathing to permit mitigate the impact of heat stress and dehydration on
greater airflow rates with less resistance and work (4–7). performance, are examined. More specifically, this
Today, physical activity and exercise are no longer review summarizes how body temperature and fluid bal-
essential to the collection of food, but rather used as a ance are regulated at rest, describes the changes occur-
means to maintain aerobic fitness and health, as well as ring during exercise in the heat, and explains how this
compete, with exercise in the heat becoming increas- may impact on performance and health. These aspects
ingly common for several reasons. Mass participation are expanded on in distinct sections. In sect. 2, a general
sporting events are growing in popularity around the overview of human thermoregulatory control and the
globe with people looking for more challenging events, factors that influence heat exchange and heat balance
which often include exercising under extreme heat (e.g., is provided. Different methodologies to assess body
Marathon des Sables). Climate change is affecting core temperature are also addressed, followed by a
global temperature with the last decade (2011–2020) summary of the major health problems that may occur
being the warmest in the 141-yr record and part of a per- when thermoregulatory function cannot be maintained
sistent long-term trend (8, 9). The six warmest years in the heat. Section 3 follows a similar pattern for fluid
have all occurred since 2015, with 2016, 2019 and 2020 balance and describes the general principles of body
being the top three. In 2020, mean global temperature fluid regulation. Subsequently, fluid disorders are
was 1.2 C above preindustrial (1850–1900) levels (9) and explained, as well as the methods to determine hydra-
is projected to increase by 1.5 C between 2030 and tion status. Section 4 summarizes the effects of heat
2052 (10). An increase in the population of major cities is stress on human performance and the underlying physi-
also causing these to become urban heat islands (11). ological mechanisms responsible for the deterioration of
These factors, along with the increased frequency and exercise performance. Section 5 examines the impact of
intensity of heat waves (12), are projected to present hydration status on performance in the heat and how
international sporting competitions (e.g., Summer systemic and peripheral hemodynamic adjustments con-
Olympics, World Athletics Championships) with increas- tribute to fatigue development. Section 6 describes dif-
ing restrictions on when, where, and how they may be ferent approaches to mitigate the detrimental effects of
held (13). Along with elite athletes, recreational competi- heat stress and exercise-induced dehydration on per-
tors also face performance and potential health chal- formance: heat acclimation, cooling interventions, and
lenges due to extreme heat exposure. These challenges hyperhydration. Finally, sect. 7 summarizes the findings of
are associated with the rise in core temperature and the review and outlines contemporary controversies
loss of body water related to exercising in the heat. This regarding the impact of heat stress and hydration status
review is therefore focused on providing an integrative on aerobic exercise in the heat and suggests avenues of
perspective of the influence of heat stress and hydration research to advance this field of study.
status on physiological responses during exercise, as
well as the impact of heat mitigation strategies. While
the focus of the review is on exercise per se, in many 2. HUMAN THERMOREGULATION AND HEAT
respects the literature described herein is directly rele- BALANCE
vant and applicable to physically demanding occupa-
tions (e.g., agricultural work, firefighting, military, and Thermoregulation constitutes one aspect of homeosta-
mining). sis and represents the ability of an organism to keep its
Although it is well established that aerobic perform- body temperature within certain boundaries in varying
ance is impaired when undertaken in hot relative to cool environmental conditions. The fundamental principles
conditions, the mechanisms mediating this impairment and theories regarding temperature regulation will be
remain contentious and differ based on the type of exer- outlined in this section and placed in the contexts of
cise being performed (i.e., incremental, constant work heat exposure at rest and during exercise. The factors
rate, and self-paced). A compromise in hydration status that constitute the human thermal environment will
(i.e., body water loss) through increased sweating is well also be examined and contextualized in the framework
recognized for exacerbating thermal strain (i.e., rise in of heat balance (i.e., interaction between heat gain
whole body temperature) and fatigue development and loss). These factors include environmental (i.e.,
under heat stress, yet debate regarding the level of ambient temperature, humidity, wind velocity, and solar
dehydration that can be incurred prior to performance radiation), task-dependent (i.e., metabolic rate and cloth-
being impacted continues. The approach used to ing), and personal (i.e., age, sex, body mass, morphol-
hydrate (i.e., ad libitum or planned drinking) when ogy, and aerobic fitness) parameters. Next, methods to

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 EXERCISE UNDER HEAT STRESS

determine body core temperature, skin temperature, 37.5

and thermal strain will be addressed, as will the spec-
trum of exertional heat illnesses that can develop during 35.0

Temperature (°C)
exercise in the heat. The intention of this section is to
provide a concise overview of the fundamental concepts 32.5
Rectal
associated with human thermoregulation and heat bal-
30.0 Head
ance, so as to contextualize the discussion on health Torso
and performance with regards to hyperthermia and Mean skin
27.5
dehydration in subsequent sections. Hands
Feet
25.0
2.1. Body Temperature 22 24 26 28 30 32 34 36

Ambient temperature (°C)

Body core (i.e., brain, heart, and other central organs) FIGURE 1. Relationship between ambient temperature and rectal,
temperature is typically regulated to 36.6 C (95% con- foot, hand, head, torso, and mean skin temperature at rest. These
fidence interval: 35.7 to 37.3 C) (14), but may deviate data indicate that changes in core temperature (i.e., rectal) are much
considerably when exposed to extreme conditions. For smaller than those of the skin and extremities to changes in ambient
temperature. Adapted with permission from Olesen (29).
example, the lowest recorded body core temperature
(i.e., rectal) survived by a human is 13.7 C (15). In contrast,
during exercise in the heat, well-trained athletes may compartments with regards to temperature: the core
reach body core (i.e., gastrointestinal) temperatures and the shell (i.e., skin and peripheral tissues). A third
of 41.5 C without any acute or long-term detrimental compartment is sometimes added to determine
effects (16). Body core temperature in humans is the changes in body heat content, that of the muscle.
main regulated variable in thermoregulation (17). Core Although measuring muscle temperature is invasive, the
temperature is most commonly determined in the diges- three-compartment model provides a more accurate
tive system (e.g., oral, esophageal, gastrointestinal, and estimate of mean body temperature during exercise
rectal) and the head (e.g., ear and forehead), next to its (33).
invasive determination in arteries or veins in clinical set-
tings (see also sect. 2.3). Body core temperature is de- 2.2. Behavioral and Autonomic Thermoregulation
pendent on measurement location as it represents the
outcome of local heat balance (18). At rest, the highest Body temperature regulation is accomplished through
body core temperatures are generally observed in the the parallel processes of behavioral and autonomic ther-
rectum (19). Resting body core temperature is also de- moregulation. Behavioral temperature regulation oper-
pendent on age, sex, ethnicity, ambient temperature, ates largely through conscious behavioral adjustments,
dew point, time of day, and month of year (14, 20). For which when in the heat includes a number of cool-seek-
example, a distinct circadian rhythm in body core tem- ing behaviors such as standing in the shade, drinking
perature occurs in humans. After a nadir in the morning cold beverages, pouring water over one’s head, and
between 0400 and 0600 h, body core temperature wearing light-colored clothing. Adjustments in work rate
steadily increases and peaks 1 to 4 h before habitual during exercise in the heat have also been suggested to
bedtime (21). The amplitude of this diurnal variation is constitute behavioral adjustments that contribute to reg-
0.5 C in healthy individuals (22), barring any exposure ulate body temperature (34). Thermoregulatory behavior
to extreme cold or heat stress, fever, or exercise. decreases the requirement for autonomic responses
Previous studies have also revealed that the elderly (35), which operate through physiological processes
have a lower resting core temperature than young that are independent of conscious voluntary behavior.
adults (23–25). The menstrual cycle significantly alters These responses include the control of vasomotor (i.e.,
body core temperature, with an upward shift of 0.4 C cutaneous vasodilation) and sudomotor (i.e., sweating)
during the luteal phase compared with the follicular function in the heat, along with metabolic heat produc-
phase in premenopausal women (26, 27). tion (i.e., shivering) and vasomotor function (i.e., cutane-
Skin acts as the interface with the environment, but ous vasoconstriction) in cold environments. A negative-
unlike core temperature, skin temperature is not regu- feedback system is typically described as the regulatory
lated (28) and varies across the body in response to the system mediating autonomic thermoregulatory responses.
thermal environment (FIGURE 1) (30, 31). Mean skin tem- This physiological control system produces graded
perature can nonetheless be categorized as cool responses according to disturbances in a regulated
(<30 C), warm (30–34.9 C), and hot (35 C) (32). The variable: body core temperature. The magnitude of
human body itself is generally divided in two main change in autonomic responses is proportional to

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 PÉRIARD ET AL.

displacement of the regulated variable in relation to is expressed as the rate of body heat storage (S):
its set point. Such control structures are called pro-
portional-control systems. In humans, central (i.e., S = M – W 6 C 6 K 6 R – E(W)
brain, spinal column, and gastrointestinal tract) and
peripheral (i.e., skin) thermoreceptors provide affer- where M is metabolic rate, W is external work rate, C is
ent input to thermoregulatory centers located in the rate of convection, K is rate of conduction, R is rate of
hypothalamus, where it is compared with the set point radiation, and E is rate of evaporation. M – W determines
(36, 37). The set point is purely a mathematical concept the rate metabolic heat gain, whereas C 6 K 6 R deter-
used to describe the thermal control of effector responses mines the rate of dry heat exchange and E reflects the
and does not imply a particular neural model of thermoreg- rate of evaporative heat loss. Four main environmental
ulation or set temperature. Rather, it describes different parameters affect the biophysical properties of human
recruitment stages within the magnitude of a load error, heat balance: ambient temperature, humidity, air veloc-
which is the difference between the input and set point ity, and solar radiation (FIGURE 2). In addition to environ-
(38). As such, central and peripheral thermoreceptors send mental factors, task dependent parameters impact on
information to a central integrator, located in the preoptic heat exchange: rate metabolic heat production and
anterior hypothalamus (39). This integrator generates a clothing; as do personal parameters: body surface area,
thermal command signal to regulate sweating, skin vasodi- body mass, sex, age, and aerobic fitness. These factors
lation, and vasoconstriction. For example, heat loss mech- are briefly addressed below, but for greater depth on
anisms are activated during a rise in core body tem- the matter the reader is referred to Refs. 51–53.
perature, while a decline in body core temperature
results in the activation of mechanisms that conserve 2.3.1. Environmental parameters.
or produce heat (37). The notion of central integration
is supported by data describing the ratio of the contri- 2.3.1.1. AMBIENT TEMPERATURE. Humans face the chal-
butions from core and skin temperature inputs in con- lenge of maintaining a stable body core temperature in a
trolling sudomotor [4:1 to 20:1 (40–43)] and vasomotor world where ambient temperature can reach 54 C in the
[3:1 to 5:1 (40, 44, 45)] responses. These responses United States, Africa, and the Middle-East and descend to
can also be altered by factors such as circadian –89 C in the Antarctic (54). During exercise, ambient tem-
rhythm, fever, menstrual cycle phase, and heat accli- peratures higher than skin temperature led to sensible (i.e.,
mation (38, 46). dry) heat gain, whereas lower temperatures lead to heat
The notion of central integration has evolved, with loss (FIGURE 3). Environments with a high ambient temper-
other regulatory models emerging. These include a ature and low humidity favor evaporative heat loss, since
model in which heat balance is achieved through heat sweat and moisture from mucosa can more easily
regulation across a range of heat loads by sensing evaporate.
heat flow to and from the body and defending body
heat content through thermoeffector responses (47, 2.3.1.2. HUMIDITY. Absolute humidity refers to the
48). Another model suggests that independent ther- amount of water vapor present in the air. In the atmos-
moeffectors loops coordinate their activities to regu- phere, absolute humidity ranges from near zero to
late body temperature around a balance point (28, 30 g·m 3 when the air is saturated at 30 C. The hu-
49). Although these thermoregulatory control models midity of the air is strongly related to the climate. Hot wet
have merit (50), the current review will rely on the tra- climates are typically found in tropical forest areas and
ditional model of a central integrator. Thermoregula- hot dry climates close to deserts. High absolute humidity
tion during exercise in the heat is regulated similarly compromises the capacity to evaporate sweat from the
as during rest and influenced by factors such as hydra- skin because the difference in water vapor (i.e., moisture)
tion state and ambient conditions, as well as work rate between the skin surface and the environment is low.
(i.e., exercise intensity). These factors are discussed in
sects. 4 and 5. 2.3.1.3. AIR VELOCITY. Standard meteorological wind
speed is determined at 10 m above ground and the high-
2.3. Heat Balance est ever air velocity recorded on earth is 113.3 m·s 1 (55).
At human level (i.e., 1–2 m above ground), air velocity
Human heat balance refers to the equilibrium between during exercise is dependent on factors such as direc-
the internal rate of metabolic heat production and rate tion of travel, wind direction and terrain (56). Air dis-
of heat exchange to the surrounding environment via placement across the body results in convective heat
sensible (i.e., convection, conduction and radiation) and exchange, depending on the thermal gradient between
insensible (i.e., evaporation) pathways. This equilibrium the air and the skin. The displacement of air also aids

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 EXERCISE UNDER HEAT STRESS

Heat exchange pathways

Environmental parameters

Diffused
radiation

Direct
radiation
Radiation

Task dependent parameters

Convection Wind

Evaporation Conduction

Reflected
radiation

FIGURE 2. Heat exchange pathways and factors influencing human heat balance. Heat exchange to the surrounding environment occurs via sensi-
ble (convection: movement of fluids; conduction: direct contact; and radiation: electromagnetic waves) heat gain or loss and insensible (evaporation: va-
porization of sweat or water) heat loss. Human heat balance is primarily influenced by environmental (ambient temperature, humidity, air velocity, and
solar radiation) and personal or task dependent (metabolic heat production and clothing) parameters. Factors such as age, sex, body mass, and mor-
phology can also influence heat balance.

with evaporative heat loss as it removes the layer of sat- temperature index (WBGT), which has been advocated
urated water vapor that may stagnate across the skin. by the American College of Sports Medicine (58) and
National Athletic Trainers’ Association (59) and used by
2.3.1.4. SOLAR RADIATION. Average annual solar radia- several international sporting organizations (e.g., World
tion directly emitted on the earth’s atmosphere is Athletics, World Triathlon).
1,361 W·m 2. The atmosphere absorbs some of this
thermal energy such that 1,000 W·m 2 reaches the
700
surface of the earth on a clear day. The amount of solar Metabolic heat production
600
radiation that reaches the human body depends on the
Heat energy (W)

500
location on earth, time of day, season, and the level of Total heat loss
400
skin area exposed.
300 Evaporative heat loss
The integration of environmental parameters can be
200
used to provide an index of the severity of the thermal
Dry heat exchange
environment, with a combination of parameters used to 100

calculate different indexes. A recent meta-analysis identi- 0

fied over 300 thermal indexes, of which 185 were included -100
10 15 20 25 35 40
in various statistical analyses (57). Temperature (98%), rela- Ambient temperature (ºC)
tive humidity (RH: 77%), and air velocity (72%) were the
FIGURE 3. Relative contribution of evaporative and dry (i.e., con-
most commonly used environmental parameters to calcu- vection and radiation) heat loss during exercise at a constant rate
late the severity of the environment, with solar radiation and metabolic heat production at different ambient temperatures.
(45%) and a combination of all four parameters (42%) less As ambient temperature increases and approaches that of the skin,
often integrated in these calculations. The most commonly dry heat loss is reduced and evaporation becomes the primary ave-
nue of heat dissipation.
used index in sport and exercise is the wet-bulb-globe

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 PÉRIARD ET AL.

2.3.2. Task-dependent parameters. active sweat glands is proportional to surface area (71).
Dry heat loss is also enhanced by having a larger body
2.3.2.1. METABOLIC HEAT PRODUCTION. Human metab- surface area when ambient temperature is lower than
olism is the sum of resting (65 W·m 2) and exercise me- skin temperature (72). Hence, for a given thermal environ-
tabolism. The oxidation of substrates during exercise ment, heat loss potential is greater in those with a large
contributes significantly to increase body core tempera- body surface area (51).
ture as only 20 to 25% (60, 61) of metabolic energy is
converted to mechanical work, with the majority released 2.3.3.2. BODY SURFACE AREA-TO-MASS RATIO. Individ-
as heat. To compete for the podium in a cycling grand uals with a high body surface area-to-mass ratio experi-
tour, such as the Tour de France, elite cyclists need to ence less heat storage during uncompensable heat ex-
deliver a power output of 6 W·kg 1 in the mountains posure than those with a lower ratio, due to the larger
(62), which leads to a sustained (e.g., 15–30 min) heat pro- area for dry and evaporative heat loss relative to body
duction of 1,400 W for a 70-kg male. The highest ever mass (51). The body surface-to-mass ratio declines with
recorded maximal rate of oxygen consumption (V_ O2max) increases in body mass and to a greater extent in
is 96.7 mL·kg 1·min 1 (63). Although not sustainable for a females (73). Thus for heavy females it is more difficult to
very long period, this level of oxygen consumption equa- release body heat than for equally heavy males. This
tes to 2,500 W of metabolic heat production, which was confirmed in a study in which a thermal model was
underscores the large contribution of exercise-induced used to assess body core temperature in females of dif-
heat production to human heat balance. ferent body morphology showing that relatively fat
females achieve considerably higher body core temper-
2.3.2.2. CLOTHING. Clothing acts as a barrier between atures during exercise in a hot/humid environment than
the skin and the environment, altering heat exchange their leaner counterparts (74). The model was validated
properties in relation to environmental conditions. The with data from six females with considerable difference
material properties and fit of a garment can affect heat in body dimensions during work in the heat (75).
strain during exercise by reducing heat dissipation and
promoting heat conservation (64). As such, the insulative 2.3.3.3. SEX. Males and females differ in body size with
properties and water vapor resistance of garments worn men generally being heavier, taller and displaying higher
during exercise in the heat should be as low as possible. V_ O2max. However, when standardized for body surface
The water absorption capacity of the material should area, metabolic heat production during several tasks is
also be low, as sweat trapped in a garment is not evapo- similar between the sexes (76). When standardized for
rated and does not provide cooling (65). Furthermore, body surface area, however, some sex-related differen-
the reflective properties of a garment are important in ces remain (e.g., sweat rate). Females have a higher den-
high radiative load scenarios (i.e., direct sunlight). It is sity of activated sweat glands during moderate exercise
not so much the color of the garment that is important, (77), but sweat rate per body surface area is higher in
but the reflective properties of the dyes used in the gar- males during light exercise in humid heat and similar
ment (66). Ventilation in the air layer between the skin between sexes in dry heat (78). These differences were
and garment (i.e., bellows effect) is important for heat suggested to stem from females having a higher onset
loss during exercise in the heat (67). An example of the threshold for sweating and better ability to suppress
bellows effect is seen in the desert, where no difference sweating when the skin is wet (78). Generally, however,
in skin temperature was observed when wearing loose when males and females are matched for body size and
fitting black or white garments (i.e., robes), despite a 6 C fitness-level (V_ O2max), differences in thermoregulation dis-
difference in the surface temperature of the garments appear (79–82). As such, there is currently no evidence
(black: 47 C; white: 41 C) (68). that females have an inherent disadvantage in thermo-
regulation when exercising in the heat compared with
2.3.3. Personal parameters. males of similar age and health status (83).

2.3.3.1. BODY SURFACE AREA. Heat generated during 2.3.3.4. AGE. Aging impacts on both thermoregulatory
metabolism is lost over the surface area of the body to capacity and fluid regulation (84, 85). Older individuals
prevent excessive heat storage. Body surface area is cal- (>60 y) have a lower resting body core temperature,
culated using a formula based on height and weight: sur- attenuated cutaneous vasodilatory capacity, less effec-
face area = 0.20247  height (m)0.725  weight (kg)0.425 tive sweat response, and decreased thermoreceptor
(69), which has been validated using three-dimensional sensitivity compared with younger individuals (84–86).
scanning techniques (70). A large body surface area is Elderly individuals also have a higher thirst sensation
beneficial for evaporative heat loss as the number of threshold (87, 88), lower total body water (89, 90),

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 EXERCISE UNDER HEAT STRESS

reduced kidney function (89, 91), and an impaired and need for accuracy. Blood temperature of the pulmo-
plasma vasopressin regulation at rest and following nary artery is considered the gold standard as it best
dehydration (92, 93). These regulatory functions deterio- represents average internal human body temperature
rate with advancing age (94) and increase the risk of (116). As a catheter is needed to determine pulmonary ar-
developing hyperthermia and dehydration (84, 85, 93, tery temperature, body core temperature is often meas-
95, 96). However, fit older individuals retain a better abil- ured at more accessible and less invasive sites, such as
ity to thermoregulate and can improve thermoregulatory the mouth, axilla, aural canal, esophagus, intestine, or
capacity with training (97). In children, thermoregulatory rectum. Oral temperature is easy to determine given its
capacity has traditionally been viewed to be less effective accessibility. It is recommended to measure oral temper-
than in adults and thermal tolerance inferior during exer- ature under the tongue, as it may vary across different
cise under heat stress due to a higher body surface area- parts of the mouth (117). Factors such as salivation, previ-
to-mass ratio, diminished sweating capacity, lower me- ous food or fluid intake, gum chewing, smoking, and
chanical efficiency, and lower cardiac output (98–100). rapid breathing are known to impact oral temperature
These responses stem from adult-child differences in (118, 119). Hence, oral temperature may underestimate
morphology, as well as endocrine, metabolic, cardiovas- core temperature, making its measurement less reliable
cular, and thermoregulatory function. However, the view in dynamic conditions or when core temperature is ele-
that children are at a thermoregulatory disadvantage has vated. Assessing axilla temperature takes longer than
evolved in recent years, with the notion that they may other body locations as more time is needed to reach an
only be at greater risk of severe hyperthermia in extreme equilibrium. Ambient temperature, local blood flow,
environmental conditions (101–103). Methodological con- underarm sweat, and closure of the axillary cavity are
siderations such as normalizing physiological responses known to impact axilla temperature (118). Axilla tempera-
to body mass and surface area have been proposed ture typically underestimates core temperature and is
when comparing children and adults, to ensure an less accurate compared with measurements at other
unbiased comparison of size-dependent responses and body locations (120, 121), especially during fever or ele-
that both children and adults are exposed to similar rela- vated vasomotor activity. Aural canal or tympanic tem-
tive heat loss requirements (104). perature is easy to determine given its accessibility.
Earwax or dirt in the ear canal, inaccurate placement,
2.3.3.5. AEROBIC FITNESS. Regular endurance exercise and/or the influence of environmental conditions (heat
leading to improved aerobic fitness (i.e., V_ O2max) has or cold) are known to reduce the reliability of aural canal
been shown to enhance heat loss capacity. Aerobic temperature (122, 123). Moreover, infrared tympanic tem-
training activates cutaneous vasodilation at a lower core perature monitors, which are purported to measure tym-
temperature and increases skin blood flow for a given panic membrane temperature, more accurately reflect a
core temperature (105–107). The increase in skin blood combination of aural canal and tympanic temperature.
flow is largely mediated by the expansion of blood vol- Esophageal temperature is measured at the level of the
ume and greater cardiac output that characterize the left atrium and provides close agreement with pulmo-
trained state (108). Endurance training has also been nary artery temperature, as placement of the sensor is
reported to reduce the internal temperature threshold close to the aorta. Esophageal temperature rapidly
for the onset of sweating, increase sweat rate at a given responds to temperature changes (124), making it a pre-
core temperature, and increase maximal sweat rate ferred method for determining core temperature. The
(106, 109–113). Modeling suggests that an exercise train- disadvantage of esophageal temperature is its place-
ing-induced increase in V_ O2max of 12 to 17% should ment, which may cause general discomfort and irritation
reduce the internal temperature threshold for the onset of the nasal passage (125). Temperature readings may
of sweating by 0.1 C (114). However, the enhanced also be affected when ingesting cool fluids or saliva.
sweating function associated with aerobic fitness may Gastrointestinal temperature can be obtained using
also relate to regular endurance training providing a ingestible temperature capsules, which are a valid, reli-
repeated thermal challenge that leads to improvements able, and easily applicable surrogate marker of core
in thermoregulatory capacity (115). The impact of aerobic temperature (126–130). To allow gastric passage and
fitness on thermoregulation is further discussed in the avoid interference with fluid ingestion (131), capsules are
context of heat acclimation in sect. 6.1.4. generally ingested 5 h before measurement. However,
it has been shown that even 8 h after ingestion, consum-
2.4. Core and Skin Temperature Measurement ing chilled water (5–8 C) can decrease capsule temper-
ature by 2–6 C (132). This decrease has been attributed
Body core temperature can be measured at different to localized cooling of areas (i.e., small and large intes-
body locations, depending on the type of equipment tines) in close proximity to the stomach and duodenum.

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 PÉRIARD ET AL.

In contrast, when fluids are not consumed during exer- studies suggest that neuromuscular fatigue induced by
cise, the timing of ingestion (40 min or 24 h) does not abnormal spinal control of motor neurons is responsible
appreciably influence gastrointestinal temperature mea- for exercise-associated muscle cramps (151, 155). Although
surement (133). The time between ingestion and mea- the underlying mechanisms responsible for heat cramps
surement (1 to 12 h) also does not appear to affect the remain contentious, they are likely to be due to a combina-
difference (0.1–0.2 C) between capsule (i.e., gastrointes- tion of sodium depletion, dehydration, and/or neuromuscu-
tinal) and rectal temperature (134). The use of ingestible lar fatigue (156, 157).
temperature capsules is especially suitable for field- Heat syncope, or orthostatic intolerance, can occur
based conditions, which is important as exercise-induced when a person is exposed to high environmental
core temperature elevations are generally higher in field temperatures (158). Heat syncope often occurs after
compared with laboratory-based settings (135). Rectal prolonged standing, immediately following exercise
temperature measurement is considered an accurate cessation or after rapid assumption to an upright pos-
method for determining core temperature, as long as the ture after resting or being seated. It generally occurs
rectal thermistor is placed 10 cm beyond the anal during the initial phase of heat acclimatization (i.e.,
sphincter (136, 137). Rectal temperature is less sensitive to first 5 days), as heat exposure increases peripheral
rapid changes in core temperature, such as observed vasodilation and postural blood pooling, diminishes ve-
during exercise, compared with esophageal temperature nous return, and reduces cardiac output. Dehydration
(116, 138). However, rectal temperature is considered the and the intake of specific medications (i.e., diuretics) may
clinical gold standard for obtaining core body tempera- further increase the risk for heat syncope, whereas heat
ture in patients suspected of exertional heat stroke (139). acclimatization induced blood volume expansion may
Finally, to determine mean skin temperature, multiple reduce the risk. Athletes can experience lightheadedness
measurements sites should be measured (e.g., chest, but also lose consciousness, which is usually quickly
upper arm, thigh, and lower leg) (140). The reader is resolved after a period of sitting or lying down to restore
referred to a recent review on skin temperature measure- cerebral perfusion.
ments (141). Heat exhaustion is the inability to continue exercising
with a core body temperature that typically ranges
2.5. Exertional Heat Illness between 38.5 C and 40 C. Cardiac output cannot be
sustained during heat exhaustion due to competing
Exercise in the heat may increase the risk for developing demands for skeletal muscle blood flow, perfusion of
exertional heat illness (EHI) as heat production often vital organs, and heat loss via the skin. Heat exhaustion
exceeds heat dissipation capacity. While the thermophy- often occurs in hot and humid conditions and is charac-
siological responses to exercise in the heat are well terized by heavy sweating, malaise, fatigue, and dizzi-
understood, individual responses vary substantially ness. Nausea, vomiting, headache, fainting, weakness,
(142, 143), as does the risk for heat related illnesses. and cold or clammy skin may also be observed (159). As
Exertional heat illnesses represent a spectrum of medi- this condition worsens, it is difficult to distinguish it from
cal conditions related to an increase in body tempera- exertional heat stroke without measuring body core
ture (58, 144). The severity of EHI varies across its temperature and organ (dys)function. However, critical
continuum, with mild complaints following exercise- to the diagnosis of heat exhaustion is a normal mental
associated muscle cramps, to more serious concerns activity and a stable neurologic status (160). Widespread
during heat syncope and heat exhaustion, and life- peripheral vascular dilatation and associated central fa-
threatening risks during heat stroke (59, 145–147). tigue and collapse are thought to be responsible for
Exercise-associated muscle or heat cramps are an heat exhaustion. Pilgrims with heat exhaustion following
early indication of EHI and arise in the form of muscle multiday desert walking demonstrated tachycardia and
spasms or cramps, which are experienced as painful high cardiac outputs with signs of peripheral vasodilata-
contractions and often result in the inability to continue tion (161). Peripheral vasodilatation attenuates increases
exercising for a short time (148, 149). Muscle/heat in peripheral vascular resistance, which subsequently
cramps typically occur during or after excessive heat ex- results in hypotension, cardiovascular insufficiency, and
posure, when fitness and heat acclimatization state are high output heart failure (162).
relatively low, but training load (150) and exercise inten- Heat stroke is the most severe condition in the EHI
sity (151) are high. Sodium loss due to heavy and/or pro- spectrum and is associated with a core temperature
longed sweating is thought to play a significant role in >40 C, central nervous system dysfunction, and multior-
the etiology of muscle/heat cramps, leading to a con- gan failure (58, 163–165). Heat stroke is characterized by
tracted interstitial fluid compartment and neuromuscular a reduction in central venous pressure and an insufficient
junction hyperexcitability (152–154). However, other cardiac output to cope with the high thermoregulatory

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 EXERCISE UNDER HEAT STRESS

demands, which accelerate the rise in core temperature. heat strain. Classic heat stroke occurs under resting con-
The combination of circulatory collapse and high core ditions, without involvement of skeletal muscle heat pro-
temperature aggravates pathophysiological processes duction. In contrast, exertional heat stroke typically
(e.g., inflammatory responses) and can lead to multiorgan affects healthy individuals such as athletes, laborers
failure (166). An alternative pathway may lie with endotox- (e.g., firefighters and agricultural workers) and military
emia in response to exercise-induced immune and gas- personnel, who are involved in strenuous physical activ-
trointestinal disturbances (167). Exercise is known to ities or exercise in which metabolic heat production
acutely suppress immune function (168–170), and lipop- overwhelms physiological heat-loss mechanisms, lead-
oly-saccharides can leak into the circulation due to ing to uncompensable heat stress.
increased gut permeability (171–173). Endotoxemia may Several personal and environmental factors are asso-
subsequently trigger a systemic inflammatory response, ciated with an increased risk for EHI and exertional heat
leading to systemic coagulation and hemorrhage, necro- stroke. A recent systematic review summarized evi-
sis, and multiorgan failure. Heat stroke is a life-threatening dence from 42 studies and clustered risk factors into
condition and can be fatal unless promptly recognized subgroups (FIGURE 4) (143). The majority of EHI risk fac-
and treated. Signs and symptoms are often nonspecific tors were attributable to intrinsic factors pertaining to
and include disorientation, tachycardia, vomiting, seiz- lifestyle. Athletes experiencing exertional heat stroke of-
ures, loss of balance, and coma. In a later stage, rhabdo- ten performed similar exercise sessions (i.e., intensity
myolysis, circulatory failure, multiorgan failure, and diss- and duration) under comparable environmental condi-
eminated intravascular coagulation may occur and could tions, without having any problems or complaints (178,
lead to death (58, 158, 160). The risk of adverse outcomes 179). These observations suggest that (temporal) chan-
(i.e., morbidity and mortality) increases the longer core ges in risk factors (e.g., a combination of mild illness,
temperature remains >41 C and is significantly reduced lack of sleep, and previous day heat stress) increase the
if core temperature is lowered rapidly (174–176). Aggr- vulnerability to develop heat stroke on that specific
essive cooling is the cornerstone of heat stroke treat- occasion. These insights are important as these risk fac-
ment, and cooling rates >0.10 C·min 1 should be tar- tors and associated behaviors are modifiable, so com-
geted to improve prognosis (177). Heat stroke can be municating this information to athletes, laborers, and
distinguished as either classic (passive) or exertional, military personal working and exercising in hot and
depending on its cause. Both subtypes result from failure humid conditions is of vital importance. The fact that
to dissipate excessive heat, but their underlying mecha- exertional heat stroke remains the third leading cause of
nisms differ. Classic heat stroke usually develops in vul- death in athletes in the United States, following cardiac
nerable populations such as the elderly or individuals disorders and head and neck trauma (160, 180), further
with comorbidities (e.g., obesity, diabetes, hypertension, emphasizes the need for early recognition of EHI symp-
heart disease, renal disease, dementia, and alcoholism) toms by healthcare professionals, appropriate equip-
due to poor heat-dissipation mechanisms or attenuated ment to treat heat stroke victims (i.e., ice baths) and
behavioral mechanisms to reduce heat exposure and education of race participants. For this purpose,

Environmental factors Individual factors Work constraints Lifestyle factors Health factors

• High wet-bulb globe • Younger age • Intense physical work • Individual volition • Previous heat illness
temperature • Female sex • Exercise duration • Overweight / obesity • Vaccination within past 48 h
• Caucasian ethnicity • Inexperienced personnel • Low Fitness • Current sunburn
• Type II fiber • Air travel within past 24 h • Current smoking • Burns
predominance • Unacclimatized personnel • Alcohol intake in past 48 h • Medication use (e.g.
• Geographical region • Illicit drugs use antihistamines, painkillers)
• Clothing (combat gear) • Supplement use • Sickle cell trait
• Military division • Dehydration • Hypohidrosis
• Previous day heat stress • Malignant hyperthermia
• Lack of sleep • Altered cytokine production
• Poor nutrition (meal skipping • Sympathectomy
in past 24 h) • Mild illness (i.e. Diarrhea,
common cold, fever)

FIGURE 4. Risk factors for exertional heat illness classified in 5 subgroups: environmental, individual, work, lifestyle, and health. Adapted with permis-
sion from Westwood et al. (143).

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 PÉRIARD ET AL.

guidelines and recommendations have been developed rehydration, respectively. Importantly, euhydration is not
for those undertaking athletic events (58, 59, 181) and a static condition but reflected in a dynamic sinusoidal
performing occupational and military tasks (182–184). fluctuation of body water loss and gain (194). The daily
regulation of total body water and fluid concentrations is
a complex process influenced by dietary intake and nu-
3. BODY FLUID BALANCE trient availability with the loss of 1% in total body water
beyond normal fluctuation typically compensated for
3.1. Body Water Balance within 24 h in free-living individuals (195). This occurs
in response to highly controlled processes via which
Total body water volume represents 60% of body changes in plasma osmolality (i.e., electrolyte-water bal-
mass (range: 45 to 75%) (185–188) and is age and sex ance) stimulate body water conservation and acquisition
dependent, with lower values for the elderly and mechanisms. The homeostatic conservation of body
females (186, 189). Body water can be divided into intra- water is regulated by the release of arginine vasopres-
cellular and extracellular fluid compartments. The intra- sin, an antidiuretic hormone, and the acquisition of water
cellular compartment represents 40% of body mass, by the stimulation of thirst. The release of arginine vaso-
whereas the extracellular compartment can be segmented pressin from the posterior pituitary is triggered by an
into the interstitial (15% body mass) and intravascular (i.e., increase in plasma osmolality of 1–2% or a 10% reduc-
plasma volume, 5% body mass) subcompartments (186, tion in plasma volume (191, 196). The increase in circulat-
190). These fluid compartments are separated by water- ing arginine vasopressin activates the reabsorption of
permeable cell membranes that allow continuous fluid water from urine by the kidneys, the main effective regu-
exchange between compartments. As such, these vol- lator of water loss (197). The sensation of thirst is stimu-
umes are not static but represent the net effect of dynamic lated in response to an increase in plasma osmolality of
fluid exchange with varying turnover rates between com- 5 to 10 mosmol/kgH2O and decrease in blood volume of
partments. Perturbations in fluid balance during exer- 10% (191, 198–200). The osmolality and volume pertur-
cise or heat exposure modify the net volumes and bations required to elicit these compensatory responses
turnover rates between fluid compartments. However, depend on the nature (i.e., intracellular vs. extracellular
the continuous exchange of fluid between compart- hypohydration) and magnitude of body water losses.
ments, driven by osmotic and oncotic gradients and Clinically, hypohydration refers to a state of hypertonic
hydrostatic pressure, promotes the maintenance of hypovolemia, which follows the net loss of hypo-osmotic
fluid balance. Human fluid balance is also regulated body water, causing a rise in extracellular tonicity (201).
by the renin-angiotensin-aldosterone system (RAAS) During such hypohydration, a shift in water from intracel-
in response to a decrease in blood pressure due to lular to extracellular compartments occurs to equilibrate
the loss of blood volume. RAAS functions to elevate osmolality between compartments, leading to intracellu-
blood volume and arterial pressure by increasing so- lar hypohydration and a rise in plasma osmolality (202,
dium and water reabsorption in the kidneys. The first 203). This triggers the osmoreceptor and endocrine
stage of RAAS is the secretion of renin into the circula- mediated cascade to conserve and acquire water. In
tion by juxtaglomerular cells when renal blood flow is contrast, extracellular hypohydration occurs when the
reduced. Circulating renin acts to cleave angiotensi- concentration of body water lost is iso-osmotic relative
nogen to angiotensin I, which is then converted into to plasma (i.e., isotonic hypovolemia), causing a contrac-
angiotensin II by angiotensin-converting enzyme. tion of the extracellular compartment, which cannot mobi-
Angiotensin II is a strong vasoconstrictor and stimu- lize water from the intracellular compartment, leaving
lates the secretion of aldosterone from the adrenal plasma osmolality unchanged. The water conservation
cortex. Aldosterone accelerates the reabsorption of and acquisition responses associated with extracellular
sodium in the kidneys and the retention of water in hypohydration are thus nonosmotic and comprise of
the circulation, which restores fluid balance. For a acute peripheral and renal vasoconstriction, along with
comprehensive description of the RAAS, including its the nonhumoral defense of blood volume (202, 204).
molecular working mechanisms, the reader is referred From a clinical perspective, the magnitude of dehydration
to Refs. 191–193. in relation to body mass loss is defined as mild (<5%),
Euhydration represents the state of being in water moderate (5–10%) and severe (>10%) and in relation to
balance, whereas hypohydration is the state of being osmolality as isotonic (275–295 mosmol/kgH2O), hypo-
in negative water balance (i.e., water deficit) and hyper- tonic (<275 mosmol/kgH2O), and hypertonic (>295 mos-
hydration the state of being in positive water balance mol/kgH2O) (TABLE 1) (206, 207). However, from a
(i.e., water excess). The processes of losing and gain- physical activity perspective lower levels of dehydration
ing body water are referred to as dehydration and have implications on exercise capacity and performance,

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Table 1. Classification of dehydration types with potential source of development

Type of Dehydration Divergence from Euhydration Potential Source

Isotonic Isotonic loss of water and sodium from extracellular fluid Gastrointestinal fluid loss (e.g., vomiting, diarrhea)
No osmotic water shift from intracellular fluid Inadequate fluid and electrolyte (e.g., sodium) intake

Hypertonic Water loss exceeds sodium loss Inadequate water intake

Osmotic water shift from cells to extracellular fluid Sweat loss
Osmotic diuresis (e.g., glucosuria)

Hypotonic Sodium loss exceeds water loss Sweat and/or gastrointestinal fluid loss
Osmotic water shift from extracellular fluid to cells Water replacement without electrolyte replacement
Diuretic therapy following excessive water intake

Adapted with permission from Ref. 205.

such that mild, moderate and severe dehydration can be secretion of arginine vasopressin to restore plasma os-
considered <3%, 3–6%, and >6% body mass loss, molality (217). It is important to note that factors associ-
respectively (see also sect. 5). ated with exercise can also stimulate arginine vaso-
pressin secretion and thirst sensation (see sect. 3.4).
While these processes ensure fluid retention during fluid
3.2. Body Water Balance during Exercise loss, the opposite responses can be expected during
hyperhydration (i.e., decreased arginine vasopressin con-
Acute exercise produces an increase in systolic and centration and increased urine secretion). The loss of
mean arterial pressure, resulting in higher capillary body water also occurs through CO2-O2 gas exchange
pressure, greater capillary filtration, and an associ- and respiratory water loss, which are dictated by exercise
ated net outward fluid shift from intravascular to intensity. These volumes are compensated for by meta-
extravascular compartments (i.e., interstitial and intra- bolic water production during metabolism (i.e., substrate
cellular) (208–210). Exercise-induced increased con- oxidation), and their overall impact is quite small (1%)
centrations of lactate, sodium, potassium, and (218, 219).
phosphate increase extravascular osmolality and Drinking behavior, drink to thirst or to a fluid
stimulate intravascular to extravascular fluid shifts replacement strategy, to maintain hydration status
(208, 211, 212). In contrast, increases in lymphatic flow and performance during exercise is complex and
enhance fluid shifts from the interstitial to intravascu- remains an area of contention within the literature
lar compartment, and elevated hydrostatic pressures (see sect. 5.6). While drinking to thirst is appropriate in
in the contracting muscles stimulate fluid shifts to- many settings, it traditionally has not been considered
ward the intravascular compartment (213). A balanced a good indicator of body water needs during exercise
state between outward and inward plasma flow may in the heat at elevated sweat rates, as ad libitum water
ultimately occur during exercise, which limits the net consumption often results in incomplete fluid replace-
fluid shift (214). Exercise also stimulates cutaneous water ment or voluntary dehydration (194, 220–226). The
loss through the formation of sweat for evaporative heat notion of voluntary dehydration, however, has been
dissipation. Sweat rate during exercise is regulated by the subject of further analysis (188, 227, 228). Drinking
several factors, including exercise intensity and duration, behavior and fluid replacement are influenced by
age, sex, training, and heat acclimatization status, cloth- physiological, psychosocial, and environmental fac-
ing, and environmental characteristics (i.e., air tempera- tors, experience and expectations, as well as issues
ture, humidity, wind velocity, and cloud cover). related to fluid palatability, food intake, and gastric
Sweat is an example of hypo-osmotic fluid loss, so distension/discomfort (229–231). It has also been sug-
volume depletion caused by excessive sweating results gested that heat acclimation improves the relationship
in a proportionally increased plasma osmolality (215). of thirst to body water needs by reducing the time to
Plasma hyperosmolality acts to mobilize fluid from the in- first drink, increasing the number of drinks consumed
tracellular to the extracellular compartment to restore per heat exposure, and increasing mean volume per
the plasma volume in hypohydrated individuals (216). If drink (225, 232), reducing voluntary dehydration by
the reduction in plasma volume exceeds 10%, changes 30% (223, 224, 233). Ultimately, fluid balance during
in arterial pressure are detected by baroreceptors in the exercise is a dynamic process influenced a several
carotid sinus, aortic arch, left atrium, and great pulmo- integrative factors. An overview of current hydration
nary veins, resulting in the sensation of thirst and guidelines is presented in sect. 5.4.

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3.3. Sodium Balance however, do not preclude impairment in cognitive func-

tion at greater levels of sustained hypohydration. Exe-
Sodium is the major determinant of plasma osmolality, rcise-induced dehydration may also increase the risk for
which is an essential regulator of arginine vasopressin postexercise hypotension (246), due to decreased car-
secretion and thirst perception. Under normal conditions, diac baroreflex sensitivity (247), which may subsequently
plasma sodium concentration is regulated between 135 lead to syncope or collapse after the cessation of exer-
and 145 mmol·L 1 (234). The regulation of sodium, how- cise (248).
ever, must be integrated with the regulation of plasma vol- Some athletes intentionally dehydrate for competi-
ume, because changes in water volume alone have tion. For example, weight category sports, such as wres-
diluting or concentrating effects on bodily fluids. tling, judo, boxing, taekwondo, and mixed martial arts,
Aldosterone, a steroid hormone that is produced by apply rapid weight loss interventions before competition
the adrenal cortex, plays a central role in sodium weigh-in. A combination of dietary restriction and sweat-
regulation. Changes in plasma osmolality are dir- induced fluid depletion by heat exposure and/or exer-
ectly sensed in the adrenal cortex, resulting in aldo- cise in vapor impermeable clothing are often employed
sterone inhibition or secretion during increased or (249–251). Although precompetition rapid weight loss is
decreased osmolality, respectively (235). During an effective way to increase the probability of competi-
hyperosmotic dehydration, more water than sodium tive success (252), rapid rehydration is needed to allow
is lost, resulting in an increase in plasma osmolality for optimal exercise performance. A systematic review
(TABLE 1). The inhibition of aldosterone release of 4,432 combat sport athletes reported hypohydration
causes less sodium to be reabsorbed in the distal levels of up to 10% body mass loss before weigh-in
tubule of the kidney nephron (236). Simultaneously, (253). Another study found that on the morning of com-
the increased osmolality causes the secretion of ar- petition, >40% of combat athletes were hypohydrated
ginine vasopressin, leading to water conservation in based on a urine sample, highlighting the short time allo-
the kidneys. The net effect is a decreased amount of cated to restore fluid balance and the risk associated
excreted urine, with an increase in urine osmolality. with entering competition with suboptimal mental and
These responses are complementary to restore so- physical performance capacity (254).
dium concentration and plasma osmolality. Exercise-induced dehydration induces intracellular and
extracellular fluid loss in proportion to the loss of water and
3.4. Fluid and Sodium Disorders solutes. Given the hypotonic concentration of sweat rela-
tive to plasma (255), the reduction in plasma volume indu-
The evaporation of sweat plays a central role in heat dis- ces an increase in electrolyte concentration (i.e., hypertonic
sipation during exercise and/or passive heat exposure. hypovolemia). Hypernatremia is an example of a hyper-
Although sweating-induced water loss can be counter- tonic hypovolemic electrolyte disorder and is defined by a
acted by increased fluid consumption and activation of plasma sodium concentration 145 mmol·L 1 (256, 257).
the RAAS, most individuals do not fully compensate their The prevalence of postexercise hypernatremia is relatively
fluid loss (194, 226, 237–239). Dehydration during pro- common among endurance athletes (>25%) given its
longed exercise in warm and hot environments impacts direct relationship with exercise-induced dehydration (258,
on thermoregulatory function and performance (see 259). Hypernatremia was also observed among 30–40%
sect. 5) and can lead to health issues. Acute dehydration of swimmers performing a short (1 min) maximal exercise
is associated with decreased glycemic regulation, wors- bout, probably due to a shift of hypo-osmotic fluid from the
ened mood, blunted blood pressure control, reduced extracellular to the intracellular compartment as exercise
cerebral blood flow during sympathoexcitation, and or- duration was too short to induce substantial fluid losses
thostatic intolerance (240). Although it is generally (260). While mild levels of hypernatremia do not lead to se-
accepted that a compromise in hydration status of 2% rious clinical symptoms, acute and severe levels of hyper-
body mass is detrimental to some aspects of cognitive natremia (>158 mmol·L 1) are associated with hyperpnea,
function (i.e., attention, psychomotor performance and restlessness, lethargy, and even coma (261).
working memory) (241–243), a recent meta-analysis To avoid the risk of hypohydration, some athletes drink
found cognitive performance not to be impaired by too much during endurance exercise events causing a dilu-
hypohydration of 2% (range: 1.2 to 4.2%) (244). A tion of circulating electrolytes (i.e., hypotonic hypervolemia).
recent systematic review also reported an inconsistent Hyponatremia is defined by a plasma sodium concentra-
effect of dehydration within 1 to 3% of body mass loss on tion of 135 mmol·L 1 or less (262), primarily due to an
cognitive function, with only 13 of 26 studies demon- increase in total body water relative to the amount of total
strating a negative influence on working memory, inhib- body exchangeable sodium. Hyponatremia can be asymp-
itory control and attention (245). These findings, tomatic or symptomatic. Asymptomatic hyponatremia has

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largely been detected in research studies collecting post- status such as osmolality, specific gravity, and color
exercise blood samples in athletes, whereas symptomatic require measurement techniques that are more cost
hyponatremia presents with mild, nonspecific symptoms effective and offer faster response times than plasma
(i.e., lightheadedness, nausea) (263–265) or more typically osmolality. Urine samples are typically evaluated as
with headache, vomiting, and/or altered mental status (i.e., first morning void or over a 24-h period, as well as im-
confusion, seizure) resulting from cerebral edema, which mediately before and after exercise. However, uri-
may progress to death (262, 266–269). Athletes with nary indexes may not accurately reflect hydration
symptomatic hyponatremia should be immediately treated status before or following exercise in situations of rapid
with hypertonic saline to reduce brain edema (267, 270, (re)hydration and isotonic and hypotonic hypohydration
271). Together with heat stroke, exercise associated hypo- (195, 283). Hydration status may also by underestimated
natremia is the most dangerous disorder for an athlete. The from urinary indexes during rapid (re)hydration following
incidence of asymptomatic hyponatremia varies widely hypertonic hypohydration incurred via sweating, as signif-
across sporting disciplines (272–274) and is dependent on icant urine production may already be occurring before
the type and duration of activity, location of the event, fluid retention responses are well activated. Although
athlete characteristics, and heat or cold exposure. Sym- urine osmolality analyzed using freezing point depression
ptomatic hyponatremia is rare, with 1% incidence in 2,135 is considered the most accurate measure of urine con-
endurance athletes (compared with 6% asymptomatic centration, it is subject to considerable (30%) day-
hyponatremia) (275) and 0.1% incidence among 669 ultra- to-day biological variations, even when nutritional
marathon runners (276). Smaller individuals and those exer- intake and exercise are controlled (282). Freezing
cising at a slower pace are more prone to develop hypona- urine samples may also alter the reliability of chemi-
tremia (267), probably due to the relatively larger drinking cal analysis techniques (284, 285) as it generates
volume-to-plasma volume ratio and increased time to urinary sediments (e.g., endogenous calcium oxa-
ingest fluid during exercise, respectively. Nonosmotic argi- late dehydrate and amorphous calcium crystals)
nine vasopressin secretion is a key contributing factor to (285). This may indicate why urine osmolality de-
hyponatremia, as elevated arginine vasopressin concentra- creases after freezing and thawing when determin-
tions stimulate the reabsorption of water from the kidneys, ing it with freezing point depression but not with re-
thereby further disturbing the balance between excessive fractometry (286).
fluid intake and fluid loss. Examples of arginine vasopressin Hydration status is difficult to accurately determine
stimuli associated with exercise include nausea/vomiting from single samples (287) and thresholds between
(277), interleukin-6 release (278), plasma volume contrac- euhydration and hypohydration difficult to establish. For
tion (279), hypoglycemia (280). and elevated body temper- example, hypohydration has been suggested to occur at
ature (281). a urine osmolality of 586 (288), 716 (289), 830 (290), and
1,052 mosmol/kgH2O (291). Urine concentration esti-
3.5. Hydration Status mated by specific gravity evaluates the ratio of the den-
sity of urine to that of pure water at a constant
The fundamental principles of body water regulation temperature. It can be measured directly via gravimetry
provide the framework for using plasma osmolality as an and indirectly using the refractive index (i.e., refractome-
index of hydration status (186). A reduction in total body try) or by change in pH of a polyelectrolyte (i.e., reagent
water reduces both intracellular and extracellular vol- strip). Although urine specific gravity via refractometry
ume. Since sweat is hypotonic relative to plasma, exer- has been suggested to correlate with urine osmolality
cise-heat stress-mediated hypohydration induces plasma (287, 291, 292), others have shown that this relationship
hypertonicity and hypovolemia that are proportionate to is not strong (293). Indeed, urine specific gravity is a
the water deficit (201). While there currently exists no con- technically less accurate method as it is influenced by
sensual gold standard to evaluate hydration status (185, both the number and molecular mass of solutes such as
195), plasma osmolality is considered under static hydra- glucose, protein and urea, temperature, pH, and age,
tion conditions to be the most precise and accurate whereas urine osmolality is affected only by the number
hydration assessment technique (185, 282). However, the of particles (294, 295). Reagent strip urine specific grav-
measurement of plasma osmolality via freezing point ity was shown to correlate with urine osmolality but not
depression or vapor pressure depression osmometry as strongly as with refractometry due to changes in pH
requires invasive (i.e., venipuncture) sampling techniques (296). In pathological specimens, a weak correlation
and expensive analysis equipment. Alternatively, urine exists between urine osmolality and urine specific
concentration reflects the renal response to alterations in gravity measured by reagent strip in acidic or alkaline
plasma osmolality and is typically well correlated with urines and those with elevated glucose, bilirubin, urobi-
plasma osmolality (195). Urinary indexes of hydration linogen, protein, and ketones. Similarly, urine specific

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 PÉRIARD ET AL.

gravity measured by refractometry correlates poorly

with urine osmolality in the presence of hemoglobin, Body mass
Morning body mass
ketones, or bilirubin (296). Among the urinary markers, within 1%
urine color is probably the least sensitive marker (195).
Another potentially viable and less invasive pathway Urine Thirst
LIKELY LIKELY
for monitoring hydration status lies with saliva and tear indices VERY sensation
osmolality, relatively accessible fluids. Saliva osmolality Specific gravity <1.020 LIKELY Not thirsty
Osmolality <700 mosmol/kgH2O
has been suggested to track acute hydration changes Color <4 units LIKELY
during hypertonic hypovolemia as sensitively as urine
osmolality (297). However, a lack of correlation between
saliva osmolality and urine osmolality and specific grav-
ity has also been shown during multiday events (298).
Urine color chart
The large inter- and intraindividual variability in saliva
1
osmolality measurements reduce its accuracy (195).
2 Euhydration
Although tear osmolality was shown to increase with
dehydration and track alterations in plasma osmolality, 3
as well as provide comparable results to urine specific 4
gravity (299), additional validation research is required. 5 Hypohydration
Bioelectrical impedance analysis of body water is a non- 6
invasive technique based on the resistance of a low am- 7 Severe
perage current (single or multiple frequencies) passed 8 hypohydration
between skin electrodes, whereas the resistant magni-
tude varies inversely with tissue water and electrolyte
FIGURE 5. Daily hydration status assessment and monitoring dia-
content. Although bioelectrical impedance analysis is
gram. The diagram combines relatively simple markers of hydration
validated in euhydrated individuals, its application is of status: morning body mass, 1st morning urine void, and subjective
less use in dynamic conditions and with dehydrated indi- thirst. As a single marker fails to provide adequate evidence for
viduals (186, 300, 301). hydration status, the combination of 2 markers provides a likely indi-
cation of hypohydration and the convergence of all 3 provides a
Given the difficulty in establishing hydration status very likely indication of hypohydration. Adapted with permission
due to measurement artifacts and precision discrepan- from Refs. 302, 303.
cies between assessment techniques, it has been sug-
gested to evaluate and monitor hydration status on a conditions, and the consequent reduction in time to
daily basis to establish personalized reference ranges exhaustion during constant work rate exercise (305–
according to a set of relatively simple indexes (FIGURE 309), or progressive decrease in work rate during self-
5) (302–304). These include changes in morning body paced exercise (i.e., time trial) (310–317). Maximal aero-
mass following first morning void, urinary indexes from bic power (i.e., V_ O2max), a key determinant of endurance
first morning void, and the sensation of thirst. While the performance (318), is also compromised under heat
lack of thirst sensation does not necessarily represent stress, in line with the severity of the environmental con-
euhydration, the presence of thirst is indicative of hypo- ditions and initial thermal strain (i.e., core and skin
hydration. The regular use of this approach will allow for temperature) (319–323). The development of hyperther-
developing personalized metrics regarding hydration mia-induced fatigue is complex, with performance
thresholds and provide a more robust diagnosis of hydra- impairments involving the interplay of several physiolog-
tion status. ical systems (146, 201, 324–327). The foremost mecha-
nisms associated with impaired aerobic exercise under
heat stress are linked to hyperthermia-mediated altera-
4. HEAT STRESS AND AEROBIC EXERCISE tions in cardiovascular, central nervous system (CNS)
PERFORMANCE and skeletal muscle function (FIGURE 6). The physiolog-
ical responses associated with these alterations impact
Prolonged high-intensity exercise is markedly impaired on perceptual responses, which can also affect perform-
by an increase in the severity of the thermal environ- ance by influencing motivation and the willingness to
ment, which is determined by the combination of ambi- continue exercising in the heat. This section will exam-
ent temperature, absolute humidity, solar radiation, and ine how skin, muscle, and cerebral blood flow are
wind velocity (see sect. 2). The impairment is character- affected during exercise in heat, describe the influence
ized by the exacerbated development of whole of hyperthermia on central neural drive and skeletal
body hyperthermia, relative to exercise in temperate muscle function and metabolism, outline the influence of

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 EXERCISE UNDER HEAT STRESS

EEG activity: ↓ attentional processing, ↓ arousal

CNS drive: ↓ voluntary activation
• Inability (motor unit excitability)
• Unwillingness (motivation)
Systemic: ↑ HR, ↓ SV, ↓ Q, ↑ a-vO2diff, ↓ VO2max Metabolism: ↑ CHO oxidation,
Perception: ↑ effort & ↑ exertion ↑ metabolite accumulation (H+, Pi)
Skin: Narrowing Tc-to-Tsk gradient, ↑ SkBF
Neural: ↑ group III & IV muscle afferents
Muscle: ↓ muscle blood flow near HRmax & VO2max
• ↑ inhibitory feedback
Brain: ↓ blood flow, ↑ a-vO2diff • Circulatory & ventilatory response
regulation

↑ Whole-body temperature

FIGURE 6. Schematic representation of the impact of exercise in the heat on cardiovascular, central nervous system (CNS) and skeletal muscle func-
tion associated with fatigue development. The rise in whole body (core, skin and muscle) temperature during exercise in the heat leads to a narrowing
core-to-skin temperature (Tc-to-Tsk) gradient and a reflex increase in skin blood flow (SkBF), which contribute to increase heart rate (HR). As thermal
strain develops, V_ O2max progressively decreases while perceived exertion increases for any given work rate. When prolonged self-paced exercise is
performed, the combination of increased thermal, cardiovascular and perceptual strain leads to a reduction in work rate. During constant work rate
exercise muscle blood flow is well maintained until HR reaches 95% of maximum (90% V_ O2max). At this point, cardiac output (Q) _ becomes compro-
mised as stroke volume (SV) markedly decreases, resulting in volitional exhaustion, despite an increase in arterio-venous oxygen different (a-vO2diff).
Blood flow to the brain is compromised at elevated exercise intensities with hyperthermia; however, the metabolic rate of oxygen is preserved. Despite
this preservation, brain activity [encephalography (EEG)] alterations occur in areas associated with the ability to inhibit conflicting attentional processing
and the capacity to sustain mental readiness and arousal. Hyperthermia also influences CNS function during maximal voluntary contractions, by sup-
pressing voluntary activation, either through an inability or unwillingness to contract exercising muscles. Occlusion of blood flow during such contrac-
tions increases muscle temperature and metabolite concentration, which alter motor unit excitability and impact on the perception of effort. Increased
1
muscle temperature also enhances carbohydrate (CHO) oxidation and metabolite (H , hydrogen ions; Pi, inorganic phosphate) accumulation during
high-intensity dynamic exercise. The increase in metabolic and mechanical disruption stimulates group III/IV muscle afferents, which provide inhibitory
feedback to the CNS and contribute to regulate circulatory and ventilatory response.

thermal strain on V_ O2max, prolonged constant work rate regulatory demands they ever face: the competition
and self-paced exercise, and examine the mechanisms between skin and muscle for large fractions of cardiac
linked to fatigue development under heat stress. output.” The concept of competition or conflict between
regulatory systems has also been suggested to represent
4.1. Adjustments in Cardiovascular Function commensalism, which is an integrated balance of regula-
tory control where one circulation benefits without sub-
Lee and Scott (328) postulated over 100 yr ago that circu- stantially affecting the other (330). Notwithstanding, the
latory adjustments contribute to limit work capacity in the development of thermal strain during exercise under heat
heat by “drafting blood away from the brain and the stress provides a robust challenge to the cardiovascular
muscles to the skin.” The cardiovascular response to pro- system, with fatigue linked to adjustments in blood flow
longed aerobic exercise in the heat includes a redistribu- to the skin, active muscles, and the brain.
tion of blood to cutaneous vascular beds for the purpose
of heat dissipation, coupled with the maintenance of per- 4.1.1. Skin blood flow.
fusion pressure and oxygen delivery to exercising
muscles. As highlighted by Rowell (329), this “forces An increase in skin temperature when exposed to envi-
humans to deal with the two most powerful competing ronmental heat stress leads to a rise in skin blood flow

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 PÉRIARD ET AL.

mediated by peripheral (i.e., local endothelial, adrener- with rest. This response is exacerbated when exercising
gic and sensory response) (331) and central (i.e., sys- in cool compared with hot environmental conditions, as
temic thermoregulatory response) pathways (332). The lower skin temperatures suppress the active vasodilator
rise in skin blood flow acts to transfer more blood from response to increasing internal temperature, thereby
the central circulation toward cutaneous vascular beds, raising the temperature threshold for vasodilation (345).
where under favorable thermal gradients dry heat loss Factors such as time of day (346), menstrual cycle phase
can occur. Once sweating is initiated, skin blood flow in females (347), and plasma osmolality (348, 349) have
serves to deliver heat to the skin where it is removed also been shown to influence the onset threshold for cu-
through evaporation. Skin temperature therefore fluctu- taneous vasodilation.r
ates in response to the balance between changes in The magnitude of the skin blood flow response dur-
blood flow and sweat evaporation (333, 334). When ing exercise-heat stress is mediated by the core-to-skin
moderate to high-intensity exercise is initiated, a vaso- temperature gradient, with a narrowing of the gradient
constrictor-mediated reduction in skin blood flow occ- leading to a reflex increase in skin blood flow (345,
urs, which contributes to provide additional blood to 350–352). Central (i.e., visceral and brain) thermorecep-
working skeletal muscles (335, 336). Shortly thereafter, tors provide a stronger thermoregulatory drive for
cutaneous vasodilation is initiated to aid in the dissipa- increasing skin blood flow at any temperature gradient
tion of metabolically generated heat. Splanchnic and re- than peripheral (i.e., skin) thermoreceptors. A 1 C
nal vasoconstriction can contribute 600 to 800 mL·min 1 increase in skin temperature accounts for 10 to 30% of
of blood to this response (337, 338). The internal tem- the thermoregulatory drive for cutaneous vasodilation
perature threshold at which active cutaneous vasodila- and sweating, whereas a 1 C increase in internal temper-
tion occurs is linked to exercise intensity, with an ature mediates 70 to 90% of the response (41, 353, 354).
increase in work rate delaying the threshold relative to It must be acknowledged, however, that changes in skin
rest (FIGURE 7) (340–344). The shift in threshold for cu- temperature are often larger than those of the core dur-
taneous vasodilation during exercise results in a lower ing exercise in the heat, providing changes in skin tem-
skin blood flow for a given core temperature compared perature significant influence on the thermoregulatory
drive for cutaneous vasodilation and sweating. Under
uncompensable heat stress where evaporative capacity
100 is limited and ambient temperature is high, the core-to-
Rest
skin temperature gradient may be reversed with skin
Dynamic exercise temperature increasing above that of the core. In such
conditions, an increase in skin blood flow would lead to
75
an increase in core temperature through convective
Skin blood flow (% of maximum)

heat gain (338), effectively compromising thermoregula-

tion (330).
C
During prolonged exercise in the heat, the rate of rise
in skin blood flow markedly decreases after 20–30 min,
50 particularly when core temperature approaches 38 C,
reaching a virtual plateau at 50 to 60% of maximum flow
capacity (FIGURE 7) (339, 351, 355). The reduced rate of
rise in skin blood flow is attributable to an attenuation of
vasodilator activity, as active vasoconstriction is progres-
25
B sively withdrawn with exercise (356). The plateauing
effect occurs in response to the perfusion requirements
A of exercising muscles (357–359) and circulatory regula-
tion (i.e., cardiac output and arterial blood pressure)
(360, 361) taking precedence over thermoregulatory
36.5 37 37.5 38
control.
Core temperature (ºC)
An increase in skin temperature has been suggested
FIGURE 7. Skin blood flow response to hyperthermia at rest and to mediate fatigue during submaximal aerobic exercise
during dynamic exercise. The response is influenced by cutaneous
under stress. The development of fatigue is purported
vasoconstriction at the onset of exercise (“A”), a shift in the core tem-
perature threshold for initiating cutaneous vasodilation (“B”), and a to stem from the greater skin blood flow and cutaneous
leveling off, or plateau, at 50-60% of maximum skin blood flow above venous compliance associated with hot skin and the
a core temperature of 38  C (“C”). Redrawn with permission from concomitant increase in cardiovascular strain (i.e., incr-
González-Alonso et al. (339) and Kenney et al. (330).
eased heart rate and decreased stroke volume

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 EXERCISE UNDER HEAT STRESS

compromising the maintenance of cardiac output and redistribution to the periphery on cardiovascular func-
blood pressure under heat stress) (362–364). This pre- tion and exercise capacity and performance in the heat,
mise is supported by early findings that a rapid lowering which reiterates the intimate relationship between ther-
of skin temperature restored work capacity following moregulation and circulatory function.
volitional fatigue, in response to a reduction in heart rate
(365, 366). A more recent study from Ely et al. (367) 4.1.2. Skeletal muscle blood flow.
demonstrated that 17% less work was performed dur-
ing a 15-min self-paced cycling task in 40 C compared Skeletal muscle blood flow requirements during physical
with 20 C conditions. The impairment was linked to the activity are linked to exercise intensity, with an increase
higher skin temperature (5 C) and heart rate (10 in oxygen demand matched by an increase in oxygen
beats·min 1) during the time trial in hot conditions, as delivery and perfusion pressure (375–377). The regula-
end exercise core temperature was similar between tri- tion of these circulatory responses is mediated by an
als (38.2 C). This corroborates previous observations increase in muscle sympathetic nerve activity (378, 379)
of a 6.5% lower mean power output in elite cyclists and functional sympatholysis (i.e., inhibition of sympa-
undertaking a 30-min time trial in 32 C compared with thetically-mediated vasoconstriction in active muscles)
23 C conditions (316). The impairment occurred in con- (380, 381). Elevated tissue and blood temperatures also
junction with the maintenance of a higher skin tempera- contribute to increase active muscle blood flow through
ture (6 C) and heart rate (4 beats·min 1) in the hotter metabolic and thermal stimuli inducing the release of
condition, as well as a higher rating of perceived exer- erythrocyte-derived adenosine triphosphate (ATP), a
tion, despite core temperature increasing at a similar potent vasodilator (382–384). Muscle blood flow in
rate during the trials (FIGURE 8). These decrements in trained individuals can reach 3 to 4 L·kg 1·min 1 during
self-paced exercise performance are supported by stud- maximal exercise with a small muscle mass (e.g., fore-
ies in which volitional exhaustion during constant work arm and isolated leg) (385). These high levels of blood
rate exercise in uncompensable heat stress (e.g., when flow are not attained, however, when performing whole
wearing encapsulated protective ensemble) coincided body maximal exercise (e.g., cycling, running and row-
with an elevated skin temperature and marked cardio- ing) (386, 387) as the cardiac output required to perfuse
vascular strain, yet relatively low core temperatures active skeletal muscles (estimated as 15 kg from a total
(<38.5 C) (368–371) compared with studies without arm and leg muscle mass of 25–28 kg) would exceed
encapsulation (>39 C) (363, 372–374). Others have 45 L·min 1, which is beyond cardiac pumping capacity,
also demonstrated exhaustion to occur earlier when even for elite endurance athletes (378, 388, 389). The
skin temperature was elevated using a water-perfused limits imposed on the ability to increase cardiac output
suit, despite similar core temperatures and heart rates at during whole body maximal exercise are mediated by
exhaustion (363, 364). These observations highlight the arterial and cardiopulmonary baroreflexes, as well as
impact of a skin temperature-mediated blood volume muscle metaboreflexes, which increase peripheral

450 200
Heart rate (beats·min-1)

Cool
*
Power output (W)

Warm 195
400
190
* * *
350 * 185
* FIGURE 8. Power output, heart rate, rec-
180 * tal, and skin temperature during a 30-min
300 cycling time trial in Hot [32 C and 60% rela-
175 tive humidity (RH)] and Cool (23 C and 60%
250 170 RH) conditions in elite road cyclists. These
data highlight the impact of an elevated skin
temperature on exacerbating the cardiovas-
39.5 36
cular response, characterized by an ele-
Rectal temperature (°C)

Skin temperature (°C)

34 vated heart rate, despite the maintenance

39.0 * * * * * * of a lower work rate (i.e., power output)
32 and similar rectal temperature. Significant
38.5
30 difference between conditions (P < 0.05).
38.0 Redrawn with permission from Tatterson et
28 al. (316).
37.5 26

37.0 24
0 5 10 15 20 25 30 35 0 5 10 15 20 25 30 35
Time (min) Time (min)

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 PÉRIARD ET AL.

resistance by augmenting sympathetic activity and flow, along with oxygen delivery, matched the rise in ox-
restricting hyperemia in the active musculature (339, ygen uptake from 50 to 90% V_ O2max during incremental
390–395). This circulatory control mechanism prevents exercise. However, beyond 90% V_ O2max a levelling off in
muscle vascular conductance from reaching unsustain- oxygen delivery occurred that attenuated the rate of rise
ably elevated levels that would significantly compromise in oxygen uptake, despite maximal increases in arterio-
the regulation and maintenance of arterial blood venous oxygen difference (a-vO2diff) and heart rate
pressure. (FIGURE 9). These findings were corroborated during
During submaximal exercise under heat stress, the supramaximal intensity cycling, and despite the greater
increased requirement and displacement of blood flow metabolic energy requirements of such exercise, pla-
to cutaneous vascular beds provides a significant chal- teaus in cardiac output and muscle vascular conduct-
lenge to the cardiovascular system, which must also ance were noted at similar levels of oxygen delivery to
maintain skeletal muscle perfusion and oxygen delivery that of maximal exercise (400). These observations indi-
(338, 396). Nevertheless, muscle blood flow can be cate an inability of the cardiovascular system to sustain
maintained during prolonged submaximal exercise in a linear increase in oxygen delivery to exercising
the heat (357, 372, 397, 398). In one of the first studies muscles, which under heat stress occurs at a lower
to examine exercising muscle blood flow in the heat, absolute work rate due to an accelerated decline in car-
Savard et al. (358) manipulated skin temperature with a diac output and mean arterial pressure, leading to a
water-perfused suit during one-legged knee extension decrease in V_ O2max. Although the relatively brief and
(20–25% V_ O2max) and two-legged cycling (50–60% intense nature of maximal and supramaximal exercise in
V_ O2max). Both exercise modalities were performed dur- the heat may be more conducive to reaching cardiovas-
ing three consecutive 25-min bouts of exercise where cular limitations, motivated individuals have also been
no water, hot water (45 C), and cold water (2 C) circu- shown to reach such limitations during prolonged sub-
lated through the suit, respectively. The authors reported maximal exercise to exhaustion (309, 363, 374, 401). For
that when additional heat stress was imposed from 25 example, a manipulation of starting esophageal temper-
to 50 min, blood flow to active skeletal muscles was main- ature (35.9, 37.4, and 38.2 C) during exhaustive cycling
tained in both exercise modalities. Others have also at 60% V_ O2max in 40 C led to a similar final heart rate:
demonstrated an uncompromised cardiac output and 98–99% of maximum (363). The increase in heart rate,
maintained skeletal muscle blood flow during prolonged along with the decline in stroke volume and cardiac out-
constant work rate exercise to volitional fatigue under put, was graded in proportion to the magnitude of
heat stress (357, 372, 398). These observations were hyperthermia, with time to exhaustion inversely related
taken to indicate that the cardiovascular system is capa- to starting esophageal temperature (63, 46, and 28 min).
ble of meeting the blood flow requirements of both the These data highlight the significance of hyperthermia in
skin and active muscles during prolonged submaximal exacerbating the development of cardiovascular strain
exercise in hot environmental conditions. It must be during constant work rate exercise to volitional fatigue
noted, however, that maximal or near maximal heart rate and the prerequisite increase in maximum or near-maxi-
was not attained at exhaustion in these studies (357, 372, mum heart rate required to reduce systemic oxygen
398), which appears to be the point at which systemic delivery. Conversely, in the absence of cardiovascular
and peripheral (i.e., skin and exercising muscles) blood limitations where heart rate is not maximal or near-maxi-
flow and oxygen delivery decrease. mal upon reaching volitional exhaustion, a lack of moti-
Indeed, González-Alonso and Calbet (399) demon- vation and/or elevated perceived exertion in response
strated during brief intensive exercise (i.e., cycling at to inhibitory afferent feedback appears to mediate the
80% of peak power output) that volitional exhaustion cessation of exercise.
was associated with a reduction in systemic and exercis-
ing muscle blood flow and oxygen delivery and uptake 4.1.3. Cerebral blood flow.
when starting with either high or normal skin and core
temperatures. These reductions were exacerbated The development of hyperthermia during dynamic exer-
under heat stress, which accelerated the decline in cise in the heat is associated with a progressive reduction
mean arterial pressure and cardiac output, ultimately in cerebral blood flow relative to levels maintained in
deceasing V_ O2max. It has also been shown that systemic cooler conditions, whether measured via transcranial
oxygen delivery is blunted at intensities below V_ O2max Doppler ultrasound [middle cerebral artery mean blood ve-
by the attainment of a plateau in cardiac output during locity (MCAV)] (401, 402), the Kety-Schmidt technique (ve-
incremental exercise and a decrease in cardiac output nous drainage) (403, 404), or near-infrared spectroscopy
during constant work rate exhaustive exercise in cool (i.e., tissue oxygenation) (374, 405). The reduction in cere-
conditions (391). Systemic and exercising muscle blood bral blood flow toward resting baseline levels has been

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 EXERCISE UNDER HEAT STRESS

200 180

Stroke volume (mL·beat-1)

Heart rate (beats·min-1)

175
160
150

125 140

100
120
75

50 100

FIGURE 9. Heart rate, stroke volume, car-

30 200 diac output, systemic arterio-venous oxygen

a-vO2 difference (mL·L-1)

Cardiac output (L·min-1)

difference (a-vO ), oxygen delivery, and

2diff
25
150 uptake during incremental exercise to
exhaustion in temperate conditions (20 C)
20
plotted against the relative increase in
100
power output. These data indicate that sys-
15
temic oxygen delivery is blunted beyond
10
50 90% V_ O2max by the attainment of a pla-
teau in cardiac output, which attenuates
5 0 the rate of rise in oxygen uptake despite
maximal increases in a-vO2diff and heart
6
rate. Redrawn with permission from
7
Oxygen uptake (L·min-1)
Oxygen delivery (L·min-1)

Mortensen et al. (391).

6 5

5 4

4 3

3 2

2 1

1 0
0 20 40 60 80 100 0 20 40 60 80 100
Cycling peak power ouptut (%) Cycling peak power ouptut (%)

attributed to an increase in cutaneous blood flow, even during moderate intensity exercise (407), it is increas-
decreases in cardiac output and arterial blood pressure, as ingly becoming apparent that this range is much narrower
well as hyperventilation-induced hypocapnia [i.e., decrease and within 5 to 25 mmHg of resting values (408, 409).
in arterial carbon dioxide pressure (PaCO2)] (401–404). Moreover, it has been shown that intense and exhaustive
Nybo and Nielsen (401) were among the first to examine exercise impairs cerebral blood flow control (410, 411).
cerebral blood flow via transcranial Doppler ultrasound Thus, given the elevated intensity sustained during self-
during constant work rate exercise to exhaustion under paced exercise (314, 412) and the progressive increase in
heat stress. The authors noted that MCAV decreased in relative intensity occurring during constant work rate exer-
parallel with the rise in body core temperature, whereas a cise in hot compared with cool conditions (319, 320), a ven-
stable elevation in MCAV was maintained during steady- tilatory-mediated decrease in PaCO2 may influence
state exercise in cooler conditions. In contrast, MCAV was cerebral vascular tone and alter the relationship between
shown to decrease regardless of ambient conditions when arterial pressure and cerebral blood flow under heat stress
performing prolonged (i.e., 45–60 min) high-intensity self- (408).
paced exercise, albeit to a greater extent in hot compared The reduction in cerebral blood flow during strenuous
with cool conditions (402). The decrease in cerebral blood exercise in the heat has been suggested to influence
flow observed during self-paced exercise was suggested central neural drive to exercising muscles in response to
to stem from the maintenance of an elevated relative exer- a compromise in oxygen delivery to the brain (401, 413,
cise intensity, resulting in a comparable hyperventilation- 414). However, the development of hyperthermia during
induced hypocapnia response. While cerebral autoreg- such exercise is associated with an enhanced cereb-
ulation has historically been purported to ensure the ral metabolism (405), manifested by a compensatory
maintenance of blood flow to the brain within a range of increase in cerebral oxygen extraction (415). For exam-
mean arterial pressures between 60 and 150 mmHg (406), ple, an esophageal temperature of 39.5 C during

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 PÉRIARD ET AL.

exercise in uncompensable heat stress, relative to by reducing mental drive (i.e., motivation) for motor per-
38 C in cool conditions, resulted in an 18% lower cer- formance. This conclusion was drawn as daily volitional
ebral blood flow at the end of exercise (403). The fatigue during a 9- to 12-day exercise-heat acclimation
decrease was accompanied by a 23% increase in regimen coincided with a final core temperature of
a-vO2diff and a 7% increase in cerebral metabolic rate. 39.7 C (372). Interestingly, cardiac output and muscle
The increase in cerebral oxygen uptake was attributed blood flow were maintained at the point of fatigue, likely
to the Q10 temperature coefficient but also to increased in response to heart rate only increasing to 160
levels of stress and mental exertion. In line with this beats·min 1. The authors further demonstrated that the
hypothesis, electroencephalography activity measure- capacity to generate force during a brief (3–5 s) maximal
ments indicate that a rise in core temperature and rating voluntary isometric contraction (MVC) of the knee exten-
of perceived exertion are associated with a decrease in sors and elbow flexors was unaltered when measured
frontal lobe b-activity during exhaustive exercise under immediately after exhaustion (372). Conversely, force
heat stress (416–419). Similar findings were reported fol- production was impaired in a subsequent study during a
lowing the completion of a self-paced time trial in the sustained (120 s) MVC conducted after volitional fatigue
heat (420) and suggested to represent a suppression of in the heat, relative to a contraction performed after
arousal, with potential links to the development of fa- steady-state exercise in cool conditions (373). The
tigue (417–419). When measured during prolonged self- impairment was attributed to hyperthermia-induced cen-
paced exercise, both a- and b-activity decreased in hot tral fatigue, a progressive reduction in voluntary activa-
relative to cool conditions across the frontal (F3 and F4) tion mediated by the rise in whole body temperature. It
and central (C3 and C4) areas (421). Elevated a-activity in was also postulated that an elevated brain temperature
these areas is associated with the capacity to maintain might trigger inhibitory signals in temperature-sensitive
attention, mental readiness and relaxed focus (422– areas of the hypothalamus to decrease motor activity
424), whereas b-activity is linked to wakefulness, mental (425, 427, 428).
activity and cortical arousal (424, 425). Prolonged high- Using active and passive heating, others have shown
intensity exercise in the heat therefore seems to induce that a progressive increase in core temperature is paral-
cerebrocortical activity alterations in areas of the brain leled by a gradual decrease in voluntary activation and
associated with the ability to inhibit conflicting atten- force production during 5 to 30 s MVCs (429–431), with
tional processing and the capacity to sustain mental read- the ability to produce force reincreasing as core temper-
iness and arousal. Whether these alterations support the ature returns toward baseline with passive cooling (429,
premise that an exacerbated reduction in cerebral blood 430). Conversely, local heating of the thigh was shown
flow under heat stress mediates a performance decre- to impair endurance capacity in the knee extensors dur-
ment via central inhibition, particularly given the robust ing a sustained contraction at 70% MVC through an
capacity of the cerebral vasculature to extract oxygen, inability to maintain maximal muscle activation, whereas
requires further elucidation. brief maximal force production was unaffected (432). It
was also shown that passive heating to a rectal tempera-
4.2. Central Neural Drive ture of 39.5 C did not deleteriously influence torque out-
put during maximal voluntary isokinetic contractions of
The role of the CNS in regulating exercise performance the knee extensors performed at three different veloc-
under heat stress spans from afferent input influencing ities (i.e., 60, 120, and 240 ·s 1) (433). Exercise-induced
the drive or willingness to continue exerting effort (i.e., hyperthermia to a tympanic temperature of 40 C also
motivation), to hyperthermia downregulating skeletal failed to influence maximal or endurance isokinetic con-
muscle recruitment. Bru €ck and Olschewski (426) pro- tractions at 240 ·s 1 (434). The neuromuscular impair-
vided the impetus to investigate these pathways after ments associated with hyperthermia-induced central
postulating that body temperature affected certain phys- fatigue therefore seem to occur during static but not
iological parameters thought to counteract motivation. dynamic contractions, sustained MVCs in particular,
More specifically, the authors suggested that increasing over the time course of whole body hyperthermia, rather
levels of hyperthermia influenced the interaction of cir- than at the attainment of a specific internal temperature.
culatory, thermal, and muscular discomfort, which pro- Although decrements in central neural drive have
gressively reduced the drive to exercise. Nielsen et al. been linked with the development of hyperthermia (373,
(357, 372) subsequently proposed that hyperthermia 430, 431, 435–437), it has also been shown that volun-
per se, rather than circulatory failure, was the critical tary activation and force production capacity are simi-
factor causing exhaustion during constant work rate larly reduced during a sustained (20 s) MVC following
exercise under heat stress. The attainment of a high self-paced exercise (i.e., 40 km time trial) in hot and cool
core temperature was suggested to influence the CNS conditions (438). The postexercise decline in voluntary

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 EXERCISE UNDER HEAT STRESS

activation accounted for 20% of the decrease in total Most of the research investigating the impact of heat
force production, indicating that the 0.8 C higher rectal stress on the central activation of skeletal muscle has
temperature at time trial completion in the heat did not focused on neuromuscular responses during maximal
exacerbate central fatigue (438). In a separate study iso- voluntary isometric contractions and evoked twitch char-
lating the effect of hyperthermia from exercise, force acteristics following passive and/or exercise-induced
production capacity of the knee extensors was shown to hyperthermia (373, 430, 431, 435–441). It is important to
decline at a faster rate following exhaustive cycling in note, however, that isometric exercise involves partial to
the heat (rectal temperature: 39.8 C), compared with complete occlusion of blood flow to active muscles
passive heating (rectal temperature: 39.5 C) (439). depending on the intensity of contraction (442, 443),
Voluntary activation was similarly reduced between con- which further increases muscle temperature and stimu-
ditions, however, with the extent of decline maintained lates chemoreflexes and mechanoreflexes (444, 445).
throughout the sustained (45 s) MVC. These studies indi- Afferent stimulation of these reflexes increases muscle
cate that the loss of force production capacity originates sympathetic nervous activity (446), which can alter motor
from both central and peripheral fatigue factors, with the unit excitability, modifying the relationship between cen-
combination of heat stress and prior contractile activity tral neural drive, motor unit recruitment, and firing rate
(i.e., exercise) exacerbating the rate of decline. Using coding (447, 448). Impairment of skeletal muscle func-
transcranial magnetic stimulation, Todd et al. (440) tion during isometric exercise under heat stress may
attempted to localize the site of voluntary activation fail- therefore relate to a failure in the peripheral transmis-
ure by passively heating participants to an esophageal sion of neural drive at any level from cortical activity to
temperature of 38.5 C and assessing brief (2–3 s) and sarcolemma depolarization (435). Afferent stimulation
sustained (2 min) MVC performance. Hyperthermia- resulting from the occlusion of blood flow during a pro-
induced decrements in voluntary torque and cortical longed isometric MVC and the accumulation of metabo-
activation of the elbow flexors were observed during lites associated with muscular contractions may also
both contractions, with greater decreases noted during influence motivation (449). A concerted effort is required
the sustained MVC. It was also noted that peak muscle to maintain force production during a prolonged MVC,
relaxation rate during the sustained contraction, the coupled with a willingness to tolerate discomfort and
steepest rate of decline of torque in the silent period im- pain. Minor discomfort is sensed at the onset of a con-
mediately following motor cortex stimulation, was 20% traction, developing into severe discomfort and pain
faster than at baseline (i.e., normothermia). This led the over time that alters the perception of sensations in the
authors to suggest that the greater central fatigue contracting musculature (450). Consequently, mental fa-
observed during longer contractions may be linked to a tigue, which involves tiredness, limited attention span,
failure in voluntary drive to account for temperature- and an aversion or decreased commitment to continuing
related adjustments (i.e., increase) in muscle contractile a task or activity (451, 452), may contribute to decrease
function. In essence, although high motor unit firing voluntary muscle activation, particularly after prolonged
rates may be transiently attained during brief MVCs, passive and active heating. Conscious signals originat-
these elevated rates may not be sustained during pro- ing from both central and peripheral afferent pathways
longed contractions (440). To further investigate this could mediate behavior and reduce motivation to mini-
premise, Pe
riard et al. (431) actively and passively mize discomfort (453), leading to the abandonment of a
heated participants from baseline rectal and muscle task in which the energetic demands (i.e., effort) out-
(vastus lateralis) temperatures of 37.1 and 35.3 C, to weigh the perceived benefits of continued performance
38.5 and 38.7 C, and then on to 39.4 and 39.3 C, (454). A lack of motivation may thus lead to inadequate
respectively. Both active and passive moderate hyper- central neural drive to solicited motor neurons, resulting
thermia increased peak muscle relaxation rate following in a loss of force (455). The loss of force production
transcranial magnetic stimulation when brief (5 s) and capacity during isometric exercise under heat stress
sustained (30 s) MVCs were performed. However, only may therefore represent a psychophysiological phe-
the increase from moderate to severe passive hyper- nomenon, wherein an integrated response related to
thermia further increased relaxation rate, albeit without both an inability and unwillingness to exercise regulates
decreasing force production capacity to a greater extent performance. Whether such a response also influences
than severe active hyperthermia. It was therefore con- prolonged dynamic exercise in the heat remains a topic
cluded that centrally mediated rates of activation are suffi- of contention.
cient to overcome both active and passive hyperthermia- Brain neurotransmitters (i.e., serotonin, dopamine, and
induced increases in peak muscle relaxation, as these fall norepinephrine) have been implicated in the control of
within physiologically relevant motor unit firing rate thermoregulation and the potential development of cen-
ranges (i.e., 10–30 Hz). tral fatigue (456, 457). On one hand, dopamine appears

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 PÉRIARD ET AL.

to display ergogenic properties by reducing perceived metabolic responses. The extent of this inhibitory influ-
exertion and thermal discomfort during self-paced exer- ence remains to be determined, however, as it has been
cise at elevated work rates in the heat (458, 459). On suggested to diminish during exercise in extreme envi-
the other hand, norepinephrine seems to produce a ronments (e.g., heat and hypoxia), effectively out-
negative effect on performance (460), while serotoner- weighed by direct disturbances to the CNS (e.g.,
gic manipulation fails to influence the development of fa- hyperthermia and hypoxemia) (485).
tigue (461, 462). As such, it appears unlikely that a Fink et al. (475) first demonstrated that muscle glyco-
particular neurotransmitter system mediates the delay gen utilization was 76% greater and blood lactate con-
or onset of fatigue during exercise in the heat (326, 463, centration twice as high following intermittent cycling in
464). Notwithstanding, fatigue is a complex phenom- hot (41 C) compared with cold (9 C) conditions. The
enon influenced by several factors of both central and increased rate of glycolysis was attributed to a thermal
peripheral origin and it is possible that different neuro- strain-mediated reduction in muscle blood flow and oxy-
transmitter systems interact with thermal, cardiovascular, gen delivery. A number of other potential mechanisms
and metabolic function to modulate fatigue. Further inte- have since been suggested to augment muscle glyco-
grative research is required in this area. genolysis through stimulation of phosphorylase activity
and other key glycogenolytic and glycolytic enzymes,
4.3. Skeletal Muscle Function and Metabolism including elevated muscle temperature (i.e., Q10 effect),
decreased energy status (i.e., degraded total adenine
Elevations in muscle temperature lead to alterations in nucleotide pool and increased free adenosine mono-
skeletal muscle function and metabolism that affect brief phosphate), and enhanced sympathoadrenal response
maximal and prolonged submaximal exercise perform- (i.e., elevated circulating epinephrine) (472, 493–497).
ance differently. An increase in muscle temperature is Conversely, some studies have not observed increased
known to enhance acute explosive exercise perform- intramuscular glycogen utilization during exercise under
ance such as sprinting and jumping (465–467) via heat stress (357, 498–500), which may in some circum-
improvements in metabolic and contractile function, stances relate to methodological issues (e.g., preexer-
nerve conduction velocity, and conformational changes cise glycogen levels, exercise intensity) (501). Others
associated with muscle contraction (468–470). In con- have also shown that carbohydrate oxidation and mus-
trast, prolonged exercise in the heat increases muscle cle glycogenolysis are lowered when the rise in whole
glycogen utilization and anaerobic metabolism, causing body temperature is attenuated during exercise in
greater accumulation of ammonia and muscle lactate cooler environments (476, 502) or by heat acclimation
(471–476). Work at high glycolytic rates is also associ- (397, 473, 500, 503) and when external cooling is pro-
ated with the release of force-depressing hydrogen (H1) vided (504). This suggests that hyperthermia is a potent
and inorganic phosphate (Pi) ions (469, 477–480). modulating factor for increasing carbohydrate metabo-
Temperature-induced impairments in sarcoplasmic retic- lism. Notwithstanding, glycogen depletion is not con-
ulum function and structural damage compromising sidered a primary factor limiting endurance exercise in
sarcoplasmic reticulum calcium (Ca21) ion regulatory the heat (324, 505–507), as high-intensity aerobic
capacity may also influence skeletal muscle force pro- exercise may be performed for extended periods
duction (469, 481). The metabolic and mechanical altera- (60 min) without muscle glycogen depletion attenuat-
tions occurring within the exercising muscles stimulate ing performance (508–511). However, protracted exer-
group III/IV muscle afferents, which relate the level of cise performed at a variable work rate results in
perturbation and fatigue to the CNS (482–484). This in- excessive muscle glycogen utilization (512), and con-
hibitory neural feedback has been suggested to influ- sidering that the oxidation rate of ingested carbohy-
ence the perception of exertion and contribute to the drate is reduced when exercising in the heat (513), it
development of fatigue during prolonged intense exer- may be speculated that glycogen depletion could be
cise in temperate conditions by decreasing central accelerated and performance impacted upon during
motor drive (485–488). Along with feedforward regula- prolonged aerobic exercise in moderate heat.
tion from central command (489, 490), group III/IV mus- Moreover, the greater reliance on carbohydrate metab-
cle afferent feedback has been linked to the regulation olism when exercising at a given work rate in hot ver-
of autonomic ventilatory and circulatory responses dur- sus temperate environmental conditions is typically
ing exercise (491, 492). As such, neural feedback regard- associated with markers of increased relative exercise
ing the level of perturbation within the skeletal muscle intensity, such as a higher heart rate, blood lactate, re-
milieu during prolonged exercise in the heat may exert spiratory exchange ratio, and rating of perceived exer-
an inhibitory influence on central motor drive and impact tion, despite systemic oxygen uptake remaining similar
on the regulation of ventilatory, circulatory, and (471–474, 500, 514, 515). It is also well established that

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 EXERCISE UNDER HEAT STRESS

a rise in exercise intensity mediates an increase in gly- rate at what is typically a submaximal work rate, forcing
cogenolysis and carbohydrate oxidation and decrease the cardiovascular system to a premature functional limit
in fat oxidation (516–519). This progressive shift in (522, 523). The traditional mechanism via which stroke
energy substrate mobilization and utilization during volume was suggested to decrease under heat stress
exercise in hot environmental conditions may repre- lay with the redistribution and pooling of blood in the pe-
sent the maintenance of a gradually increasing relative riphery (i.e., cutaneous circulation), which decreased
exercise intensity, mediated by a hyperthermia- central blood volume and concomitantly ventricular fill-
induced decrease in maximal aerobic capacity (see ing pressure and end-diastolic volume (338, 352, 524).
sects. 4.4–4.6). A more contemporary hypothesis proposes that the
reduction in stroke volume is primarily related to shorter
4.4. Maximal Aerobic Power in the Heat ventricular filling time and possibly filling pressure, con-
sequent to a hyperthermia-mediated increase in heart
Rowell (338) previously highlighted that V_ O2max is unal- rate compared with when exercising at a similar work
tered during brief (<15 min) incremental exercise under- rate in cool conditions (i.e., normothermia) (525–529).
taken in hot conditions, as regional vasoconstriction The tachycardic response in the early stages of exercise
allows for redistributing a sufficient fraction (80–85%) of in the heat is suggested to stem from a thermoregula-
cardiac output to working muscles. The similarity in tory-mediated rise in cutaneous blood flow (526, 530).
response between hot and cool environments stems As thermal strain develops, the increase in heart rate
from the capacity to achieve maximal cardiac output at has been attributed to withdrawal of parasympathetic
similar work rates, despite marginally greater levels of outflow and increased cardiac sympathetic neural activ-
whole body hyperthermia in the heat. Indeed, when ity in response to baroreflex modulation and/or a hyper-
core temperature remains <38 C and skin temperature adrenergic state (531–536), along with the direct effect
does not exceed 35 C during incremental exercise in of blood temperature on the sinoatrial node (i.e., cardiac
the heat, V_ O2max remains similar to cool conditions (314, pacemaker) (537–542).
319, 520, 521). When preceded by active or passive The reduction in V_ O2max occurring during incremental
whole body heating, however, a marked decrease in exercise to exhaustion under heat stress following pre-
maximal cardiac output occurs during exhaustive exer- heating has been extensively studied (320–323, 543).
cise in the heat, which reduces V_ O2max (FIGURE 10). The Arngrimsson et al. (319) demonstrated a proportio-
decrement in maximal cardiac output results from a nal decrease in V_ O2max in relation to increases in
lower stroke volume at the attainment of maximal heart mean body temperature (= [esophageal  0.87] 1 [mean

Cool Hot
22 22

18 18
Skin
Cardiac output (L·min-1)

Heart, brain, etc.

14 14 Viscera
Muscle

10 10

6 HR: 195 6 HR: 195

SV: 114 SV: 95
a-vO2diff: 166 a-vO2diff: 162
2 2

0 0
0.25 1 2 3 4 0.25 1 2 3 4

Oxygen uptake (L·min-1) Oxygen uptake (L·min-1)

FIGURE 10. Estimated distribution of cardiac output during incremental exercise in temperate (26 C) and hot (43 C) environments and its conse-
quent influence on maximal aerobic capacity. Incremental exercise to exhaustion in the heat following whole body heating is associated with a greater
redistribution of cardiac output to the skin and an elevated heart rate for any given level of oxygen uptake (i.e., work rate). The elevated heart rate
response is influenced by withdrawal of parasympathetic outflow, increased cardiac sympathetic neural activity, and the direct effect of blood tempera-
ture on the sinoatrial node. The outcome of this elevation in heart rate is the attainment of maximum heart rate at a lower work rate than in cool condi-
tions, which coupled with a lower stroke volume, leads to decrease in maximal cardiac output, forcing the cardiovascular system to a functional limit at
what is typically a submaximal work rate. HR, heart rate (beats·min 1); SV, stroke volume (mL·beat 1); a-vO , arterio-venous oxygen difference
2diff
(mL·L 1). Redrawn with permission from Rowell (338).

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 PÉRIARD ET AL.

skin  0.13]) in both men and women (FIGURE 11). These 4.5. Constant Work Rate Exercise in the Heat
increases in mean body temperature were associated
with exercise or passive preheating in ambient tempera- Prolonged constant work rate exercise (e.g., 50–75%
tures of 35, 40, and 45 C, leading to 4, 9, and 18% V_ O2max) in temperate conditions leads to cardiovascular
reductions in V_ O2max, relative to 25 C. Unlike exercise at drift, a time-dependent phenomenon characterized by a
altitude where V_ O2max is acutely decreased in relation to progressive change or drift in certain cardiovascular
the severity of the hypoxic stimulus (544, 545), the responses after 10 to 15 min of exercise (337, 352, 546).
decrease in V_ O2max under heat stress appears to occur This phenomenon is characterized by an increased
progressively in response to the rise in whole body tem- heart rate and oxygen uptake, decreased stroke vol-
perature, not the prevailing climatic conditions per se. It ume, and diminished mean arterial and pulmonary pres-
has also been shown that an elevated skin temperature sure, while cardiac output remains constant. Under heat
alone does not compromise V_ O2max. Utilizing a water- stress, these adjustments in cardiovascular function are
perfused suit, Trangmar et al. (521) manipulated skin exacerbated, with the increase in heart rate strongly cor-
(16 C) and whole body (skin: 16 C, core: 11 C) temper- related to the rise in rectal temperature when exercising
ature before participants undertook an incremental cy- at 60% (r = 0.83) and 75% (r = 0.68) V_ O2max in 40 C and
cling test to exhaustion. Relative to a control condition, 50% RH (309). The high core temperatures (e.g., 39.5 to
whole body hyperthermia decreased V_ O2max by 8%, 40 C) reached at volitional fatigue (i.e., exhaustion) dur-
whereas an increase in skin temperature alone did not ing such exercise in laboratory settings often coincide
affect maximal aerobic power. This observation reinfor- with considerable cardiovascular strain (i.e., heart rate
ces the notion that a marked rise in whole body thermal >95% of maximum) (363, 396, 418, 439). Previous stud-
strain is required to elicit a decrement in V_ O2max. ies have suggested that fatigue was the result of attain-
ing a “critically” elevated core temperature (363, 372,
373, 401). This concept has been the focus of some dis-
cussion (547, 548) with a recent commentary suggesting
5 that using such terminology in a reductionist manner to
describe the impact of hyperthermia on the develop-
ment of fatigue during prolonged exercise in the heat
0 may be misleading (549). Fatigue during exercise in the
heat is not caused by a sole factor but by the interaction
' Maximal oxygen uptake (%)

of several physiological processes, as well as the inter-

-5 pretation of afferent feedback in the CNS (FIGURE 6).
The elevated heart rate observed at volitional fatigue
during constant work rate exercise in uncompensable
-10 Men Women conditions is associated with an increased a-vO2diff and
25N significant declines in stroke volume, cardiac output,
25A and mean arterial pressure (364, 396, 399), coupled
-15 with increases in thermal sensation, discomfort, and per-
35A
40A ceived exertion (309, 418). The combination of these fac-
45N tors leads to the premature termination of exercise in
-20
45A the heat, with the increase in perceived exertion stem-
45P ming from an increase in relative exercise intensity
(%V_ O2max), concomitant to the attainment of V_ O2max at
-25
37.5 38.0 38.5 39.0 39.5 40.0 submaximal work rates.
Mean body temperature (ºC) Relative exercise intensity as a determinant of endur-
ance performance is not a novel concept. Gleser and
FIGURE 11. Proportional relationship between changes in V_ O2max
Vogel (550, 551) proposed nearly 50 yr ago that endur-
and mean body temperature at exhaustion in 7 conditions: 1) 25 C
without warm-up (25N); 2) 25  C with a 20-min warm-up at 33% of ance capacity (i.e., time to exhaustion) was a function of
control V_ O2max (25A); 3) 35  C with warm-up (35A); 4) 40  C with relative (i.e., %V_ O2max) rather than absolute (i.e., work
warm-up (40A); 5) 45 C without warm-up (45N); 6) 45  C with warm- rate) exercise intensity. By manipulating absolute work
up (45A); and 7) 45  C with passive preheating to elevate core tem-
perature to the same extent as 45A (45P), all of which in 50% relative
rate and inspired oxygen fraction in a series of studies,
humidity. These data indicate that the reduction in V_ O2max under the authors proposed that prolonged exercise perform-
heat stress is associated with whole body temperature, rather than ance decreased exponentially with a rise in %V_ O2max. A
the prevailing ambient conditions per se. Redrawn with permission hypothetical model was developed whereby muscle ox-
from Arngrimsson et al. (319).
ygen demand increased as a function of relative

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 EXERCISE UNDER HEAT STRESS

intensity, and oxygen delivery as the product of blood before terminating exercise. Volitional fatigue in such
flow and oxygen content. In the model, oxygen delivery circumstances would relate to the attainment of V_ O2max
at lower work rates increased proportionally to meet ox- and a consequent impairment in oxygen delivery to
ygen demands. At very high work rates, however, a exercising muscles, in response to a compromise in sys-
compromise in muscle blood flow occurred that led to temic blood flow (i.e., maximal cardiac output) (see sect.
insufficient oxygen delivery, causing a rise in anaerobic 4.1). In the second scenario, despite a similar rate of
glycolysis and reduction in endurance time (550). A simi- increase in whole body temperature to the previous sce-
lar phenomenon appears to occur during prolonged nario, heart rate at the point of volitional fatigue might be
exercise in the heat, with premature fatigue linked to the well below maximum, which would allow for adequate
progressive decline in V_ O2max (FIGURE 12). As thermal blood flow and oxygen delivery to active skeletal
strain develops during constant work rate exercise in muscles. Although the attainment of cardiovascular limita-
the heat, V_ O2max decreases, an increase in relative exer- tions may not represent the primary mechanism media-
cise intensity and perceived exertion then ensues for a ting the termination of exercise in the second scenario,
given absolute work rate (320, 453, 552–554). Voli- the progressive increase in thermal and cardiovascular
tional fatigue during such exercise is therefore de- strain may play a role in augmenting the perception of
pendent on the severity of the thermal strain exertion and thermal discomfort, leading to the cessation
imposed by the interaction of several factors, includ- of exercise. These scenarios indicate that the progressive
ing ambient conditions (305, 364), initial body tem- increase in thermal and cardiovascular strain play a mod-
perature (363), relative exercise intensity (309, 555), ulatory role in the volitional termination of exercise during
and fitness level (309, 370, 555). constant work rate efforts, albeit with different physiologi-
Fatigue or volitional exhaustion during constant work cal endpoints.
rate exercise may also arise through a similar pathway
but occur at different physiological endpoints. In the first 4.6. Self-Paced Exercise in the Heat
scenario, motivated individuals exercising at a predeter-
mined work rate (e.g., 60% V_ O2max) for a prolonged pe- The regulation of prolonged self-paced exercise in the
riod may reach maximal or near-maximal heart rate heat has been attributed to the development of thermal
strain impacting on cardiovascular function (312, 367,
Oxygen
556), thermal perception (i.e., discomfort) exacerbating
demand perceived exertion (34, 557, 558), and the rate of heat
storage influencing locomotor muscle recruitment (317,
559, 560). In most instances, work rate at the start of a
VO2max prolonged time trial in hot environmental conditions is
Oxygen equivalents

Oxygen
similar to that of cooler conditions (311–314, 560–563).
delivery As a greater level of thermal strain develops in the
hotter environment, work rate progressively decreases
(FIGURE 13). This gradual reduction in work rate is asso-
ciated with the integration of several factors related to
Endurance
time increases in thermal, circulatory, metabolic, and percep-
Anaerobic
metabolism tual strain.

riard et al. (312–314, 402, 421,
In a series of studies, Pe
564) demonstrated that a thermoregulatory-mediated
rise in cardiovascular strain was associated with a pro-
25 50 75 100 gressive reduction in work rate during prolonged
50 75 100
intense self-paced cycling in the heat, relative to when
Relative intensity (%VO2max) undertaken in cooler conditions. The reduction in work
rate under heat stress was significantly correlated with
FIGURE 12. Conceptual model of muscle oxygen demand, oxygen
delivery, and anaerobic metabolism relative to exercise intensity declines in stroke volume, cardiac output and mean ar-
(%V_ O2max) on endurance capacity (i.e., time to exhaustion) during terial pressure during a 40 km time trial (FIGURE 14)
constant work rate exercise in hot (red lines and text) and cool (blue (312). Heart rate throughout the time trial in the heat
lines and text) conditions. Under heat stress, a gradual increase in
thermal strain (i.e., rise in whole body temperature) leads to a pro-
(35 C) was also 8 beats·min 1 higher than in cool
gressive decrease in V_ O2max, which results in a rise in relative exer- (20 C) conditions. This elevated cardiovascular resp-
cise intensity for any given work rate and a greater reliance on onse has been shown to exacerbate the decrease in
anaerobic metabolism, reducing endurance time. Adapted with per- peak oxygen consumption (V_ O2peak) measured during
mission from Gleser and Vogel (550).
the end-spurt of prolonged (45–60 min) time trial efforts

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 PÉRIARD ET AL.

400 protracted however, as a disassociation develops

Cool between %V_ O2peak, heart rate and perceived exertion.
350 Hot The %V_ O2peak sustained during self-paced cycling is
* related to the duration or distance of the event, with
Power output (W)

300 * time trials of 45–60 min conducted at 85% V_ O2peak

* * * * * and shorter efforts performed at a greater fraction of
* *
maximal aerobic power (313, 314, 412, 565–567).
250
Perceived exertion during such trials in the heat is simi-
lar and often higher than in cooler conditions (312, 316,
200
402, 560). From a performance perspective, the pro-
gressive decrease in V_ O2peak and concomitant increase
150
0 25 50 75 100
in relative intensity for any given work rate appears to
represent the primary determinant mediating the decline
Time trial completion (%)
in work rate (e.g., power output) observed in hot condi-
FIGURE 13. Power output during a 40-km cycling time trial in Hot tions. This premise is reinforced by data indicating that
[35 C and 60% relative humidity (RH)] and Cool (20  C and 40% RH) breathing a hyperoxic gas mixture with fractional oxygen
conditions. These data indicate that work rate (i.e., power output) is
similar at the start of self-paced exercise in hot and cool conditions,
content (FIO2) of 0.45 during the final 25% of a 40 min
as the difference in thermal (i.e., core and skin temperature) strain time trial in the heat (35 C) increased power output rela-
between conditions is relatively small. As exercise progresses, the tive to breathing normoxic air (FIO2 of 0.21) (564). The
development of hyperthermia under heat stress mediates a reduc- improvement in performance was attributed to a hyper-
tion in work rate. *Significant difference between Cool and Hot
(P < 0.05). Reproduced with permission from Pe
riard et al. (312). oxia-mediated increase in arterial oxygen content and
delivery to active muscles, effectively reversing part of
the decrease in V_ O2peak and allowing for a greater
in the heat by 12%, compared with a similar effort power output to be maintained. Interestingly however,
undertaken cool conditions (312, 314, 402). The reduc- the extent of the improvement from breathing hyperoxic
tion in V_ O2peak occurs progressively during self-paced air was greater in a time trial conducted in cooler condi-
exercise in the heat and is accompanied by a gradual tions (18 C), which suggests that the elevated level of
decline in absolute work rate (i.e., power output). The lat- thermal and cardiovascular strain experienced during
ter response has been suggested to occur to maintain prolonged self-paced exercise in the heat might partly
relative exercise intensity (i.e., %V_ O2peak) within a narrow attenuate the beneficial effect of hyperoxia. Taken to-
range, similar to that of time trial efforts performed gether, these findings provide support for the regulation
in cooler environmental conditions (314). This range of self-paced exercise involving the conscious interpre-
widens under heat stress when exercise becomes tation of sensory information relating to effort (i.e.,

200 190
Stroke volume (mL·beat-1)
Heart rate (beats·min-1)

Cool
175
190 Hot
160 * * *
180
* * * *
* * * 145
170 * 130
115
FIGURE 14. Cardiovascular responses
160 during a 40-km cycling time trial in Hot
100
150 [35 C and 60% relative humidity (RH)] and
85
Cool (20 C and 40% RH) conditions.
140 70 These data indicate that the development
of thermal strain during self-paced exer-
Mean arterial pressure (mmHg)

30 140 cise in the heat increases the cardiovascu-

Cardiac output (L·min-1)

lar response, despite the maintenance of

27 130
* a lower work rate in the heat. *Significant
* * * * * * difference between Cool and Hot
* 120
*
†
24
* 110
(P < 0.05). Significantly lower than 10 min
21
(P < 0.05). Reproduced with permission
100 from Pe
riard et al. (312).
18
90

15 80
0 25 50 75 100 0 25 50 75 100

Time trial completion (%) Time trial completion (%)

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 EXERCISE UNDER HEAT STRESS

amount of mental and physical energy allocated toward induce the feeling of coolness, did not drive changes in
completing a task) and exertion (i.e., level of strain expe- work rate during the early stages of a 40-km time trial in
rienced during a task) (552, 568). More specifically, self- warm conditions relative to control and control spray condi-
paced exercise regulation appears to be an integrative tions, nor did it affect overall performance. Although work
process during which a balance is achieved between an rate in the first few minutes (5–10 min) of prolonged self-
efferent copy of central motor command (i.e., corollary paced exercise in the heat is often similar to that of cooler
discharge) and afferent sensory input (i.e., physiological conditions (311–314, 560–563), the progressive decrease in
signals) originating from peripheral receptors (569–571), speed or power output during such exercise is typically initi-
which is altered in response to the progressive rise in ated before a marked rise in thermal strain. As such, work
thermal and cardiovascular strain. The comparative bal- rate in the initial 10–15 min of self-paced exercise may con-
ance between effort and exertion, or the predicted and sciously be reduced in response to a thermal perception
actual sensory feedback, may therefore allow for sus- mediated increase in perceived exertion. Alternatively,
taining an optimal performance intensity in different experienced individuals may modify work rate and adopt a
environments (e.g., hot, cold, and hypoxic). more conservative pacing strategy to avoid larger decre-
In 1916, Lee and Scott (328) wrote that “it is a fact of ments in work rate later on during an event, although this
common experience that a human being in a hot and approach may not enhance performance (578).
humid atmosphere feels a disinclination to perform mus- An alternative pathway suggested to mediate the
cular work.” Indeed, thermal discomfort is associated impairment in self-paced exercise performance in the
with decreased work and athletic performance under heat lies with anticipatory regulation of muscle recruit-
heat stress (572). Accordingly, behavioral thermoregula- ment (317, 559, 560). Derived from the central governor
tion has been suggested as a mechanism by which self- model of exercise (579, 580), anticipatory regulation is
paced exercise performance may be regulated in the purported to ensure the prevention of thermal injury by
heat. It is proposed that the integration of physiological preventing excessive increases in body heat storage
and psychological influences can formulate a behavior and debilitating levels of hyperthermia from developing
that establishes optimal conditions for heat exchange (581). It is proposed that the moment exercise is initiated,
with the environment (573–575). For example, it is the rate of body heat storage regulates work rate
known that heat balance during exercise at a constant through its influence on perceived exertion. Therefore,
work rate is mediated by autonomic responses and the work rate decreases to match the maximum tolerable
prevailing environmental conditions as metabolic heat rating of perceived exertion before harmful disturbances
production is fixed. In contrast, self-paced exercise can disrupt homeostasis. This hypothesis stems from a
allows for behavioral thermoregulatory adjustments to study in which power output during a 20-km cycling
alter or improve the compensability of an environment time trial began to decline in 35 C conditions at a point
by adjusting work rate (i.e., metabolic heat production) where core temperature was similar, but skin tempera-
(557, 574). This coordinated behavioral response is pre- ture was 7 C higher than in a 15 C environment (560).
ceded by modifications in subjective thermal perception In a follow-up study it was reported that the rate of body
(i.e., comfort and sensation), primarily driven by skin tem- heat storage measured in the very early stages (i.e., first
perature. Thermal perception is thus purported to play a 4 min) of self-paced exercise in 35 C conditions was
modulatory role in exacerbating the rating of perceived greater than in 15 C and 25 C conditions, leading the
exertion, with the conscious decision to reduce work authors to surmise that the more rapid reduction in work
rate (e.g., power output or running velocity) occurring rate under heat stress was mediated by afferent feed-
primarily to maintain a desired perceived exertion (34, back to the CNS regarding the rate of body heat storage
557, 558, 575). Thermal perception is further suggested (317). However, the method used by Tucker et al. (317) to
to impact on perceived exertion and to reduce work rate calculate the rate of heat storage has been criticized
only in the early stages of self-paced exercise in the (582), with recent studies demonstrating no association
heat, when the increase in body core temperature is between the initial rate of heat storage and the reduc-
minimal, but skin temperature is elevated. Thereafter, tion in self-paced exercise performance in the heat (583,
when whole body temperature is elevated, factors asso- 584). A field-based study has also shown no correlation
ciated with cardiovascular strain are suggested to modu- between the rate of heat storage and 8-km running
late perceived exertion and the consequent voluntary speed in 17 C and 30 C conditions, with runners capa-
reductions in work rate (34). While behavioral thermo- ble of accelerating toward the end of the test, despite a
regulation represents a powerful mechanism via which rectal temperature >40 C (562). As such, support for
conscious decisions contribute to preserve thermal ho- the hypothesis that the rate of heat storage during the
meostasis (576), Barwood et al. (577) demonstrated that early stages of exercise mediates changes in self-
thermal perception, modified by using a menthol spray to selected work rate is limited.

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 PÉRIARD ET AL.

Ultimately, the regulation of self-paced exercise perform- As a result, “the subject gradually feels worse and
ance involves making decisions based on prior experi- worse, and eventually becomes incapacitated from
ence, accurate knowledge of a task and an understanding exhaustion of dehydration, no matter how tough or well
of one’s physical abilities, while interpreting and reacting acclimatized. Administration of water combats all of
to physiological cues (i.e., sensory information) associated these undesirable changes, and in general the more
with effort and exertion. Under heat stress, pacing is a pro- nearly water intake approximates sweat loss, the better
cess informed by awareness and influenced by factors off the subjects remains.” In his seminal book,
such as the prevailing ambient conditions, the develop- Physiology of Man in the Desert, Adolph (220) high-
ment of thermal and circulatory strain, the integrity of meta- lighted a few years later that acute dehydration limits
bolic processes, and adjustments in skeletal muscle the ability to work through a reduction in circulating
function. Thus self-paced exercise performance in the heat blood volume and impairment in cardiovascular function.
appears to be regulated by interpreting sensory informa- Following on from these early observations and those of
tion influenced by increases in thermal, cardiovascular, others (221, 586–591), it was described that both exer-
and metabolic strain. cise-induced hypohydration and dehydration impact on
thermoregulatory function by reducing whole body
4.7. Summary sweat rate and skin blood flow, thereby increasing the
rate of heat storage (i.e., hyperthermia) and intensifying
Several factors and mechanistic pathways have been physiological and perceptual strain. The extent of physi-
proposed to mediate the impairment in endurance exer- ological strain imposed by hyperthermia and dehydra-
cise capacity and performance under heat stress. These tion relates to the magnitude of thermal strain and body
pathways include hyperthermia-induced 1) adjustment water loss, as well as the prevailing ambient conditions
cardiovascular function, which impact on blood flow dis- and mode and intensity of exercise being performed.
tribution, oxygen delivery and heat dissipation, 2) altera- This section will examine how an elevated whole
tions in central motor drive, which influence muscle body temperature and compromised hydration status
activation and force production capacity, and 3) pertur- alter thermoregulatory, cardiovascular, and metabolic
bations in skeletal muscle function, which compromise function, and how these alterations impact on aerobic
metabolic and structural characteristics of the muscle exercise performance. The history of recommendations
and influence autonomic responses. The commonality regarding fluid intake during exercise will also be exam-
with all of these responses is the increase in whole body ined and the latest recommendations addressed and
temperature that accompanies prolonged moderate-to- contextualized.
high intensity exercise in the heat and the concomitant
link between the development of hyperthermia, sympa- 5.1. Adjustments in Thermoregulatory Function
thetic activity, and circulatory function. These factors
appear to cause a gradual decrease in V_ O2max during Whole body sweat rate during physical activity is deter-
both constant work rate and self-paced exercise in the mined by exercise intensity and climatic conditions but
heat, which leads to an increase in perceived exertion typically ranges between 0.5 and 2.0 L·h 1 with some
for any given work rate. The integrative decision to athletes (2%) sweating >3.0 L·h 1 (592). Gradual
cease exercising (i.e., constant work rate exercise) or to reductions in body mass (e.g., 2 to 5%) from water deficit
decrease work rate (i.e., self-paced exercise) can occur result in marked decrements in plasma (10%) and
across a spectrum of physiological and perceptual end- blood (6%) volume (593–595). The loss of plasma vol-
points, which are exercise, intensity, environmental, con- ume with exercise leads to a state of hyperosmotic hy-
text, and participant specific. povolemia that is proportional to the decrement in total
body water (596). Although the composition of the pre-
cursor secretory fluid contained in eccrine sweat glands
5. HEAT STRESS, HYDRATION STATUS, AND is similar to that of plasma, a considerable amount of the
EXERCISE PERFORMANCE ions (e.g., sodium and chloride) within the fluid are reab-
sorbed as it traverses the duct of the gland, leading to a
Endurance exercise is impaired under heat stress with a sweat osmolality approximately half that of plasma (597,
compromise in hydration status exacerbating the delete- 598). The increase in intravascular osmotic pressure
rious effects of thermal strain. Pitts et al. (585) reported resulting from plasma hyperosmolality causes a shift in
over 75 yr ago that dehydration steadily increased rectal fluid from the intracellular to the extracellular compart-
temperature, heart rate, and oxygen uptake, while sweat ment, which helps defend plasma volume (257). At ele-
rate decreased and plasma osmolality increased during vated whole body sweat rates, however, the volume of
prolonged marches in hot/dry and hot/humid conditions. fluid mobilized from the intracellular compartment into

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 EXERCISE UNDER HEAT STRESS

the vasculature is insufficient to restore plasma volume 600

and leads to intracellular dehydration.
The influence of dehydration on exacerbating hyper-
thermia during work in the heat is well established (585, 500

587–590). In a 1923 review, Marriott (599) synthesized

the effects of anhydremia (i.e., reduced fluid content of
the blood) on circulatory, metabolic, and thermoregula- 400

Sweat rate (g·m-2·h-1)

tory responses, highlighting that “when the blood and
tissues become concentrated by water loss the amount
of water available for evaporation is diminished and ulti- 300

mately becomes less than that required for removal of

the heat of metabolism. Fever then occurs.” Several dec-
ades later, in an attempt to determine the link betw- 200 0%
een hydration status, core temperature and sweating, 3%
Greenleaf and Castle (600) examined the impact of 5%
hyperhydration (11.2% body mass) and severe ( 5.2% 100
7%
body mass) hypohydration on the rectal temperature
response during exercise at 50% V_ O2max in temper- 37.0 37.5 38.0 38.5 39.0
ate conditions. The authors demonstrated increased Rectal temperature (ºC)
oxygen uptake, heart rate, and rectal temperature
responses in the severe hypohydration trial, along with a FIGURE 15. Influence of euhydration and 3 different levels of
hypohydration (3.1, 5.0, and 6.7% body mass loss) on the relationship
reduced sweat rate compared with hyperhydration. The
between sweat rate and rectal temperature at the completion of 3 (2
reduction in sweat rate was attributed as the primary for 7% hypohydration) bouts of exercise (10-min rest 1 25 min of
pathway exacerbating the rise in rectal temperature treadmill walking) in 49  C and 20% relative humidity. The data indi-
(0.1 C per 1% body mass loss) (600). In a subsequent cate a systematically lower sweat rate for a given rectal temperature
with increased severity of hypohydration. Reproduced with permis-
review, Sawka et al. (601) compared the effects of hypo- sion from Sawka et al. (215).
hydration on the rise in body core temperature across
eight studies and determined that participant character-
istics, environmental conditions, and exposure duration threshold for cutaneous vasodilation (0.42 C) during
influenced thermoregulatory responses. The increase in 30 min of running in the heat, relative to euhydration and
core temperature during exercise in the heat with hypo- hyperhydration (2.4% body mass gain). Along with the
hydration (2 to 7% body mass loss) appeared to be elevated onset threshold, there was a reduction in cuta-
slightly greater with an estimated 0.15 C per 1% body- neous blood flow for a given temperature with hypohy-
mass loss. Several studies have demonstrated that hyp- dration (FIGURE 16). The authors suggested that the
ohydration-induced hyperosmotic hypovolemia delays attenuation in cutaneous blood flow contributed to
thermoregulatory sweating and cutaneous vasodilation maintain an already compromised venous return, but
at rest and during exercise and reduces the sensitivity of it also decreased internal (i.e., core-to-skin) heat trans-
the relationship between thermoeffector responses and fer and exacerbated hyperthermia. These data indi-
core temperature (348, 349, 602–606). Although both cate that arterial and cardiac filling pressure are
hypovolemia (602, 607–609) and hyperosmolality (610– maintained through baroreflex modulation, at the
613) influence these responses, the increase in plasma expense of internal heat transfer, to preserve cardiac
osmolality appears to be more strongly correlated with output and muscle perfusion (355, 360, 618). These
the reduction in sweating during exercise-heat stress data further highlight that hypovolemia can stimulate
than the decrease in blood volume (614). Sawka et al. circulatory adjustments in the absence of hyperosmo-
(215) further demonstrated that sweat rate decreased lality, although in the context of exercise-induced
and thermal strain increased proportionally with the se- dehydration, hyperosmotic hypovolemia may further
verity of hypohydration during prolonged intermittent exacerbate these adjustments.
exercise in the heat (FIGURE 15). Adjustments in the onset threshold and sensitivity of
An attenuated skin blood flow response for a given thermoeffector responses are associated with factors of
level of thermal strain has also been reported (594, 603, both central and peripheral origin. Hypohydration and
605, 615–617). Nadel et al. (605) demonstrated that a dehydration may reduce the responsiveness of central
four-day diuretic-induced hypohydration (i.e., iso-osmotic neural structures regulating evaporative heat loss, with
hypovolemia) of 2.7% body mass loss (17.5% plasma vol- an increase in the onset threshold for sweating associ-
ume contraction) increased the esophageal temperature ated with a hyperosmolality-induced inhibition of warm-

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 PÉRIARD ET AL.

25 decline in systemic and regional perfusion is associated

Hyperhydration
Forearm blood flow (mL·min-1·100 mL-1) with a decrease in cardiac output, increase in total pe-
Euhydration
ripheral resistance, and reduction in mean arterial pres-
Hypohydration
20 sure during whole body exercise at intensities above
60% V_ O2max (594, 595, 616, 618). Conversely, skin,
15
muscle, and cerebral blood flow are uncompromised by
the combination of hyperthermia and dehydration dur-
ing exercise at low intensities or with a small muscle
10 mass (629, 630). The additive effect of dehydration and
hyperthermia during exercise is therefore mediated by
the severity of each factor. In a study examining different
5 magnitudes of dehydration on thermal and cardiovascu-
lar responses, Montain and Coyle (595) demonstrated a
linear relationship between the extent of body mass loss
0
36.5 37.0 37.5 38.0 38.5 39.0
and the increase in esophageal temperature and heart
Esophageal temperature (ºC) rate, as well as the decrease in stroke volume, cardiac
output, and skin blood flow (FIGURE 17).
FIGURE 16. Influence of hypohydration (2.7% body mass loss) The progressive rise in heart rate and decline in
and hyperhydration (2.4% body mass gain) on the relationship
between skin (forearm) blood flow and esophageal temperature dur-
stroke volume and cardiac output during aerobic exer-
ing 30 min of cycling at 55% V_ O2max in 35 C and 38% relative humid- cise with dehydration in hot (594, 616, 631–633) and
ity. The data indicate a lower cutaneous (forearm) blood flow for a temperate (e.g., 22 C) (634) conditions represent funda-
given esophageal temperature with hypohydration. Reproduced mental responses associated with dehydration-induced
with permission from Nadel et al. (605).
cardiovascular strain. The reduction in cardiac output is
primarily related to a decrease in stroke volume, owing
to hyperthermia-induced tachycardia and concomitant
sensitive neurons within the hypothalamus (i.e., median
reduction in blood volume, suppressed venous return,
preoptic nucleus) (619, 620). Osmotically driven periph-
and impaired cardiac filling (525, 526, 528, 529, 594,
eral interference with the function of sweat glands may
635). Maintaining euhydration through fluid ingestion
also reduce sweating (600, 621). While the influence of
allows for preventing severe hyperthermia and preserv-
hypovolemia-induced baroreceptor unloading (simu-
ing cardiovascular stability (594, 595, 616). Cold condi-
lated via lower body negative pressure, head-up tilting,
tions (2–10 C) also preserve circulatory function during
and pharmacological agents) on the modulation of
hypohydrated and dehydrating exercise (4% body
sweating remains controversial (622–627), it may occur
mass loss), as wide core-to-skin and skin-to-air tempera-
under mild to moderate heat stress but is unlikely to
ture gradients ensure dry heat loss to the environment
occur in relatively acute settings (628). Hypovolemia has
and minimal heat storage (594, 616, 636). González-
further been suggested to increase the onset threshold
Alonso et al. (616) demonstrated that hyperthermia with
for cutaneous vasodilation by reducing cardiac preload
dehydration leads to cardiovascular instability (i.e.,
and altering atrial baroreceptor activity (602), which pro-
impaired ability to maintain cardiac output and blood
vides afferent input to the hypothalamic thermoregula-
pressure) by having participants cycle for 30 min at
tory centers that regulate both cutaneous blood flow
70% V_ O2max in either 2 C or 35 C while 1) euhydrated
and sweating (216). Ultimately, unreplenished (i.e., hypo-
with an esophageal temperature of 38.2 C (normo-
hydration) or inadequately replaced (i.e., dehydration)
thermic), 2) euhydrated with an esophageal temperature
body water losses during exercise under heat stress
of 39.3 C (hyperthermic), 3) dehydrated (4% body
reduce blood volume and increase osmolality with the
mass) and hyperthermic with a skin temperature of
severity of these responses impacting on thermoregula-
34 C, 4) dehydrated and hyperthermic with a skin tem-
tory capacity.
perature of 21 C, and 5) previously dehydrated (i.e.,
restored blood volume) and normothermic with a skin
5.2. Adjustments in Cardiovascular Function temperature of 21 C. Hyperthermia and dehydration in
isolation were shown not to influence cardiac output or
Hyperthermia coupled with progressive dehydration mean arterial pressure during exercise, as their individ-
poses a significant challenge to thermoregulatory ual effects were similar and increased heart rate by 5%
capacity and cardiovascular control during prolonged and reduced stroke volume by 7–8% (616). In contrast,
exercise, characterized by a reduction in systemic, cuta- the combination of hyperthermia and dehydration
neous, active muscle and cerebral blood flow. The increased heart rate by 9% and decreased stroke

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 EXERCISE UNDER HEAT STRESS

35 0

Stroke volume (mL·beat-1)

Heart rate (beats·min-1)

30
-10
25
-20
20

15 -30
10 FIGURE 17. Influence of graded dehydra-
-40
5 tion (1.1, 2.3, 3.4, and 4.2% body mass loss)
on changes in heart rate, stroke volume
0 -50
and cardiac output from 10 to 110 min and
forearm blood flow from 50 to 105 min of
1.0 3.0
cycling at 65% V_ O in 33 C and 50%
2max
Cardiac output (L·min-1)

relative humidity. The data indicate that the

Forearm blood flow

magnitude of these responses is propor-

(mL·min-1·100mL)
2.0
0.0
tional to fluid losses experienced via sweat-
1.0 ing. Reproduced with permission from
-1.0 Montain and Coyle (595).
0.0

-2.0
-1.0

-3.0 -2.0
0.0 1.0 2.0 3.0 4.0 5.0 0.0 1.0 2.0 3.0 4.0 5.0

Body mass loss (%) Body mass loss (%)

volume by 20%, resulting in a 13% decrease in cardiac also resulted in a greater increase in esophageal tem-
output. Because heart rate was near maximum (96%) perature (1.5 C) than euhydrated exercise at the same
at the end of exercise, the cardiac output generated time point, along with a higher heart rate (28
was the highest possible but inadequate for maintaining beats·min 1) and lower stroke volume (40 mL·beat 1).
cardiovascular function, as evidenced by a decline in ar- Cardiac output was therefore reduced, as were mean
terial blood pressure and increase in systemic vascular arterial pressure and systemic vascular conductance,
resistance. These systemic circulatory adjustments leading to a 2 L·min 1 reduction in exercising muscle
reduce blood flow and impair oxygen delivery to active blood flow (FIGURE 18). The reciprocal relationship
muscles and the brain, both mechanisms that have been between systemic (i.e., cardiac output) and regional
implicated in the development of fatigue during aerobic (i.e., exercising limb) blood flow has been demon-
exercise in the heat. strated within various experimental paradigms, includ-
ing maximal exercise in the heat (399, 521) and
5.2.1. Skeletal muscle blood flow and metabolism. hyperthermia-induced local tissue hyperemia (382,
384). Others have also demonstrated a proportional
The loss of body water through sweating during exer- change in exercising muscle blood flow and cardiac
cise under heat stress leads to hyperosmotic hypovo- output using pharmacological agents to induce
lemia and increased heat storage due to a decreased changes in limb blood flow (637–641). Similar to maxi-
ability to dissipate heat. The increase in thermal strain mal exercise under heat stress (399), exercising mus-
during prolonged whole body exercise is associated cle vascular conductance remains unchanged or
with a compromised cardiovascular response, charac- slightly increases during whole body exercise with
terized in part by reductions in systemic and active hyperthermia and dehydration (618, 629). This indi-
muscle blood flow. Previous studies have demon- cates that the fall in exercising muscle blood flow dur-
strated that exercising muscle blood flow is main- ing prolonged exercise is associated with gradual
tained during prolonged euhydrated exercise in the systemic circulatory strain, rather than increased neu-
heat when marked cardiovascular strain is avoided ral vasoconstriction in the active musculature (642).
and the capacity to maintain cardiac output and oxy- The fall in muscle blood flow and subsequent fatigue
gen delivery is preserved (sect. 4.5). In contrast, during aerobic exercise have been linked to inad-
González-Alonso et al. (618) reported that progressive equate substrate delivery, energy deficiency, metabo-
dehydration (3.9% body mass loss) reduces exercising lite accumulation (i.e., H1 and Pi), and elevated muscle
muscle blood flow and oxygen delivery toward to end temperature, factors that may influence intracellular
of prolonged (135 min) exercise to exhaustion under metabolic processes (643, 644).
heat stress, in response to a decrease in perfus- When prolonged exercise is undertaken in a euhy-
ion pressure and systemic blood flow. Dehydration drated state with adequate systemic and skeletal

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 PÉRIARD ET AL.

24 glycogen utilization and lactate accumulation

increase during prolonged exercise with progres-
Cardiac output (L·min-1)
22 sive dehydration (1–3% body mass loss) in temper-
ate conditions (494–496, 647). Under heat stress, a
20
*† similar increase in muscle glycogen utilization and
lactate production occurs with dehydration (3.9%
*†
Euhydration *† body mass loss), along with a decrease in free fatty
18
Dehydration acid uptake (515). This occurs despite the reduction in
exercising muscle blood flow not compromising the
16
delivery of free fatty acids and glucose or lactate re-
126 moval. The reduction in free fatty acid uptake and
increase in carbohydrate oxidation reflects a shift in fuel
Mean arterial pressure

122
selection (648), with both hyperthermia and dehydra-
118 tion augmenting glycogen utilization, but hyperthermia
(mmHg)

114
potentially being the more potent stimulator. In a recent
study, Fernández-Elías et al. (514) had participants cycle
110
*† *† for 40 min at a submaximal work rate in temperate con-
106 ditions in a hypohydrated state (4.4% body mass loss)
and in temperate and hot conditions in a rehydrated
102
state (mild hypohydration: 1.3%). The authors reported
20
that hypohydration increased muscle glycogen utiliza-
Systemic vascular conductane

tion by 35% during exercise in temperate conditions.

Intestinal temperature during the hypohydrated trial
(mL·min-1·mmHg-1)

increased to 39.2 C, which was similar to the rehy-

19

drated trial in hot conditions and higher than the rehy-

18
drated trial (38.5 C) in temperate conditions. Despite
*† * † an 11% lower muscle water content at the start of the
17
hypohydrated trial in temperate conditions, glycogen
utilization was similar to that of the rehydrated trial in
16 the heat, indicating that hyperthermia and likely muscle
temperature are the primary factors stimulating glyco-
17
genolysis during intense whole body exercise. As with
Leg blood flow (L·min-1)

16
euhydrated exercise in hot environmental conditions
(see sect. 4.5), the physiological and perceptual
15 responses associated with dehydrated exercise at a
constant work rate under heat stress are commensurate
14
*† with the maintenance of a greater relative exercise in-
*† tensity (494–496, 514, 647). The elevated rate of carbo-
13
hydrate oxidation (i.e., skeletal muscle glycogenolysis)
12 and diminished rate of fat oxidation during exercise in
0 20 40 60 80 100 120 140 160
hot environmental conditions with concomitant hyper-
Time (min)
thermia, with or without dehydration, may reflect a pro-
FIGURE 18. Influence of euhydration and progressive dehydration gressive rise in relative exercise intensity in response to
(3.9% body mass loss) on cardiac output, mean arterial pressure, sys- a decrease in V_ O2max (see sect. 4.3). Given muscle gly-
temic vascular conductance, and muscle blood flow during exercise at cogen content is a primary determinant of aerobic per-
60% V_ O2max in 35 C and 45% relative humidity. The data indicate that
active muscle blood flow decreases during prolonged exercise in the
formance (511, 649–651), the increased rate of muscle
heat with dehydration in association with a decline in cardiac output glycogenolysis experienced under heat stress may
and systemic vascular conductance. Significantly lower than 20 min expedite the onset of fatigue during constant work rate
†
(P < 0.05). Significantly lower than euhydration (P < 0.05). Reproduced exercise. When performing self-paced exercise, work
with permission from González-Alonso et al. (618).
rate adjustments (i.e., reductions) would be required to
muscle blood flow, the delivery of substrates and re- continue exercising. Collectively, the development of
moval of metabolites within the active musculature hyperthermia and dehydration during aerobic exercise
are closely matched, both in temperate (645, 646) under heat stress compromise active muscle blood flow
and hot conditions (357, 372). However, net muscle and oxygen delivery, and increase the reliance on

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 EXERCISE UNDER HEAT STRESS

carbohydrate metabolism, both of which may contribute delayed the decline in MCAV, which occurred earlier
to premature fatigue development. with dehydration, concomitant with an elevated hyper-
thermia and tachycardia. As with the previous study, cer-
5.2.2. Cerebral blood flow and metabolism. ebral metabolism was preserved through enhanced
oxygen and glucose extraction across the brain (654).
Heat stress has been shown to reduce cerebral blood This observation is supported by data demonstrating an
flow during prolonged submaximal and brief maximal uncompromised cerebral metabolic rate for oxygen dur-
exercise (374, 401–405) in response to hyperventilation- ing the transition from rest to moderate intensity exer-
induced hypocapnia (i.e., decreased PaCO2), mediated cise (655–657), followed by a rise in cerebral meta-
by hyperthermia and the maintenance of an elevated bolism at intensities approaching maximum (404, 405,
exercise intensity, typically >60% V_ O2max. At rest, Ogoh 658). These data indicate that dehydration exacerbates
et al. (652) demonstrated that whole body passive cerebrovascular instability during brief exercise to voli-
heating (1.5 C increase in esophageal temperature) tional fatigue and prolonged strenuous exercise in the
increased cardiac output by 60% but failed to increase heat by accelerating the decline in cerebral blood flow.
intracranial blood flow (i.e., internal carotid and vertebral The accelerated decline in intracranial blood flow with
arteries) as a 15% reduction was noted. It was sug- dehydration is accompanied by a decrease in cerebro-
gested that blood flow was distributed to extracranial vascular conductance stemming from an increase in va-
(i.e., external carotid artery) vascular beds for heat dissi- soconstrictor activity, modulated primarily by a decline in
pation. It has further been reported during progressive PaCO2 (415, 654). The reduction in extracranial blood flow
passive heating that cerebral blood flow (i.e., MCAv) is during prolonged exercise in the heat with dehydration
reduced in response to hyperthermia-induced hyper- appears to be influenced by regulatory mechanisms akin
ventilation and the peripheral redistribution of cardiac to those of the cutaneous circulation (see sect. 4.1.1).
output (653). The authors further demonstrated that mild Given the metabolic stability exhibited by the brain,
hypohydration (1.5% body mass loss), in the absence of the notion that a compromise in oxygen delivery to the
hyperthermia, was associated with an elevated cerebral brain might mediate the development of fatigue or
blood flow at rest. In contrast, the reduction in cerebral impair performance during exercise under heat stress,
blood flow appears to be accelerated during dehydrated with or without concomitant dehydration, by compromis-
exercise under heat stress. For example, Trangmar et al. ing central neural drive (401, 404, 413, 414) appears
(415) demonstrated during incremental exercise to unlikely. Rather, the suppression of exercising muscle
exhaustion that the combination of dehydration (3% perfusion and aerobic metabolism associated with
body mass loss) and hyperthermia (0.7 C) precipitated greater thermal strain and cardiovascular instability dur-
the decline in intracranial (i.e., internal carotid and mid- ing exercise-induced hyperthermia and dehydration
dle cerebral arteries) blood flow without affecting extrac- appear to represent the primary determinants accelerat-
ranial (i.e., common carotid artery) blood flow. The ing fatigue development. This premature fatigue is asso-
combination of hyperthermia and dehydration decre- ciated with a decline in blood flow and oxygen delivery
ased the absolute work rate attained at V_ O2max by that requires an increase in oxygen extraction (i.e.,
20%, albeit with equivalent cerebral blood flow values a-vO2diff) to support aerobic metabolism in the active
to those without dehydration. The decline in cerebral musculature. The decline in blood flow is temporally
blood flow during incremental exercise in the heat, with associated with the attainment of upper limits to func-
or without dehydration, was accompanied by a compen- tional oxygen extraction, which blunts exercising muscle
satory increase in oxygen extraction, which allowed for oxygen uptake, and thus whole body V_ O2max. Trangmar
maintaining the cerebral metabolic rate for oxygen (415). and González-Alonso (659) developed an elegant con-
In a follow-up study, prolonged submaximal exercise in ceptual framework outlining the combined influence of
the heat was undertaken with and without eliciting dehydration and hyperthermia during maximal and sub-
exhaustion, in both a euhydrated and dehydrated state maximal exercise on regional (i.e., cerebral, skin, and leg
(654). Euhydration through fluid ingestion allowed for muscle) and systemic (i.e., cardiac output) hemodynam-
preserving intracranial and extracranial blood flow dur- ics, and the concomitant alterations in aerobic metabo-
ing nonfatiguing exercise, with progressive dehydration lism (FIGURE 19). The framework highlights how
(3% body mass loss) and greater hyperthermia dehydration-induced reductions in skin blood flow exac-
(0.5 C) accelerating the decline in internal carotid ar- erbate physiological strain by increasing thermal strain
tery blood flow and MCAV and eliciting a decline in and how the cerebral metabolic rate for oxygen is pre-
extracranial blood flow (i.e., common and external ca- served and unlikely to contribute to fatigue development,
rotid arteries) at the end of nonexhaustive exercise but that a reduction in exercising muscle aerobic metabo-
(120 min). During exhaustive exercise, euhydration only lism mediates dehydration-induced fatigue development.

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 PÉRIARD ET AL.

combined with hypohydration, the decrease in V_ O2max

Severe exercise-induced under heat stress might be expected to worsen, particu-
hyperthermia and dehydration larly given a recent meta-analysis reporting that a 4%
reduction in body mass leads to a 2.5% reduction in
V_ O2max in temperate conditions (20.5 C) (660). Under
heat stress however, when hyperthermia is combined
↓ Cerebral
blood flow
↓ Skin
blood flow
↓ Leg
blood flow
↓ Cardiac
output
with hypohydration, most of the reduction V_ O2max
appears attributable to the magnitude of thermal strain.
After inducing a 4% loss in body mass or maintaining
euhydration via fluid ingestion, Nybo et al. (321) had en-
↓ Systemic and regional durance-trained participants complete four maximal
oxygen transport
(402 W) cycling tests to exhaustion (<8 min): control,
hypohydration, hyperthermia, and a combination of
↑ Systemic and regional hypohydration and hyperthermia (FIGURE 20). Thermal
oxygen extraction strain was carefully manipulated with a water perfused
jacket so that starting esophageal and skin tempera-
tures were 37.5 C and 31 C in normothermia, and
38.5 C and 37 C in hyperthermia. A 16% reduction in
= Cerebral ↓ Leg oxygen ↓ Systemic V_ O2max was reported with hyperthermia, regardless of
metabolism uptake oxygen uptake
hydration status, along with a 52% reduction in exercise
time relative to the normothermic and euhydrated trial.
In the normothermic and hypohydrated trial a 5% reduc-
Fatigue
tion in V_ O2max and 26% decrease in exercise time were
Volitional exhaustion noted. The reduction in V_ O2max with hyperthermia was
ascribed to a decline in cardiac output, reducing blood
FIGURE 19. Conceptual framework of the impact of dehydration
flow and oxygen delivery to exercising skeletal muscles
on regional and systemic hemodynamics and aerobic metabolism. (321). The similar reduction in V_ O2max under heat stress,
The combination of dehydration, hyperthermia, and strenuous exer- with or without hypohydration, supports previous find-
cise markedly reduces cerebral, leg (i.e., muscle) and systemic (i.e., ings of a 26% decrease with hyperthermia alone (322)
cardiac output) blood flow. Dehydration-induced reductions in skin
blood flow exacerbate physiological strain by increasing body heat
and in combination with hypohydration (4.3% body mass
storage. The reduction in cerebral blood flow is associated with a loss) (661), the latter study also reporting a 48% reduc-
hyperventilation-induced fall in arterial carbon dioxide pressure. The tion in exercise time. In a separate study, V_ o2max was
reduction in cardiac output is due to a progressive decrease in measured immediately after 60 and 120 min of submaxi-
stroke volume in response to an increase in heart rate toward maxi-
mum and concomitant to a fall in end-diastolic volume that is not
mal cycling in warm conditions without fluid ingestion
compensated for by the reduction in end-systolic volume. The fall in (2.3% and 3.7% body mass loss, respectively) and after
whole body perfusion requires tissue and systemic oxygen extrac- 120 min with fluid ingestion (0.7% body mass loss) (662).
tion to increase to support aerobic metabolism. Although the cere- A significant reduction in V_ O2max of 8.7% was observed
bral metabolic rate for oxygen is well preserved, and unlikely to
contribute to fatigue development during short-duration maximal
after 120 min without fluid ingestion, in conjunction with
and prolonged submaximal exercise, reductions in active muscle greater hyperthermia (0.3 C), relative to the other con-
and systemic aerobic metabolism are likely candidates to mediate ditions in which V_ O2max remained unchanged. Pichan et
dehydration-induced fatigue development. Adapted with permission al. (663) also demonstrated following heat acclimation
from Trangmar and González-Alonso (659).
that hypohydration of 1.3, 2.3, and 3.3% body mass
decreased V_ O2max in hot/dry conditions (45 C, 30% RH)
by 8.7, 11.0, and 21.7% and in hot/humid conditions
5.3. Heat Stress, Hydration Status, and Maximal (39 C, 60% RH) by 5.6, 8.0, and 20.4%. The environmen-
Aerobic Power tal conditions (i.e., dry vs. humid) led to a similar
decrease in V_ O2max, which was more pronounced when
The progressive rise in thermal strain when exercising in hypohydrated by 3% body mass. Altogether, these data
increasingly hot ambient conditions is associated with indicate that V_ O2max declines markedly upon exceeding
an exacerbated decrease in V_ O2max (319). The magni- the 3% body mass loss threshold (642, 660) and may
tude of the decrease is reliant on marked elevations in only slightly exacerbate the effects of hyperthermia. This
both core and skin temperature, which in turn drive an suggests that an elevated whole body temperature (e.g.,
increase in physiological strain that suppresses systemic core temperature >38 C and skin temperature >35 C)
and exercising muscle oxygen delivery (321, 521). When exacerbates cardiovascular strain and precipitates the

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 EXERCISE UNDER HEAT STRESS

5 To further investigate the influence of hydration status

on exercise capacity and performance, we explored the
4
scientific literature and segmented dehydration and
Oxygen uptake (L·min-1)

hypohydration in body mass deficits of 0.5–1.4, 1.5–2.4,

2.5–3.4, 3.5–4.4, and 4.5% across ambient conditions
3
above and below 30 C. In addition to utilizing the
reviews highlighted above, a systematic search of the lit-
2 erature was conducted on PubMed (August 2020) to
identify aerobic-based constant work rate (excluding
1 Normo & Euhy Hyper & Euhy incremental/graded V_ O2max tests) and self-paced exer-
Normo & Hypo Hyper & Hypo cise protocols evaluating the impact of dehydration and
hypohydration. To be included in our analysis, studies
0
0 1 2 3 4 5 6 7 had to be compared with a euhydration (control) trial and
Time (min) provide environmental condition information (otherwise
assumed to be <30 C, i.e., Ref. 667). Studies examining
FIGURE 20. Influence of hyperthermia and hypohydration on max-
imal aerobic and endurance capacity. Oxygen uptake during maxi- the influence of fluid or beverage composition (e.g., so-
mal cycling to exhaustion at 402 W in normothermic (Normo) and dium or carbohydrate) were excluded, unless controlled
hyperthermic (Hyper: esophageal and mean skin temperature: 11 C for between trials (i.e., Refs. 668, 669). The observations
and 16 C higher, respectively) states, while euhydrated (Euhy) or
hypohydrated (Hypo: 4% body mass loss). The data indicate hyper-
from our review of the literature are summarized in the
thermia with or without hypohydration similarly reduces V_ O2max and sections below. We identified 11 constant work rate stud-
that part of this reduction is restored when normothermic but hypo- ies providing 22 comparisons (TABLES 2 and 3; addi-
hydrated, such that most of the decline in V_ O2max with combined tional details provided in APPENDIX A) and 33 self-paced
hyperthermia and hypohydration is associated with hyperthermia.
Redrawn with permission from Nybo et al. (321).
exercise studies providing 58 comparisons (TABLES 4
and 5; additional details provided in APPENDIX A). For
ease of comparison, all performance outcomes were
attainment of V_ O2max to a greater extent than hypohy- converted to percent change in time relative to euhydra-
dration of 3–4% during maximal exercise. Whether a tion by equating a 1% change in power output to a 1%
similar relationship persists with severe hypohydration change in running time-trial speed or time and a 0.4%
(e.g., >6%) remains to be determined. Notwithstanding, change in time during a cycling time trial (709).
hyperthermia and hypohydration/dehydration interact in Decrements in exercise capacity and performance were
modulating systemic and regional blood flow (i.e., oxy- converted to negative percent changes such that a
gen delivery), such that their influence is integrative. shorter time to volitional exhaustion during constant
work rate exercise and longer time to complete a time
5.4. Heat Stress, Hydration Status, and Prolonged trial or less distance completed during self-paced exer-
Aerobic Exercise cise are expressed as negative values. Several perform-
ance trials, both at a constant work rate and self-paced,
The combination of environmental heat stress and a were performed following prolonged exercise (e.g., 60-
compromised hydration status during constant work rate to 90-min preload). While the exercise preload was not
exercise is characterized by an exacerbated rise in body included in the analysis of performance, its implications
core temperature; decreased systemic, muscle, and skin on physiological responses and performance are impor-
blood flow; and increased reliance on muscle glycogen tant and so it has been acknowledged where relevant.
and anaerobic metabolism (215, 595, 605, 618). These The separation of dehydration and hypohydration is im-
responses lead to premature fatigue with several narra- portant when investigating the influence of hydration sta-
tive and meta-analytical reviews reporting that a body tus on performance as initiating exercise with a particular
mass loss exceeding 2% impairs exercise capacity, body water deficit (e.g., 3%: hypohydration) has different
particularly when ambient temperature surpasses 30 C physiological implications to reaching such a deficit dur-
(204, 660, 664, 665). In contrast, exercise-induced ing the final stages of a prolonged effort (e.g., final 15 min
dehydration to 4% body mass loss does not appear to of a 90-min exercise bout: dehydration). It must also be
impact on performance during ecologically valid self- acknowledged that exercise capacity and performance
paced exercise tasks (e.g., cycling or running time trials) are not suddenly and markedly impaired upon reaching a
performed in 20 to 33 C conditions (665, 666). particular level of dehydration, but progressively affected
However, hypohydration of 1.7 to 5.6% body mass has as dehydration develops. Moreover, while constant work
been shown to impair aerobic exercise performance in rate exercise allows for isolating independent variables
ambient temperatures ranging from 19 to 40 C (660). (e.g., fluid intake) in a well-controlled environment to

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 PÉRIARD ET AL.

Table 2. Influence of different levels of dehydration on exercise capacity during constant work rate exercise to
exhaustion in ambient temperature conditions below and above 308C
Body Mass Loss
Study 0.5–1.4% 1.5–2.4% 2.5–3.4% 3.5–4.4% >4.5% Exercise Time, %

Ambient temperature <308C

McConell et al. (670) – 1.8 – – – 24.4

Maughan et al. (671) – 1.8 – – – 7.9

Fallowfield et al. (672) – 2.0 – – – 24.6

McConell et al. (670) – – 3.2 – – 47.9

Ambient temperature 308C

de Melo-Marins et al. (673) 1.0 – – – – 2.6

Marino et al. (674) 1.0 – – – – 1.5

de Melo-Marins et al. (673) 1.3 – – – – 2.6

Marino et al. (674) – 1.7 – – – 21.1

Negative exercise capacity percent values represent a shorter time to volitional exhaustion relative to euhydration. Protocol details provided in TABLE
A1. P < 0.05, significantly different from euhydration/control.

examine their effect on dependent variables (e.g., voli- seems to corroborate. A 19% (range: 24.6 to 7.9%)
tional fatigue), it has been argued that this model of exer- reduction in endurance time was noted with a body mass
cise lacks ecological validity (229, 666, 710, 711). loss <2.5% and ambient temperature <30 C. These data
Endurance athletes competing in real-world settings typi- represent three studies in which a similar relative intensity
cally complete a known distance as quickly as possible, (70% V_ O2max) was prescribed, twice to exhaustion (671,
rather than maintain a given work rate for as long as possi- 672) and once for 120 min and then followed by an
ble. As such, self-paced time trials are typically viewed as increase in work rate to 90% V_ O2max until fatigue (670).
more representative of a true competitive environment, as With a body mass loss of 3.2%, a much larger reduction
athletes can adjust their work rate and regulate their effort. (47.9%) in time to exhaustion was reported and coincided
The within-subject reliability of self-paced exercise trials is with greater thermal and cardiovascular strain (670). In
generally greater than time to exhaustion tests (712–714), ambient conditions 30 C a 7.0% (range: 21.1 to 1.5)
although both appear to display similar reliability when the reduction in exercise capacity was observed when body
curvilinear relationship between exercise intensity and du- mass losses remained <2.5%. Although no study met the
ration is accounted for (715) and have similar sensitivity inclusion criteria for dehydration 2.5% body mass, one
(716). Moreover, it has been argued that exercise to voli- did demonstrate a 25% decrease in endurance time
tional fatigue does have some relevance to competitive with a 6.4% body mass loss (717). This study was not
race scenarios, such as when athletes adopt the pace set included, however, as the euhydration trial was termi-
by faster competitors until unable to follow (714). nated after a predetermined time frame, rather than voli-
Notwithstanding, differentiating the influence of a compro- tional fatigue. Although available data are generally
mise in hydration status between constant work rate and limited, they indicate that aerobic exercise capacity is
self-paced exercise provides insight into how fatigue largely preserved when body mass loss remains 1.0%
develops when hyperthermic and hypovolemic. but is impaired when dehydration approaches and sur-
passes 2.0%, both in temperate and hot conditions.
5.4.1. Constant work rate exercise and
dehydration. 5.4.2. Constant work rate exercise and
hypohydration.
Dehydration in excess of 2% body mass has been
reported to impair constant work rate exercise to voli- A marked body water deficit (i.e., hypohydration) before
tional fatigue in warmer environments, which TABLE 2 undertaking exercise influences physiological responses

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 EXERCISE UNDER HEAT STRESS

Table 3. Influence of different levels of hypohydration on exercise capacity during constant work rate exercise to
exhaustion in ambient temperature conditions below and above 308C
Study Body Mass Loss Exercise Time, %

0.5–1.4% 1.5–2.4% 2.5–3.4% 3.5–4.4% >4.5%

Ambient Temperature <308C

Ebert et al. (675) 2.5 28.7

0.5–1.4% 1.5–2.4% 2.5–3.4% 3.5–4.4% >4.5%

Ambient temperature 308C

Walsh et al. (676) – 1.8 – – – 30.6

Cheung and McLellan (677) – 1.9 – – – 4.4

Cheung and McLellan (368) – 1.9 – – – 12.5

Baker et al. (668) – 2.0 – – – 33.3

Cheung and McLellan (677) – 2.0 – – – 11.9

Cheung and McLellan (368) – 2.0 – – – 18.6

Cheung and McLellan (368) – 2.1 – – – 14.6

Cheung and McLellan (368) – 2.2 – – – 12.4

Cheung and McLellan (678) – 2.2 – – – 10.7

Cheung and McLellan (678) – 2.2 – – – 18.2

Cheung and McLellan (677) – – 2.6 – – 20.5

Cheung and McLellan (677) – – 2.8 – – 20.6

Baker et al. (668) – – 3.3 – – 61.9

Negative exercise capacity percent values represent a shorter time to volitional exhaustion relative to euhydration. Protocol details provided in TABLE
A2. P < 0.05, significantly different from euhydration/control.

from the onset of exercise and exacerbates the rise in a body mass deficit of 1.8 to 2.0% (368, 668, 676, 677).
whole body temperature. As such, undertaking constant The studies performed by Cheung and McLellan (368,
work rate exercise in a hypohydrated state is clearly detri- 677, 678) are noteworthy as participants were dehy-
mental to endurance capacity, regardless of the prevail- drated 15 h before undertaking a walking heat tolerance
ing ambient conditions (TABLE 3). One study reported test to volitional fatigue while wearing protective clothing,
that hypohydration of 2.5% body mass yielded a 28.7% such that the environment was uncompensable. Alt-
reduction in exercise capacity during a simulated hill hough some participants terminated exercise because of
climb (8% gradient) in 29 C conditions (675). Despite reaching the ethically imposed upper limit for rectal tem-
being 1.9 kg lighter, time to exhaustion was reduced in perature (39.3 C), they reported being very near the point
conjunction with an elevated rectal temperature (0.5 C) of voluntary termination. Moreover, the average endpoint
and heart rate (4 beats·min 1). When ambient tempera- rectal temperature in each study was 38.8 C (677),
ture exceeds 30 C, a 17% (range: 33.3 to 4.4%) 38.6 C (368), and 39.0 C (677) due to the uncompen-
decrease in endurance time is noted with hypohydration sable nature of the protocol. As such, these studies were
<2.5% body mass and 34% (range: 61.9 to 20.5%) included in the current section. The series of studies indi-
reduction with hypohydration 2.5%. The impact of hypo- cated that even mild hypohydration impairs endurance
hydration in hotter conditions is quite marked, even with capacity under uncompensable heat stress and that

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Table 4. Impact of different levels of dehydration on exercise performance during self-paced efforts with ambient
temperature below and above 308C
Body Mass Loss
Study 0.5–1.4% 1.5–2.4% 2.5–3.4% 3.5–4.4% >4.5% Performance Time (%)

Ambient Temperature <308C

Bachle et al. (679) 1.0 – – – – 1.3

McConell et al. (680) 1.0 – – – – 0.7

Backx et al. (681) 1.3 – – – – 0.1

Backx et al. (681) – 1.7 – – – 0.5

Kay and Marino (682) – 1.8 – – – 3.3

McConell et al. (680) – 1.9 – – – 0.7

Bardis et al. (683) – 2.2 – – – 5.8

Robinson et al. (684) – 2.3 – – – 1.4

Daries et al. (685) – – 2.6 – – 1.3

Hillman et al. (686) – – 3.0 – – 2.0

Daries et al. (685) – – 3.2 – – 2.6

Ambient temperature 308C

Bardis et al. (687) – 1.8 – – – 4.7

Below et al. (669) – 1.9 – – – 6.5

Dugas et al. (688) – 1.9 – – – 0.6

Dugas et al. (688) – 2.1 – – – 1.0

Perreault-Briere et al. (689) – 2.2 – – – 0.2

Adams et al. (690) – 2.2 – – – 4.7

Kay and Marino (682) – 2.2 – – – 0.0

Dugas et al. (688) – – 2.9 – – 3.6

Perreault Briere et al. (689) – – 2.9 – – 0.5

Dion et al. (691) – – 3.1 – – 1.1

Hillman et al. (686) – – – 3.8 – 5.0

Dugas et al. (688) – – – 3.9 – 3.2

Dugas et al. (688) – – – 4.3 – 2.3

Negative performance percent values represent a longer time to complete a known distance, or less distance completed over a given time period.
Protocol details provided in TABLE A3. P < 0.05, significantly different to euhydration/control.

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Table 5. Influence of different levels of hypohydration on exercise performance during self-paced efforts with ambi-
ent temperature below and above 308C
Body Mass Loss
Study 0.5–1.4% 1.5–2.4% 2.5–3.4% 3.5–4.4% >4.5% Performance Time, %

Ambient Temperature <308C

Slater et al. (692) 1.3 – – – – 0.8

Armstrong et al. (693) – 1.6 – – – 7.2

Merry et al. (694) – 1.8 – – – 5.2

Merry et al. (694) – 1.8 – – – 2.4

Armstrong et al. (693) – 1.9 – – – 3.4

Slater et al. (692) – 2.0 – – – 0.5

Armstrong et al. (693) – 2.1 – – – 6.7

Stearns et al. (695) – 2.1 – – – 4.6

Casa et al. (696) – 2.3 – – – 4.8

Logan-Sprenger et al. (494) – 2.3 – – – 13.0

Fleming and James (697) – 2.4 – – – 5.8

Fleming and James (697) – 2.4 – – – 1.2

Cheuvront et al. (698) – – 2.9 – – 1.0

Cheuvront et al. (698) – – 3.0 – – 3.2

Burge et al. (667) – – 3.1 – – 4.9

Oliver et al. (699) – – 3.2 – – 2.8

Stewart et al. (700) – – – 3.8 – 3.0

Castellani et al. (701) – – – 4.0 – 5.2

Kenefick et al. (702) – – – 4.1 – 1.1

Kenefick et al. (702) – – – 4.2 – 3.8

Ambient temperature 308C

Bardis et al. (703) 1.0 – – – – 2.1

Berkulo et al. (704) 1.1 – – – – 1.6

Slater et al. (692) 1.1 – – – – 0.8

Berkulo et al. (704) 1.3 – – – – 0.3

Slater et al. (692) – 2.0 – – – 0.1

Cheung et al. (705) – 2.0 – – – 0.6

Continued

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 PÉRIARD ET AL.

Table 5.—Continued
Body Mass Loss
Study 0.5–1.4% 1.5–2.4% 2.5–3.4% 3.5–4.4% >4.5% Performance Time, %

Wall et al. (706) – 2.1 – – – 0.1

Cheung et al. (705) – 2.1 – – – 2.1

James et al. (707) – 2.4 – – – 3.1

Wall et al. (706) – – 3.0 – – 0.1

Funnell et al. (708) – – 3.0 – – 11.4

Funnell et al. (708) – – 3.0 – – 10.1

Kenefick et al. (702) – – – 4.0 – 4.9

Kenefick et al. (702) – – – 4.1 – 8.7

Negative performance percent values represent a longer time to complete a known distance, or less distance completed over a given time period.
Protocol details provided in TABLE A4. P < 0.05, significantly different to euhydration/control.

short-term aerobic training and heat acclimation fail to during 60-min cycling time trials interspersed with
enhance exercise-heat tolerance in such conditions, sprints efforts in 20 C and 33 C conditions, both with or
whereas long-term aerobic fitness from regular physical without mild dehydration (2% body mass loss). These
activity is beneficial. The larger reductions in performance observations are notable for the similar performance
capacity noted in the Baker et al. (668) and Walsh et al. outcome in 20 C and 33 C conditions without dehydra-
(676) studies likely reflect differences in protocol, with tion, which contrast previous studies where prolonged
participants in both studies running or cycling at 70% time trial performance in the heat was impaired relative
V_ O2max for 60–120 min before exercising to exhaustion at to cool conditions (311–314, 560, 718). The lack of differ-
85–90% V_ O2max. The higher exercise intensity sustained ence between hot and cool conditions indicates a
following the initial bout of exercise to induce hypohydra- potential lack of statistical power (n = 7) and/or task famil-
tion may have exacerbated the impairment in subsequent iarity. The findings of Dugas et al. (688) of comparable
performance. Hence, mild to moderate hypohydration performances during 80-km cycling time trials across six
reduces exercise capacity in both hot and cool condi- fluid intake conditions may also have been subject to
tions, with exercise performed at higher intensities possi- type II error (n = 6). To address this, the authors created
bly hastening fatigue development. two body mass deficit groups (i.e., above and below
2.5%), which highlighted the significant impairment in
5.4.3. Self-paced exercise and dehydration. performance afforded by dehydration. The similar ther-
mal responses observed between conditions may be
The influence of dehydration on self-paced exercise associated with the 10.5 m·s 1 airflow provided during
performance appears to be quite equivocal, particularly exercise, which does provide greater convective and
in cooler environments. During time trial efforts in ambi- evaporative heat loss and more accurately reflects an
ent conditions of <30 C, a similar 0.2% reduction in per- outdoor cycling setting. Bardis et al. (683) also reported
formance is noted with body mass losses <2.5% (range: a decrease in performance during a 5-km cycling hill
5.8 to 3.3%) and 2.5% (range: 2.0 to 2.6%). At ambi- climb in 28–30 C outdoor conditions following 60 min
ent temperature 30 C, a slightly greater impairment in of indoor cycling. Airflow during the hill climb likely
performance is noted, which is again similar between matched that of moving speed (4.7 m·s 1), yet perform-
body mass losses below ( 2.2%, range: 6.5 to 1.0%) ance was impaired. Other studies have also shown that
and above ( 2.1%, range: 5.0 to 1.1%) 2.5%. The lack of 10- to 20-min time trial performance is decreased in
a persistent effect of dehydration on self-paced exercise warmer environments with limited airflow after an initial
performance likely stems from the progressive nature of 90 min of submaximal exercise (669, 686). In contrast,
body water loss and the duration of most efforts being Daries et al. (685) reported unaffected 30-min running
60 min. Of note, Kay and Marino (682) reported similar time trial performances after 90 min of steady-state run-
thermal, physiological, and performance outcomes ning in 25 C conditions with an airflow commensurate

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 EXERCISE UNDER HEAT STRESS

with running speed (3.8 m·s 1), despite 2.6% and 3.0% of fluid status on performance outcomes because of dif-
body mass losses. ferences in water deficit before and during exercise,
Ambient temperature, relative humidity, and airflow (in environmental conditions, exercise task (i.e., constant
studies reporting them) were 26.9 C, 55.3%, and 5 m·s 1 work rate versus self-paced), and participant characteris-
in the cycling studies and 27.5 C, 48.5%, and 4.0 m·s 1 in tics (i.e., age, sex, fitness, and acclimation state). It must
the running studies identified in TABLE 4. This indicates also be acknowledged that while laboratory-based stud-
that airflow in the cycling studies was less than encoun- ies offer control and provide significant mechanistic
tered when competing in an outdoor environment and insight regarding the impact of hydration status on exer-
may have influenced performance outcomes. Notwith- cise capacity and performance in the heat, several fac-
standing, self-paced exercise performance is relatively tors relative to exercising in a real-world environment
well maintained with dehydration <4% body mass, partic- reduce the validity of certain findings. These factors
ularly in cooler conditions even when exercise is include familiarization to the stressor (i.e., hypohydra-
>60 min, due to the progressive nature of body mass tion), ability to drink ad libitum, airflow provided during
loss. However, some studies may have been underpow- exercise, being blinded to hydration status, and under-
ered (i.e., small sample size) to draw firm conclusions. standing the consequences of hypohydration (229).
Notwithstanding, based on the data discussed above it
5.4.4. Self-paced exercise and hypohydration. appears that constant work rate exercise is well main-
tained with dehydration and hypohydration around 1%
The impact of hypohydration on self-paced exercise per- body mass, even in the heat. However, a 2% body
formance is more consistent and pronounced than that mass deficit incurred before or during exercise leads to
of dehydration (TABLE 5). A body water deficit <2.5% is a marked decrease in exercise capacity over a range of
associated with a 4.6% (range: 13.0 to 0.5%) impair- ambient temperatures (20 to 40 C). Although fewer data
ment in time trial performance in temperate conditions are available to compare the effects of hydration status
(<30 C) and 3.1% (range: 5.2 to 1.0%) decrement with on constant work rate exercise relative to self-paced
hypohydration 2.5% body mass. In warmer environ- exercise, the influence of dehydration and hypohydra-
ments (30 C), a body mass deficit <2.5% before exer- tion are much clearer in the former. Indeed, the impact
cise appears not to influence performance ( 0.6%, of dehydration during time trial exercise is equivocal
range: 3.2 to 2.1%), whereas a deficit 2.5% leads to a and performance appears to be preserved up to a 4%
7.0% (range: 11.4 to 0.1%) impairment. The lower impair- loss in body mass in 20 to 33 C environments. Beyond
ment in performance noted with hypohydration under this level of dehydration, the data are ambiguous but
2.5% may be influenced by four experimental trials in indicate a loss of performance. However, hypohydration
which body mass before exercise was only reduced by is associated with a reduction in performance when a
1.0 to 1.3%, which is within the range of day-to-day body time trial is undertaken with a body mass deficit around
mass fluctuations (282, 719). In studies where hypohy- 3% or larger across a spectrum of ambient temperatures
dration was 2.0 to 2.1% of body mass, intravenous infu- (10 to 40 C). These observations support those of previ-
sion of isotonic saline was used to manipulate hydration ous reviews (204, 660, 664, 665) and emphasize the
state. In the study of Wall et al. (706), intravenous saline impact of a reduction in total body water and blood/
infusion was shown to restore blood volume, which plasma volume in augmenting thermal strain and com-
probably alleviated the effects of hypovolemia on cardi- promising systemic and regional blood flow and oxygen
ovascular function, as evidenced by a similar cardiovas- delivery. The data also highlight the importance of con-
cular (i.e., heart rate) response to euhydration. In vective and evaporative cooling, with studies providing
contrast, hypohydration 3% yielded consistent per- an airflow commensurate with the activity (e.g., running
formance impairments in ambient conditions of 30 to or cycling) associated with less of a performance impair-
40 C (702, 708). Kenefick et al. (702) reported increas- ment (685, 688, 689, 691, 694, 706), although several
ingly larger performance reductions with hypohydration factors interact to regulate performance (FIGURE 6).
of 4% body mass when ambient temperature increased
from 10 to 20, 30, and 40 C. Although the influence of 5.5. Blinded Rehydration
hypohydration is less robust during self-paced com-
pared with constant work rate exercise, it does appear The effect of hypohydration on thermoregulatory, cardi-
to impair performance when exercise is initiated with a ovascular, and perceptual responses during prolonged
body water deficit of 3% or greater in temperate and hot exercise in the heat forms the mechanistic basis on
environments. which performance impairments occur. Conventional
In summary, caution should be employed when com- methods used to induce different levels of hypohydra-
paring the results of investigations assessing the impact tion (e.g., active or passive heat exposure with fluid

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 PÉRIARD ET AL.

restriction and diuretic administration) before an exer- body mass loss) during intermittent cycling in warm con-
cise task allow for participants to know the hydration sta- ditions with moderate airflow (4.5 m·s 1). Despite elicit-
tus under which exercise will be conducted. This ing only mild dehydration, performance was reduced
knowledge may partly influence performance (706, 708) (8%) in the latter states of exercise compared with
through either a placebo (euhydration) or nocebo (hypo- euhydration, in conjunction with an elevated rectal tem-
hydration) effect (720), given that athletes are aware of perature (0.4 C). Previous findings from that laboratory
the impact of hypohydration on endurance performance support the notion that mild dehydration or hypohydra-
(721). Several recent studies have therefore attempted tion impair aerobic exercise performance in the heat
to blind hydration status by manipulating total body (683, 687, 703).
water via intravenous infusion of isotonic saline (705, The intravenous infusion of isotonic saline following
706, 722) or gastric infusion of water with a nasogastric exercise-induced hypohydration restores blood/plasma
feeding tube (690, 707, 708). volume to varying degrees without affecting plasma os-
The first study attempting to blind hydration status molality, such that subsequent exercise is performed
rehydrated participants following exercise in the heat under an atypical hydration status. To replicate the phys-
through intravenous isotonic saline infusion to elicit iological and perceptual responses associated with
hypohydration of 0, 2, and 3% body mass loss before a exercise-induced hypohydration (i.e., decreased plasma
25-km cycling time trial in the heat with an ecologically volume and increased plasma osmolality and thirst)
valid airflow (9 m·s 1) (706). As a result of the infusion, while keeping participants naïve to hydration status,
blood volume was restored to baseline levels or above James et al. (707) used a combination of oral and intra-
before commencing each time trial and remained ele- gastric rehydration to maintain (0% body mass loss) and
vated during exercise via continuous infusion to match elicit a 2.4% body mass loss before a 15-min cycling time
sweat rate. Consequently, performance, physiological, trial in the heat with minimal airflow (0.35 m·s 1). The
and perceptual responses, including thirst sensation, intermittent exercise protocol performed before the time
were similar between trials, although rectal temperature trial elicited the physiological and perceptual responses
was 0.3 C higher from 17 km onward in the 3% hypohy- commensurate with dehydration (i.e., increased heart
dration trial. The similarity in responses was attributed to rate, rating of perceived exertion, serum osmolality, and
saline infusion preventing greater cardiovascular strain thirst and reduced plasma volume). Performance during
by restoring blood/plasma volume and cardiac filling. the subsequent time trial was reduced by 7.5% with
Serum osmolality, which drives the thirst sensation (723, hypohydration, while heart rate and gastrointestinal tem-
724), was also similar between trials. It has been argued perature were similar to euhydration, although a non-
that the sensation of thirst, rather than the loss of body significant increase in final gastrointestinal temperature
water, modulates performance impairments during aero- of 0.35 C was noted with hypohydration (707). Given
bic exercise to ensure that brain osmolality remains the low facing airflow in this study, it is likely that evapo-
within homeostatic range (711, 725). To investigate how rative heat loss was affected in both the hypohydrated
thirst and hydration status might affect performance, and euhydrated trials (315, 729). It has also been shown
Cheung et al. (705) used intravenous saline infusion af- during a 5-km cycling time trial in the heat with an airflow
ter 90 min of dehydrating exercise in the heat to create of 4.5 m·s 1 that hypohydration (2.2% body mass loss)
body mass deficits of 0% and 3% before completing a impairs performance, independently of thirst, when
20-km time trial in hot conditions with moderate airflow manipulated by intragastric water delivery and drinking
(3 m·s 1). Thirst during the time trial was manipulated by small amounts of water (690). The 6% decrement in
altering the sensation of dryness in the mouth by rinsing performance was associated with a similar heart rate to
with water. This approach reduced the sensation of the euhydrated trial but greater increase in rectal tem-
thirst but performance was unaffected, regardless of perature (0.4 C).
hydration status and despite hypohydration leading to Taken together, these observations indicate that the
greater increases in rectal temperature (0.7 C) and effects of hypohydration on endurance performance are
heart rate (5 beats·min 1). Although the sensation of not entirely mediated by dipsogenic drive, occurring in
thirst was reduced with mouth rinsing, it has been shown conjunction with both high and low sensations of thirst.
that oral fluid ingestion increases exercise performance Moreover, it appears that knowledge of hydration status
relative to mouth rinsing (726), by stimulating oropharyn- does not exacerbate the impairment in performance
geal reflex inhibition of vasopressin secretion and dipso- stemming from hypohydration. Indeed, the influence of
genic drive (i.e., thirst) (727, 728). Using both intravenous blinded and unblinded hypohydration on self-paced
infusion of isotonic saline and oral fluid ingestion to elicit exercise performance in warm conditions with high air-
a similar perception of thirst, Adams et al. (722) main- flow (5.9 m·s 1) was investigated by controlling for thirst
tained euhydration and elicited mild dehydration (1.8% and maintaining euhydration (0.5% body mass loss) or

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 EXERCISE UNDER HEAT STRESS

inducing hypohydration (3% body mass loss) via intra- typically aimed at individuals exercising for protracted
gastric rehydration and oral ingestion of small amounts periods of time in hot outdoor environments. These
of fluid (708). Hypohydration similarly impaired 15-min recommendations have evolved since first introduced
cycling time trial performance whether blinded (11%) or 50 yr ago, to account for the sport or activity (i.e., du-
unblinded (10%) to hydration status, with similarly exa- ration and intensity), setting (i.e., recreational or com-
cerbated alterations in heart rate, rating of perceived petitive), individual (i.e., training and acclimatization
exertion, gastrointestinal temperature, serum osmolality, status), and environmental conditions.
thirst, and plasma volume, relative to euhydration. This Interest regarding the impact of hydration status and
reinforces the observations and interpretation of previ- fluid ingestion during athletic events emerged in the
ous studies that hypohydration equivalent to 3% of 1960s but mostly focused on marathon running.
body mass is detrimental to performance, despite partic- Following its inception in the first Olympic Games in
ipants knowledge of hydration status. 1896, drinking and eating during a marathon were dis-
couraged for a variety of reasons, ranging from pride to
5.6. Hydration Guidelines digestive discomfort (742–744). While research regard-
ing the effects of dehydration on work performance was
The influence of hydration status on aerobic performance advancing in occupational and military settings (220,
and the approach used to hydrate (i.e., ad libitum or 221, 223, 224, 585, 588, 590, 745), studies focusing on
planned drinking) during exercise are highly debated athletic performance appeared later and mainly investi-
topics. It is not the intention of this section to participate gated the impact of severe body water loss on heat dis-
in this debate or to address optimal fluid composition (i.e., sipation and hyperthermia. For example, Pugh et al.
carbohydrate and electrolyte), as previous papers have (746) reported that the winner of a marathon in temper-
discussed this in detail (204, 725, 730, 731). Instead, this ate conditions experienced a 6.7% loss of body mass
section outlines the evolution of hydration (i.e., fluid and final rectal temperature of 41.1 C. Such elevated rec-
replacement) recommendations and contextualizes the tal temperatures had been reported previously in
most recent guidelines to exercise performance in the shorter (e.g., <10 km) warm, humid races (747). Of inter-
heat. est, however, was that average water intake during the
On one hand, performance impairments have been marathon was 420 mL and the concomitant body
shown to occur when body mass losses exceed 2% mass deficit 5.2% (746). It was concluded that the
during exercise in well-controlled laboratory settings capacity to dissipate heat limits performance and that
under temperate conditions (667, 669, 670, 672, 692, successful runners have elevated sweat rates. To avoid
698, 732, 733). Avoiding such losses with a planned fluid the detrimental effects of dehydration, Wyndham and
intake strategy has been suggested to optimize per- Strydom (748) subsequently suggested to drink 300 mL
formance by preserving thermoregulatory and cardio- of water every 20 min from the beginning of a marathon
vascular function (59, 146, 201, 204, 734–736). On the (748). This suggestion was derived from the significant
other hand, some studies have shown endurance per- linear relationship (r = 0.67) established between the
formance to be uncompromised in temperate conditions magnitude of dehydration (beyond 3% body mass loss)
despite a 2% body mass loss (680, 684) and reported and final rectal temperature during a 32-km run. A simi-
that the fastest finishers in endurance events (e.g., mara- lar correlation (r = 0.58) between dehydration (6%
thon and triathlon) often experience the greatest body body mass loss) and rectal temperature was originally
mass losses (e.g., 10%) (275, 737, 738). As such, it has observed following the Boston Marathon by Buskirk and
been proposed that exercise performance may be maxi- Beetham (749), a relationship that improved (r = 0.66)
mized by drinking according to the dictates of thirst (i.e., when controlling for work rate (i.e., speed  body mass).
ad libitum) (665, 666, 739, 740). This notion is based on Costill et al. (750) contextualized the issues surrounding
the thirst mechanism being optimized to preserve se- hydration and marathon running at the time by stating
rum/plasma osmolality within normal range and protect that “while there appears to be significant value in the
intracellular volume, thus preserving homeostasis (741). replacement of body fluids during prolonged, severe
Although contention exists regarding the impact of running, the rapid fluid loss, limited rate of gastric empty-
hypohydration and dehydration on aerobic performance ing, current competitive rules, and feeding habits during
in cold and temperate conditions, there is general the marathon makes this practice largely ineffective.”
agreement that a compromise in hydration status is det- These issues, although identified in the context of mara-
rimental to endurance exercise in warm and hot conditions thon running, are inherent to most endurance sports
(see sects. 5.3 and 5.4). Recommendations regarding performed within the heavy-to-severe intensity domains
fluid replacement for optimizing performance and in a structured competitive environment (e.g., cycling,
reducing the risk of thermal injury are therefore race-walking). Notwithstanding, these early observations

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 PÉRIARD ET AL.

provided the impetus for developing hydration guide- dehydration (i.e., %body mass loss). For example, to
lines regarding fluid intake during exercise. reduce physiological strain and preserve optimal per-
The American College of Sports Medicine published formance, a panel of experts recommended in a consen-
its first position stand regarding the prevention of heat sus statement on training and competing in the heat that
injuries during distance running in 1975, recommending body mass loss from water deficit should be minimized
to frequently ingest fluids during competition (751). The during prolonged intense exercise in the heat, within the
position stand was expanded in 1984 to consider com- constraints of the competition setting (e.g., fluid availabil-
munity joggers, fun runners, and elite athletes participat- ity and event characteristics) (181). It has further been
ing in distance running with the recommendation to suggested that high-intensity exercise eliciting elevated
drink 100 to 200 mL of water every 2–3 km (752, 753). sweat rates, along with activities >90 min in the heat,
These recommendations latter evolved to drink early should be accompanied with a planned hydration strat-
and often during exercise to replace all body mass lost egy, whereas drinking to thirst may be sufficient to offset
via sweating or consume the maximal amount of fluid fluid losses during low-intensity exercise of shorter dura-
tolerable (754). Adjustments to this position were then tion (<90 min) in cooler climates (760). A meta-analysis
made indicating that to maintain performance an individ- examining the impact of fluid intake strategy on endur-
ualized fluid replacement plan should be adopted to ance exercise in warm conditions concluded that
prevent excessive dehydration (>2% body mass loss) planned and ad libitum drinking yielded similar perform-
and pronounced alterations in electrolyte balance (734). ance outcomes, with body mass losses of 1% and
In 2000, the National Athletic Trainers Association pub- 2%, respectively (739). The slightly greater loss of
lished their first statement on fluid replacement during body mass with ad libitum drinking is a common obser-
physical activity advising that fluids should be consumed vation given that when provided with access to fluids,
to offset sweat and urine losses and maintain body humans replace <75% of body water losses during exer-
mass loss <2% by consuming 200–300 mL every 10 to cise (194, 226, 237–239). Nevertheless, the findings of
20 min (755). This recommendation was advocated for the meta-analysis indicate that the two hydration strat-
several years (59, 158) and recently amended to indicate egies should be viewed as complementary with the de-
that health and performance are optimized when body cision to use a particular one based on several factors,
mass losses are limited to 2% or less, without gaining including exercise duration, fluid availability, food inges-
body mass through water ingestion (756). The caution tion, ambient conditions, heat acclimatization status, and
against gaining body mass was added following the first various logistical factors. A position statement from
case of symptomatic hyponatremia linked to endurance Sports Dieticians Australia on nutrition for exercise in
exercise (757) and the subsequent increase in docu- hot environments highlighted that the divergence in
mented cases (265, 266, 758) (see also sect. 3.4). In total fluid intake between planned and ad libitum drink-
contrast to statements emphasizing the prescription of ing may increase with exercise duration, particularly
fluid intake based on body mass loss, the International under heat stress, and opportunities to access fluid dur-
Marathon Medical Directors Association suggested in ing real-life sporting events were more limited than in
2003 that athletes drink 400–800 mL·h 1 ad libitum, laboratory studies (304). To address both the practicality
with faster and heavier runners racing in warm condi- and value of fluid intake during a competitive event, it
tions drinking at the higher rate, and slower runners was suggested that individualized fluid replacement
competing in cool conditions at lower rates (759). These plans be informed by prior assessment of fluid balance,
recommendations were updated 3 yr later, with the perceived thirst, gastrointestinal tolerance and perform-
advice that runners understand their individualized fluid ance metrics in similar settings to competition and
needs but defer to physiological cues to increase (i.e., adjusted according to real-time assessment.
thirst) or decrease (i.e., increased urination, bloating, and Finally, to accurately determine the impact of hydra-
weight gain) fluid intake when running (741). It was fur- tion status on athletic performance, careful establish-
ther indicated that running in extreme heat (>38 C) may ment of a euhydrated baseline is required. Given the
require fluid intake beyond the dictates of thirst. day-to-day fluctuations in body mass (1%) attributable
Following on from the evolution of these recommen- to variations in total body water (282, 719), at least 3 con-
dations and expanding research regarding the impact of secutive days of measurements should be performed
hydration status on performance and whether to drink to nude, following first morning void and after ingesting flu-
a plan, or to thirst, balanced and practical hydration rec- ids (1–2 L) the evening prior (204). Total body water loss
ommendations have emerged to incorporate a broader provides an estimate regarding how much dehydration
spectrum of sports and physical activities. These place may impact on physiological and perceptual responses,
greater emphasis on the context in which exercise is within the context of an exercise task in particular envi-
performed than avoidance of a particular level of ronmental conditions. For example, in cold and

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 EXERCISE UNDER HEAT STRESS

temperate conditions, a greater level of dehydration performance stemming from hyperthermia and dehydra-
(e.g., 2 to 4% body mass loss) is better tolerated during tion may be alleviated. Firstly, human adaptation to
prolonged high-intensity exercise, even with an elevated repeated heat exposure (i.e., heat acclimation) is dis-
body core temperature, due to attenuated physiological cussed, as are some of the contentious issues regarding
and perceptual responses. the adaptive process and consequent benefits. Secondly,
the potential for external and internal cooling methods to
5.7. Summary improve performance is outlined, along with the time
frame (i.e., before and during exercise) for using different
A rise in core temperature and loss of body water via approaches and their physiological underpinning. Finally,
sweating are natural consequences of prolonged moder- the effects and pathways via which hyperhydration influ-
ate to high-intensity exercise. When undertaken in the ences exercise performance in the heat are described.
heat, exercise-induced hyperthermia and dehydration
are augmented, with excessive body water loss reducing 6.1. Heat Acclimation
blood volume and increasing osmolality. This response
influences thermoregulatory capacity by reducing the The development of thermal strain when physically active
sensitivity of thermoeffector responses to a given core in the heat intensifies the physiological and perceptual
temperature, further increasing thermal strain. The rise in responses associated with exercising at a given work
whole body temperature augments skeletal muscle gly- rate, leading to impaired endurance capacity. Progressive
cogenolysis and anaerobic metabolism and coupled with dehydration as a result of excessive sweat loss in the
hypovolemia progressively compromises systemic and heat exacerbates this impairment by further reducing
regional (i.e., cutaneous, active muscle, and cerebral) per- evaporative heat loss and increasing cardiovascular
fusion and oxygen delivery. These adjustments lower strain. However, repeated exposure to heat stress, such
V_ O2max and accelerate the development of fatigue during as during natural heat acclimatization or laboratory-based
constant work rate exercise, primarily by attenuating oxy- heat acclimation, induces adaptations that allow for better
gen delivery and uptake in exercising skeletal muscles. fluid balance and increased cardiovascular stability.
Although likely unrelated to modifications in cerebral per- Although elicited in different settings, heat acclimatization
fusion, adjustments in central neural drive may also impact and heat acclimation induce similar physiological adapta-
on the ability to continue exercising when hyperthermic tions and are often used interchangeably (761, 762).
and dehydrated. Performance impairments during self- These adaptations include increased total body water
paced exercise relate to similar hemodynamic adjustments and expanded plasma volume, reduced heart rate,
intensifying physiological and perceptual responses. While increased stroke volume and better sustained cardiac
hyperthermia is unavoidable during prolonged high-inten- output during exercise, increased myocardial function (in
sity exercise in hot environmental conditions, ensuring animal models), enhanced skin blood flow and sweating
euhydration before exercise and replacing sweat losses responses, improved skeletal muscle metabolism, and
during exercise contribute to mitigate the compounding increased thermal tolerance when exercising at a given
effect of hyperthermia and dehydration. The choice of work rate (146, 761, 763–768). TABLE 6 outlines the func-
which approach to utilize, drink to thirst or plan to drink, tional benefits associated with the heat acclimation/accli-
should be dictated by the nature of the exercise task matization that improve performance and comfort in the
(i.e., intensity, duration), ambient conditions, availability of heat when exercising at a given work rate, as well as
fluids, and an understating of one’s fitness and acclimation reduce the risk of exertional heat illness and thermal
status. injury (146, 763). This section will further outline the time
course of human heat adaptation, explain the different
approaches that can be used to induce heat acclimation,
6. MITIGATING THE IMPACT OF detail the performance benefit conferred by acclimation
HYPERTHERMIA AND DEHYDRATION when exercising in hot and possibly cool conditions,
detail the process of sudomotor and vasomotor adapta-
Section 4 described how the increase in thermal strain tion, describe the process of total body water and plasma
during aerobic exercise under heat stress intensifies volume expansion, and examine whether permissive
physiological and perpetual responses to detrimentally dehydration enhances the adaptive process.
impact on performance. In sect. 5, it was demonstrated
that the loss of body water during prolonged exercise 6.1.1. Time course of heat adaptation.
can further intensify these responses and exacerbate
performance impairments. This section discusses Heat acclimation is considered the primary intervention
the potential pathways via which reductions in one can adopt to reduce physiological strain and

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 PÉRIARD ET AL.

Table 6. Physiological adaptations and functional overview of the responses associated with heat acclima-
consequences associated with the heat acclimation tization, suggesting that the human organism adapted to
phenotype in humans that improve performance at a hot climatic conditions by modifying either its constitu-
given work rate and increase maximal aerobic power
tion or function. The author highlighted that a lowering
Adaptation Consequence of heart rate and improved maintenance of blood pres-
sure were fundamental adaptive responses. The hema-
Core temperature Reduced tological adaptations occurring following prolonged
Rest: decreased
sojourns in different climates were later described by
Exercise: decreased
Barcroft et al. (771) with an account of “blood volume
Sweating Improved
increasing as the temperature rose and decreasing as it
fell.” A comprehensive understanding of the essential
Onset threshold: decreased
adaptations to heat stress at the time was summarized
Rate: increased
by Sundstroem (772), including those related to body
Sensitivity: increased
temperature, heat exchange, metabolism, blood distri-
Skin temperature Reduced
bution, heart rate, blood pressure, endocrine, and nerv-
Exercise: decreased
ous system function. The time frame and magnitude of
Skin blood flow Improved
heat adaptations, along with the mechanistic pathways
Onset threshold: decreased via which they developed, were greatly elucidated dur-
Sensitivity: increased ing the last century by research conducted in military
Fluid balance Improved and occupational settings (e.g., mining) (773–779). This
Thirst: improved knowledge was expanded on with more recent research
Electrolyte losses: reduced findings, some of which within a sporting context (563,
Total body water: increased 780–791).
Plasma volume: increased Heat acclimation is a highly individualized process
Cardiovascular stability Improved and dependent on several factors such as the active or
Heart rate: lowered passive nature of the regimen, the duration, and fre-
Stroke volume: increased quency and number of heat exposures, along with the
Cardiac output: better sustained environmental conditions in which it occurs. Acquisition
Blood pressure: better defended of the heat acclimation phenotype occurs relatively
Skeletal muscle metabolism Improved quickly with a substantial fraction of adaptations in cer-
Muscle glycogen: spared tain physiological parameters developing within the first
Lactate threshold: increased week of heat exposure (e.g., plasma volume expansion
Muscle and plasma lactate: lowered and decreased heart rate) (761, 792, 793). However, reg-
Muscle force production: increased
imens of 14 days or longer are recommended to achieve
Whole body metabolic rate Lowered
maximal adaptations and the associated benefits
Acquired thermal tolerance Increased
(FIGURE 21) (765, 794). This recommendation aligns
with the biphasic model of heat acclimation proposed
Heat shock proteins expression: increased
by Horowitz et al. (795–797) in which the kinetics of ad-
Cytoprotection: improved
aptation are mediated by interactions between central
This table was adapted with permission from Sawka et al. (146). thermoregulatory autonomic outflow and effector organ
responsiveness. The initial short-term phase (1–5 days)
is characterized by a decreased effector organ output-
optimize performance in anticipation of exercising in hot to-autonomic signal ratio, whereby increased efferent
environmental conditions (181). The adaptive capacity of activity overrides impaired peripheral responsiveness to
humans to environmental heat stress has been recog- produce adequate effector output. In the second longer
nized for centuries, with reports of Europeans relocating term phase (>21 days), the effector organ output-to-au-
to East and West Indian climates initially being adversely tonomic signal ratio is increased, as both central and pe-
affected by the environment but over time habituating ripheral adaptations enhance physiological efficiency
and living comfortably (769). This habituation process and reduce the requirement for increased excitation.
included behavioral modifications (e.g., reduced work The extensive work by Horowitz and colleagues (797–
rate, rescheduled work periods, and use of shelters) and 807) using an animal model (i.e., rats) over protracted
potential blood adaptations allowing for “a pretty good periods (up to 60 days) of continuous heat exposure
state of health” (769). In 1884 Jousset (770) expanded (34 C) has provided a breadth of mechanistic insights.
on these observations by providing a comprehensive As a result, the genomic responses, molecular signaling

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125

120 Plasma Volume

Heart Rate
115
Core temperature

Adaptation (% Day 1)
110 Skin Temperature
Sweating Rate
105
Thermal Comfort
100 Exercise Capacity

95

90

85

80

75
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15
Days of heat acclimation
FIGURE 21. Generalized time course of adaptations related to exercise-heat acclimation. Within a week of acclimation plasma volume expansion
occurs and heart rate is reduced during exercise at a given work rate. Core and skin temperatures are also reduced when exercising at a given work
rate, whereas sweat rate increases when in uncompensable conditions. Perceptually, the rating of thermal comfort is improved. As a result of these
adaptations, aerobic exercise capacity is increased. During the second week of heat acclimation some adaptions can further develop or reach a pla-
teau. The magnitude of these adaptations is dependent on the active or passive nature of the regimen, the duration, frequency and number of heat
exposures, and the environmental characteristics. Adapted with permission from Pe
riard et al. (765).

and epigenetic mechanisms associated with the acquisi- the diversity of heat acclimation protocols and the rela-
tion of heat acclimation homeostasis have begun to tively few studies that have examined the rate at which
emerge. This includes insight into the neuroplasticity of adaptations deteriorate, there is contention regarding
the thermoregulatory system (e.g., changes in tempera- the rate of decay for heat acclimation. It was suggested
ture-thresholds for activating heat dissipation effectors), that 1 day of exercise-heat exposure is required for every
the increase in hypothalamic and cardiac cytoprotective 5 days spent outside of the heat to maintain adaptation
molecules (e.g., heat shock proteins and hypoxia-induci- (773, 812) or that 1 day of heat acclimation is lost for ev-
ble factor-1a), alterations in the expression (i.e., faster ery 2 days spent without heat exposure (813). In a recent
activation and suppression) of genes involved in cross- meta-analysis of 21 studies, it was concluded that the
tolerance (e.g., ischemic-reperfusion), and cardiac remod- rate of decay for the main adaptations following heat
eling of the myosin isoform profile increasing contractile acclimation (i.e., lowered heart rate and core tempera-
efficiency (i.e., greater pressure generation and slower ture) is 2.5% per day without heat exposure and that
contraction and relaxation velocities) (763, 808, 809). there are insufficient data to make a good estimate for
These insights, however, emphasize the gap in knowl- the decay in sweat rate (814). As such, in the 2 wk follow-
edge between the mechanistic understanding of long- ing heat acclimation, a well-acclimated individual may
term heat adaptations in animals and that of human physi- lose 30–35% of the heart rate and core temperature
ological heat acclimation, particularly as it relates to adaptations if regular heat exposure is removed.
long-term biphasic acclimation. Moreover, although a Notwithstanding, there is support for the notion that aer-
generalized categorization of short (<7 days)-, medium obic fitness and regular exercise in cool conditions con-
(8–14 days)-, and long-term (>15 days) heat acclimation tribute to maintain adaptations or reduce the rate of
has been proposed for humans (781), the heterogeneity decay (773, 815).
between heat acclimation regimens necessitates a classi-
fication more appropriately based on the adaptive stimu- 6.1.2. Heat acclimation approaches.
lus provided by a chosen regimen, such as the
cumulative adaptation impulse (810). To date, however, a Heat adaptation occurs following a series of prolonged
representative index of the adaptive stimulus provided by daily or semidaily exposures to an environment that ele-
heat acclimation and the consequent level of adaptation vates whole body temperature, increases skin blood
has yet to be developed and utilized. flow, and elicits profuse sweating. Differences in endog-
The physiological adaptations associated with heat enous (i.e., metabolic heat production) and exogenous
acclimation are transient in nature and steadily decay (i.e., ambient and radiative temperature, humidity, and
without consistent heat exposure. It has been proposed air velocity) thermal loads allow for creating or utilizing
that the adaptations developing most rapidly (e.g., environments suitable for different heat acclimation and
decreased heart rate) during the acclimation process acclimatization approaches. As highlighted in FIGURE
are also those that decay most quickly (773, 811). Given 22, these include self-paced exercise, constant work

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 PÉRIARD ET AL.

Heat training

Heat acclimatization Heat acclimation

Natural environment Artificial environment
(outdoor/field training) (indoor/laboratory training)

Self-paced Constant work Passive Post-exercise Controlled Controlled

exercise rate exercise heating heating hyperthermia heart rate

Activity Activity Activity Activity Activity Activity

Cycle or run at constant Exercise/rest to attain and Exercise to attain and

Cycle or run at Water immersion Water immersion maintain a given heart
work rate maintain a given core
self-selected work rate Sauna bathing Sauna bathing
(e.g. 185 W or 15 km/h) temperature (e.g. ~38.5ºC) rate (e.g. 65% VO2peak)

Conditions Conditions Conditions Conditions Conditions Conditions

Outdoor: variable Outdoor: variable Outdoor: variable
Water: 40ºC Water : 40ºC Indoor: 35 to 40ºC,
Indoor: 35 to 40ºC, Indoor: 35 to 40ºC, Indoor: 35 to 40ºC,
Sauna: 70 to 90ºC Sauna: 70 to 90ºC 20 to 80% RH
20 to 80% RH 20 to 80% RH 20 to 80% RH

Duration Duration Duration Duration Duration Duration

Water: 30 to 60 min Water: 20 to 40 min
60 to 90 min 60 to 90 min 60 to 90 min 60 to 90 min
Sauna: 15 to 30 min Sauna: 10 to 20 min

FIGURE 22. Schematic overview of the methods used for heat acclimation and heat acclimatization, with examples for activity selection, environmen-
tal conditions and duration. Manipulation of temperature and humidity is recommended in accordance with the anticipated environmental conditions to
be encountered during upcoming competitions. RH, relative humidity. Adapted with permission from Daanen et al. (814).

rate exercise, passive heating, postexercise passive inter- and intraindividual stimulus for adaptation within
heating, controlled hyperthermia, and controlled heart and between training sessions, stemming from the
rate heat acclimation. Although all of these approaches self-regulated nature of the regimen. Notwithst-
can be utilized in artificial environments (i.e., indoor or anding, self-paced exercise-heat acclimatization pro-
laboratory settings) to heat acclimate, only the self- vides an individual with the ability to control their
paced exercise model can be employed with relative effort based on the integration of objective measures
ease in a natural outdoor environment to acclimatize. such as heart rate and time, as well as subjective per-
Constant work rate and controlled heart rate protocols ceptual cues like the perception of exertion, thermal
can also be used to heat acclimatize but with greater dif- comfort, and sensation.
ficulty due to the logistical constrained (e.g., terrain) Similar to self-paced heat acclimatization, the constant
associated with maintaining a given work rate or heart work rate approach was developed within military and
rate. occupational (e.g., mining) settings (779, 792, 823–826).
The self-paced exercise-heat acclimatization app- It provides significant improvements in work capacity
roach was originally developed by the military to ensure under heat stress through enhanced thermoregulatory,
the safety of large and diverse groups of recruits during cardiovascular, metabolic, and cellular adaptations (112,
basic training and to prepare unacclimatized soldiers for 372, 398, 473, 827, 828). It has also been shown to
rapid deployment to hot environments (816, 817). In an improve time trial performance (785, 787) and intermit-
athletic context, self-paced heat acclimatization offers a tent sprinting (829) in the heat. Because the endoge-
sport-specific means of inducing adaptation in several nous (i.e., work rate) and exogenous (i.e., ambient
individuals exercising together but self-regulating their conditions) thermal loads are fixed during constant work
effort according to fitness level and the parameters of rate exercise, it has been suggested that a progressive
the training session and prevailing ambient conditions. It reduction occurs in the forcing function driving adapta-
is therefore often used with team-sport athletes (818– tion, as physiological strain decreases with acclimation,
822) and has been successfully utilized to enhance per- potentially attenuating the adaptive response (768,
formance in trained cyclists following an outdoor training 830). This limitation was accommodated for in a rec-
camp (563, 783). The potential shortcomings of this ent study examining the effects of prolonged (5 wk)
approach lay with the difficulty in standardizing the exercise-heat acclimation (cycling at 60% V_ O2max),

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 EXERCISE UNDER HEAT STRESS

whereby ambient temperature was set to 35 C (30% maintain a given heart rate increases as acclimation
RH) in the first week of training and increased by 1 C in develops, providing a constant stimulus for adaptation.
subsequent weeks (787, 831). The authors reported that For example, the power output required to hold a heart
rectal temperature was elevated to 38.5 C within 35– rate equivalent to 65% V_ O2max during the last 75 min of a
40 min and increased to 39.6 C at the end of all 60- 90-min session in 40 C and 40% RH increased by
min training sessions, providing a consistent thermal 25 W (15%) throughout a 10-day protocol (846).
impulse for adaptation. Constant work rate heat acclima- Controlling heart rate also allowed for maintaining an av-
tion has also been shown in a meta-analysis to provide a erage rectal temperature of 38.4 C for those final
similar magnitude of improvement in exercise perform- 75 min. Other studies have utilized the controlled heart
ance to that of controlled hyperthermia heat acclimation rate model to induce heat acclimation and demon-
(794). A direct comparison between approaches also strated a lowered core temperature and heart rate dur-
found that controlled hyperthermia did not provide ing exercise at a given work rate in the heat, increased
greater adaptations than constant work rate exercise sweat output and reduced sweat sodium concentration,
(832, 833). It appears, therefore, that constant work rate plasma volume expansion, improved cerebral perfusion,
heat acclimation is a viable and potent means of induc- enhanced heat dissipation (i.e., evaporative heat loss),
ing adaptations to the heat. and improved time trial performance under heat stress
Controlled hyperthermia, or isothermic heat acclima- (113, 846–849). Given that the maintenance of a greater
tion, was developed by Fox et al. (830, 834, 835) in an relative exercise intensity during exercise-heat acclima-
attempt to define the stimulus for adaptation based on tion may hasten the adaptive process (794), the con-
the degree and duration of thermoregulatory imbalance trolled heart rate approach appears to offer both a
(i.e., elevation of body temperature), rather than the practical and time-efficient manner by which to heat
characteristics of the climate in which participants were acclimate.
exposed. This approach is purported to provide a forc- Passive heat acclimation (i.e., without an exercise
ing function that increases in proportion to adaptations component) involves regular exposure to a high exoge-
by manipulating endogenous and/or exogenous thermal nous heat load provided by a hot bath (e.g., 40 C),
loads to attain and maintain a target core temperature, environmental chamber (e.g., >45 C), or sauna (e.g.,
typically around 38.5 C (768, 781). Numerous studies 70–90 C) for 30 to 90 min, depending on the medium.
have demonstrated that controlled hyperthermia heat The approach has been shown to yield adaptations
acclimation leads to several hallmark adaptations, commensurate with exercise-heat acclimation, such as a
including a lower heart rate and core temperature dur- decrease in heart rate and rectal temperature and an
ing exercise, higher sweat rate, and improved aerobic increase in sweat rate during exercise at a given work
exercise capacity in the heat (833, 834, 836–841). It has rate in the heat (850–853). Passive heat acclimation has
also been reported that the expansion of plasma volume also been shown to lower the onset threshold for sweat-
may be sustained during controlled hyperthermia heat ing and increase sweat sensitivity (854, 855), initiate
acclimation, as it allows for maintaining a consistently hyperthermia-induced ventilation at a lower core tem-
elevated physiological strain throughout the adaptive perature (105), and improve skeletal muscle contractility
process (842). These findings remain to be replicated, (i.e., twitch amplitude) and force production capacity
however, as the early expansion of plasma volume gen- without altering central activation or peripheral neural
erally regresses during prolonged heat acclimation activity, evidence of enhanced skeletal muscle function
(826, 843–845). Notwithstanding, the controlled hyper- (788). Although passive heat acclimation has been
thermia model of heat acclimation offers a safe and shown to increase V_ O2peak in temperate conditions
effective way of inducing adaptation due to the constant (854), changes in endurance performance under heat
monitoring of core temperature. From a practical per- stress have not been evaluated and it remains undeter-
spective, however, it may lack real-world application and mined whether this approach can lead to improvements
relevance to athletes and coaches training with heart in prolonged exercise capacity. Based on the principles
rate, rather than with body core temperature. of adaptation theory (768), it has been suggested that
An alternative approach to controlled hyperthermia exercise-heat acclimation regimens replicating the work
was recently proposed with the adaptive stimulus regu- rate and environmental conditions in which competition
lated by manipulating work rate to maintain a given will occur may be more effective at developing sport-
heart rate (765). With this approach, the level of strain specific adaptations that contribute to improve perform-
attained and sustained within each acclimation session ance (765, 856). However, in highly trained individu-
corresponds to the heart rate associated with a relative als, thermoregulatory heat adaptations may suffice to
intensity specific to exercise in cool conditions (e.g., % enhance performance in the heat, due to an already
V_ O2max). Hence, the absolute work rate required to well-developed aerobic capacity.

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 PÉRIARD ET AL.

In an effort to maintain a strong training impulse and decrease in power output following the onset of exer-
induce heat acclimation, passive heat exposure is now cise in the heat on the first day of training in hot (34 C)
frequently being used immediately after exercise in cool and dry (18% RH) outdoor conditions, leading to a 16%
conditions. This approach has the benefit of allowing lower mean power output than in the cool trials (FIGURE
athletes to complete regular training without heat stress 23). However, after 1 wk of training in the heat, the dec-
affecting training quality, coupled with acquiring the rement was partly recovered with mean power output
adaptations related to chronic heat exposure. Post-exer- only 8% lower than that of the cooler trials and almost
cise passive heating for 30 to 45 min can be achieved fully restored (i.e., 3% lower) after 2 wk of training in
via sauna exposure (789, 857) or hot water immersion the heat. Interestingly, heart rate was similarly elevated
(791, 858–861) as it induces an increase in whole body throughout the time trials in the heat and slightly higher
temperature beyond that achieved with exercise in than in the cooler trials, which supports the notion that a
cool conditions. The adaptations associated with this similar relative exercise intensity (i.e., %V_ O2max) is main-
approach are akin to those of more traditional heat accli- tained during self-paced exercise in hot and cool condi-
mation protocols. In a series of studies, Zurawlew et al. tions (312, 314, 864), with heat acclimation/acclimatization
(791, 859–861) demonstrated that 6 consecutive days of increasing the absolute intensity (e.g., power output) that
postexercise (i.e., 40 min run at 65% V_ O2max) immersion can be sustained. Other potential adaptations conferred
in 40 C water lowered core and skin temperature, heart by heat acclimation that could benefit endurance per-
rate, perceived exertion, and thermal sensation in both formance include a reduction in oxygen uptake (767,
endurance-trained and recreationally active individuals 865) and blood and muscle lactate accumulation (473)
during a 40 min run in the heat. Part of these adaptations during submaximal exercise in the heat, as well as an
were also retained for 2 wk after completion of the regi- increase in lactate threshold (785, 838). The mechanisms
men (861). From a performance perspective, postexer- responsible for these adaptations remain unclear but
cise water immersion has been shown to improve 5-km could stem from the increase in total body water
treadmill performance by 5% in hot but not cool condi- enhancing lactate removal through increased splanch-
tions (791). In contrast, a 32% increase in run time to nic circulation (866) or through increased cardiac output
exhaustion in cool conditions was noted in fit individuals and decreased metabolic rate delaying lactate accumu-
after heat acclimation via postexercise sauna bathing, lation (500, 865). Heat acclimation has also been shown
which is equivalent to a 2% improvement in 5-km run- to reduce muscle glycogen utilization during submaxi-
ning time trial performance (857). Although the evidence mal exercise in the heat (397, 500, 503), in part due to a
is limited, it appears that passive heating following exer- reduction in plasma epinephrine (473). Collectively,
cise in cool conditions provides a practical approach to these adaptations provide the integrative framework
heat acclimate in those that may have difficulty adopting upon which endurance performance is improved when
more traditional exercise-based regimens, or those that heat acclimated.
wish to maintain training quality (862, 863).
400
*
6.1.3. Performance benefits in hot conditions. §
350
†
Power output (W)

The benefits of heat acclimation on exercise perform-

300
ance in the heat are well established. For example, exer-
cise-heat acclimation has been shown to increase
V_ O2max by 4% when undertaken in 49 C following 250
Cool
whole body preheating (543) and by 8 to 10% in 38 C Hot 1
200
(785, 847). Heat acclimation has also been shown to Hot 2
enhance endurance exercise capacity by 23% (i.e., Hot 3
time to exhaustion or task failure) and performance by 150

7% (i.e., self-paced time trial) under heat stress, with 0 20 40 60 80 100
Time trial completion (%)
medium to long-term acclimation providing more robust
improvements than short-term regimens (794). In a heat FIGURE 23. Power output during 43.4-km cycling time trials per-
acclimatization study with well-trained cyclists, Racinais formed in Cool (8 C; average of trials performed before and after
heat acclimatization) and Hot (37 C) conditions on day 1 (Hot 1) and
et al. (563) demonstrated that three cycling time trials after 6 (Hot 2) and 14 (Hot 3) days of training in the heat. These data
(43.3 km) undertaken in hot outdoor conditions (36 C) indicate the magnitude of improvement that can occur in time trial per-
were initiated at a similar power output to that of pre- formance with heat acclimatization in trained cyclists. § Cool time trial †
and postacclimatization time trials performed in cooler power output significantly higher than Hot 1, Hot 2, and Hot 3, respec-
tively (P < 0.05). Redrawn with permission from Racinais et al. (563).
conditions (9 C). The authors reported a marked

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 EXERCISE UNDER HEAT STRESS

6.1.4. Performance benefits in cool conditions. dominantly within the control group (877). Following 28
sessions over 5–6 wk of heat (35–40 C) or control
Observations of performance enhancement in cool con- (<15 C) training, Mikkelsen et al. (787) showed that 15-
ditions following heat acclimation have sparked debate km time trial performance in cool conditions (14 C) was
as to whether heat adaptations provide a benefit to improved by 6% in both groups, with V_ O2max and peak
exercise performance in cooler conditions (867, 868). power output remaining unchanged. Taken together,
For example, one group demonstrated significant the benefits of training in hot compared with cool condi-
improvements in V_ O2max (180 mL·min 1) and 60-min tions for improving performance in cooler environments
time trial performance (16 W) in cool conditions follow- appear to be unclear, potentially due to nature and in-
ing 10 days of constant load heat acclimation (785), while tensity (i.e., moderate to intense) of the training regi-
another reported no such improvement, despite similar mens used to induce exercise-heat acclimation.
changes in V_ O2max (200 mL) and 30-min time trial per- Moreover, training per se, even in cool conditions, leads
formance (6 W) following controlled heart rate heat to adaptations commensurate with heat acclimation.
acclimation (847). Several other studies have reported Indeed, even when undertaken in cool conditions, en-
that training in the heat enhances different aspects of durance training reduces physiological strain and
aerobic performance in cool conditions (13 to 23 C), increases exercise capacity in the heat, with aerobically
such as V_ O2max (543, 869), power output at V_ O2max trained individuals exhibiting several characteristics of
(838, 840, 870), lactate threshold (785, 838, 840), and the heat-acclimated phenotype (e.g., lowered resting
endurance performance (840, 857, 871). These heart rate and core temperature) (878, 879). A recent
improvements have been reported following a vari- meta-analysis examining the impact of heat mitigation
ety of short- to long-term heat acclimation regimens strategies on lowering core temperature at the start of
using passive, active, and controlled hyperthermia exercise, attenuating the rate of rise in core temperature
protocols in participants of different fitness levels during exercise, and improving endurance performance
and within different phases of their competitive sea- determined that the most influential strategy was being
son. Similarly, team-sport athletes participating in aerobically fit, followed by heat acclimation, precooling,
preseason (820), in-season (819), and off-season and fluid ingestion (880). Sotiridis et al. (881) recently
(818) training camps have been shown to experience demonstrated that 10 sessions of aerobic training in tem-
improvements in performance in cool conditions fol- perate conditions (24 C) elicited a 10% improvement in
lowing a period of intensified training in the heat. V_ O2max under heat stress in untrained but not trained
Cardiovascular, hematological, thermoregulatory, individuals, with both groups exhibiting a lower resting
skeletal muscle, and cellular adaptations stemming rectal temperature and increased whole body sweat
from heat acclimation have been suggested to pro- rate during exercise in the heat. The lower resting core
vide the ergogenic stimulus for enhancing perform- temperature of fit individuals has been proposed to
ance in cooler environments (785, 872, 873). How- stem from a training-induced increase in blood volume
ever, similar to the contention regarding the effects enhancing core-to-skin heat conductance through
of altitude training on endurance performance at increased cutaneous blood flow (882). Ravanelli et al.
sea-level (874–876), the transfer of benefits stem- (849) also demonstrated that 8 wk of aerobic training in
ming from training in the heat to performance in cool 23 C conditions led to reductions in resting and end-
environments (i.e., cross adaptation) is difficult to exercise core temperature in previously untrained indi-
accurately determine given the heterogeneity viduals, as well as an increase in whole body sweat rate
between the studies highlighted above. during uncompensable exercise-heat stress, adapta-
The absence of a control group in several studies pre- tions that were further enhanced following 6 days of
cludes the ability to adequately distinguish between the heat acclimation. The authors suggested that adapta-
effects of heat acclimation and those of training per se tions related to aerobic training, rather than fitness per
on performance enhancement in cool conditions. In a se (i.e., V_ O2max), mediated these thermoregulatory
study that included both hot and control (i.e., cool condi- improvements when exercising at a fixed rate of heat
tion) training groups, it was shown that 30-min time trial production per kilogram of total body mass (115). The in-
performance, V_ O2max and peak power output increased dependent effect of training, fitness, and acclimation
only in the heat acclimation group when testing was status on thermoregulatory responses during uncom-
undertaken in the heat (847). In a separate study, 2 wk pensable heat stress remains difficult to determine, how-
of outdoor training in hot (34 C) or cool (<15 C) condi- ever, as these factors are intimately linked. The addition
tions failed to improve 43.30km time trial performance of a control group to heat acclimation research studies
in cool conditions in either group, despite an overall is also complex, as exercise performed at a given work
improvement in V_ O2max in cool conditions, pre- rate in cool conditions will elicit a lower thermal and

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 PÉRIARD ET AL.

cardiovascular response than in the heat, whereas exer- decrease the internal temperature threshold for cutane-
cise performed to produce a given thermal or cardiovas- ous vasodilation without altering the slope of the blood
cular response will lead to a lower work rate being flow-internal temperature relationship (i.e., sensitivity)
sustained in hot compared with cool conditions. The (106, 900, 901). However, Lorenzo and Minson (902)
nature of the exercise stimulus (i.e., absolute work rate showed that heat acclimation does improve cutaneous
and metabolic rate) along with the thermal and cardio- vascular sensitivity to locally applied acetylcholine, an
vascular responses would therefore differ, which to a endothelium-dependent vasodilator, without altering
certain extent is the goal of adding a control group. The maximal skin blood flow. More recently, Barry et al. (903)
decision regarding what type of stimulus to provide a demonstrated that heat acclimation lowers the change
control group should be based on the research ques- in mean body temperature required to activate heat loss
tion, with the inclusion of both matched exercise stress thermoeffector responses (i.e., cutaneous vasodilation
and physiological strain groups likely providing valuable and sweating). The change in mean body temperature
insight. Ultimately, the addition of at least one control needed to trigger skin sympathetic nerve activity did not
group to heat training studies would allow for better simply reflect the reduction in resting core temperature
identifying the extent to which heat stress and/or training associated with heat acclimation, but occurred after a
stress provide the adaptive benefit for enhancing per- smaller change in mean body temperature. It remains to
formance in hot as well as cool conditions. be determined, however, if the reduction in onset
threshold for skin sympathetic nerve activity reflects ear-
lier vasomotor or sudomotor activation, as recordings
6.1.5. Sudomotor and vasomotor adaptations. reflect sympathetic outflow to both the cutaneous vas-
An improved sweating response is considered a hall- culature and eccrine sweat glands (904). The mechanis-
mark indicator of heat acclimation with both central and tic pathway via which heat acclimation improves the
peripheral adaptations contributing to the improvement. neural control of body temperature remains unresolved
Centrally, a shift in the internal temperature threshold for but may relate to augmented thermal sensitivity of pe-
the initiation of sweating occurs in response to a heat ripheral warm receptors, as well as an increased thermo-
acclimation mediated reduction in core temperature sensitivity and/or plasticity of central (i.e., hypothalamic)
(106, 112, 883). The onset threshold for sweating occurs neurons (903).
at a lower internal temperature but following a similar
change in absolute temperature (884). Peripherally, 6.1.6. Total body water and plasma volume
adaptations occur at the level of the sweat gland with an expansion.
enhancement of both secretory capacity and sensitivity An increase in total body water (i.e., intra- and extracellu-
(835, 885–888). These adaptations stem from enh- lar fluid) following repeated exposures to heat stress is a
anced cholinergic sensitivity along with an increase in classic response associated with the heat acclimation
size (i.e., hypertrophy) and efficiency of eccrine glands phenotype (771). During the first week of heat acclima-
(889, 890). An increased resistance to hidromeiosis has tion total body water can increase by 2–3 liters (5–7%)
also be reported, such that higher sweat rates can be (826, 842, 843, 905) with expansion mostly occurring
sustained (830, 891). The composition of sweat is also within the extracellular fluid compartment (i.e., intravas-
influenced by heat acclimation with electrolyte (e.g., so- cular and interstitial space) (842, 905). The increased
dium, chloride and potassium) concentration decreasing retention of fluid within the vascular space (i.e., plasma
in response to an increase in their conservation (891– volume expansion) has long been considered a primary
895). The mechanistic pathways via which sweat elec- adaptation supporting cardiovascular stability during
trolyte conservation occurs remain unclear, although so- exercise-heat stress through improved cardiac filling
dium conservation has been linked to aldosterone- (146, 216, 338, 591, 766, 843, 906–908). Plasma volume
mediated sodium ion reuptake within the reabsorptive expansion is purported to enhance vascular filling and
duct of the sweat gland (896–898). atrial pressure (i.e., preload), thereby decreasing heart
Assuming that prevailing ambient conditions allow for rate and increasing stroke volume and arterial blood
evaporation, the enhanced sweating response associ- pressure during exercise at a given work rate in the heat
ated with heat acclimation results in improved evapora- (591, 826, 907). This response is akin to the expansion
tive cooling and decreased skin temperature, reducing of blood volume (i.e., plasma and erythrocyte) that
thermoregulatory skin blood flow requirements. A occurs with an increase in fitness following aerobic train-
decrease in skin temperature may also reduce cutane- ing, which is considered an important contributor to
ous venous compliance and allow for a redistribution of improvements in performance via larger stroke volume
blood volume from the peripheral to central circulation and greater ventricular filling (878, 909). Recent studies,
(233, 899). Historically, heat acclimation was thought to however, have reported that 5-day passive (910) and 10-

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 EXERCISE UNDER HEAT STRESS

day exercise-heat (911) acclimation have minimal effects correlated, albeit moderately (r = 0.49), with the
on left-ventricular volumes, function, and systemic increase in total hemoglobin mass, leading the
hemodynamics at rest and during exercise. It must be authors to speculate that there may be an erythro-
noted that postacclimation echocardiography meas- poietic compensatory response occurring, secondary
urements in these studies were undertaken at similar to the expansion of plasma volume. A subsequent
core temperatures and heart rates as preacclimation, study utilizing a similar 5-wk heat acclimation training
along with a similar plasma volume (1–3% expansion). approach reported a 4.6% increase in total hemoglo-
Additional research is thus required to clarify the link bin mass and 4.8% expansion of plasma volume, with
between blood/plasma volume expansion and car- red cell volume and blood volume remaining
diac function during exercise under heat stress in the unchanged (925). A moderate correlation between
heat acclimated state. Framing improvements in car- changes in plasma volume and changes in hemoglo-
diovascular stability in the broader context of integra- bin mass was also reported (r = 0.54). The pathway
tive heat acclimation adaptations is important, as via which this is purported to occur is associated with
other factors can influence cardiac function. For the hypothesis that the kidney functions as a “crit-
example, a reduction in resting core temperature meter” to adjust hematocrit within normal values
contributes to the attenuated elevation in core tem- (e.g., 45%) by regulating red blood cell volume and
perature and thus heart rate during exercise at a plasma volume to stabilize arterial oxygen content
given work rate in the heat following heat acclimation (926). Although an attractive premise, additional
(912). Plasma volume expansion also increases the research is required to elucidate the magnitude and
specific heat capacity of blood (913), which improves time course of the erythropoietic response to exer-
heat transfer from the core to the skin, potentially cise-heat acclimation.
allowing for a reduction in the skin blood flow The rapid expansion of plasma volume during heat
response (146). acclimation was traditionally viewed as transient phe-
The expansion of plasma volume is mediated by the nomenon, with a small contraction typically occurring
retention of fluid in response to increases in plasma col- after 1 wk of acclimation, despite continued heat ex-
loid (i.e., protein) and crystalloid (i.e., electrolyte) osmotic posure (826, 843–845). This phenomenon has been
pressures (209, 826, 844, 914, 915). Intravascular protein suggested to be an experimental artifact stemming
content increases via acclimation-induced albumin syn- from a failure to maintain a constant adaptation stim-
thesis (916, 917), coupled with a decrease in cutaneous ulus, due to utilizing the constant work rate heat
blood flow (209) and capillary permeability (915, 918) acclimation approach. By clamping core temperature
that allow for protein to remain within the intravascular at 38.5 C during 16–17 days of controlled hyperther-
space. The oncotic effect created by the net increase in mia heat acclimation, Patterson et al. (842, 905)
intravascular protein content during heat acclimation induced an increase in plasma volume of 13% that
causes a shift in fluid from the interstitial to the intravas- remained expanded for the duration of the regimen.
cular space (844, 907, 914), with each gram of albumin The authors also reported an expansion of interstitial
osmotically attracting 15 mL of fluid (919). In parallel, fluid that decreased slightly from the midpoint (11–
the conservation of sodium chloride through the incr- 15%) to the end (6–9%) of heat acclimation, sugges-
eased secretion of aldosterone (920, 921) during heat tive of a ubiquitous expansion of the extracellular
acclimation helps maintain extracellular fluid osmolality compartment. Despite these observations, conten-
and in turn to conserve or expand extracellular fluid vol- tion remains as to the extent plasma volume can be
ume (216, 257, 842, 905). The expansion of plasma vol- expanded and maintained during heat acclimation.
ume following heat acclimation varies between 2 and Recently, 5 wk (28 sessions) of constant rate exercise
16% (765, 794) and appears within the first few days of heat acclimation with a weekly increase in ambient
heat exposure (907, 922) with erythrocyte volume typi- temperature (1 C) to maintain the adaptation impulse
cally remaining unchanged (923). The latter response yielded a 7% expansion of plasma volume (831).
may be influenced by the relative brevity of most Unfortunately, plasma volume was not measured
heat acclimation interventions, as longer periods of throughout the acclimation process (e.g., midpoint),
training (4–6 wk) are required to expand red blood but the extent of increase is less than that observed
cell volume and total hemoglobin mass (924). In a by Patterson et al. (842, 905), despite core tempera-
recent heat acclimation study conducted over 5 wk, it ture increasing to 39.6 C during each 60-min train-
was reported that a 7.6% plasma volume expansion ing session (831). Additional research is therefore
was accompanied by a 4.2% increase red blood cell required to more clearly elucidate the time course of
volume and 3.2% increase in total hemoglobin mass expansion and retention of plasma volume to a given
(831). The expansion of plasma volume was thermal impulse.

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 PÉRIARD ET AL.

6.1.7. Heat acclimation with permissive active individuals experienced a body mass loss of
dehydration. 2.5% within each 90-min exposure. On day 8, an 11%
increase in plasma volume, 5 beats·min 1 decrease in
Physical activity performed under heat stress relies pri- resting heart rate and 0.20 C reduction in resting core
marily on evaporative cooling to dissipate metabolically temperature were observed, as well as an increased
generated thermal energy, which can lead to varying sweat rate (0.22 L·h 1) and decreased exercising heart
levels of dehydration depending on the compensability rate (10 beats·min 1) and core temperature (0.40 C)
of the thermal environment and fluid intake. The fluid during constant work rate semirecumbent cycling. The
secreted in sweat is initially drawn from the interstitium adaptations were sustained until the end of acclimation
and then from the intravascular and intracellular com- on day 22, prompting the authors to conclude that the
partments (593, 927–931). This sequence occurs as expansion of plasma volume can be sustained during
hypo-osmotic sweat, relative to plasma, increases os- long-term heat acclimation, provided the stimulus for ad-
motic pressure within the extracellular fluid compart- aptation is maintained (842). In a follow-up study, it was
ment, resulting in the transmembrane flow of water from reported that heat acclimation does not confer preferen-
the intracellular compartment. The loss of body water tial protection against plasma volume loss when exercis-
and fluid shift between compartments activates regula- ing in humid heat, with a greater hemoconcentration
tory processes to maintain blood volume, plasma osmo- noted on days 8 (3.4%) and 22 (4.6%) of acclimation,
lality and blood pressure. As such, restricting fluid intake relative to day 1 (i.e., baseline) (905). It was suggested
(i.e., permissive dehydration) during heat acclimation that the greater plasma loss was advantageous, as it
has been proposed to provide a thermally independent supported greater sweat secretion and facilitated post-
stimulus to enhance the adaptive process by further exercise plasma volume restoration due to an increase
challenging fluid regulatory responses (781, 810, 812). in plasma osmolality, and to a lesser extent the oncotic
The magnitude of dehydration imposed during such reg- pressure gradient, which modulated a rapid influx of
imens should be well regulated, as large body water def- fluid within the intravascular space after transitioning
icits result in greater heat storage and physiological from an exercising to a resting state. Garrett et al. (938)
strain (220, 595, 604, 616, 618), which could impair the also reported a plasma volume increase (4.5%) along
adaptive process (846). In the animal model, adjustment with reductions in core temperature (0.3 C) and heart
in cardiovascular and thermoregulatory responses com- rate (14 beats·min 1) during exercise-heat stress after
pensate for small changes in hydration status but are only 5 days of controlled hyperthermia heat acclimation
altered at severe levels of hypohydration (>10% body with restricted fluid intake (2.1% daily body mass loss).
mass loss) (932). Severe hypohydration has thus been Although these observations offer insight into fluid regu-
shown to dampen long-term heat adaptation in rats at latory processes during heat acclimation, the lack of a
the phenotypic and genomic levels through attenuated euhydrated control group limits the scope of evidence
thermoeffector responses (i.e., onset and gain) (933) and upon which firm conclusions regarding permissive dehy-
altered hypothalamic gene expression (934). The damp- dration promoting a sustained expansion of plasma vol-
ened adaptative response was associated with continu- ume can be drawn.
ous exposure (30 days) to 34 C and 35% RH with severe Studies in which a control group was employed to
hypohydration. While these findings provide novel examine the role of hydration status on the adaptative
insights into the impact of severe hypohydration on the response to heat acclimation offer conflicting results. A
long-term adaptive process to environmental heat stress short-term (5 days) controlled hyperthermia heat accli-
in rats, the regimen in which this occurred differs greatly mation regimen using a crossover design in which
to those adopted by free-living, exercise-trained euhydration (0.3% body mass loss) or permissive deh-
humans. Indeed, it has been suggested that eliciting a ydration (1.8% body mass loss) were induced demon-
body mass loss of 2–3% within each acclimation session strated a trend for plasma volume expansion to be
may induce beneficial adaptations in humans (810, 842, greater with dehydration (8 vs. 4%) (935). Although final
935), as this level of dehydration initiates fluid conserva- heart rate was 9 beats·min 1 lower during exercise-
tion and stimulates thirst (196, 239, 724, 936, 937), with- heat stress after dehydrated heat acclimation, similar
out compromising the adaptive response by the overly changes in exercising core and skin temperature were
impacting on thermoregulatory and cardiovascular noted. In contrast, Neal et al. (870) reported that under
function. similar levels of thermal strain (i.e., 10 days of controlled
Patterson et al. (842, 884) were the first to investigate hyperthermia heat acclimation), dehydration (2.7 vs.
the impact of permissive dehydration on the adaptive 0.6% body mass loss) did not influence the induction
response to chronic heat stress. A 3-wk controlled or decay (7 days) of heat adaptations in trained individu-
hyperthermia protocol was employed wherein physically als. While heart rate, sweat rate, and core and skin

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 EXERCISE UNDER HEAT STRESS

temperature were improved following heat acclimation, mass loss) at inducing adaptation, as evidenced by an
the magnitude of these responses was equivalent enhanced sweat rate, decreased skin temperature and
between the euhydrated and dehydrated regimens in improved self-paced exercise performance in the heat
this crossover design study, as was plasma volume (846). Conversely, dehydration consistently impaired the
expansion. The similar expansion of plasma volume exercising component of heat acclimation at the targeted
was attributed to the comparable increase in aldoste- heart rate and limited adaptations beyond day five of the
rone concentration noted between regimens, along intervention. Although heat acclimation resulted in a sig-
with plasma osmolality in the dehydration regimen not nificant expansion of plasma volume (4% on day 5), no
surpassing the 2% threshold required to stimulate differences between or within either intervention were
renal water conservation (204). Others have also identified. The lack of difference occurred despite the
shown in recreational athletes that 3 days of exercise- 3% reduction in daily body mass exceeding the 2%
heat training with 1.4% (euhydration) or 2.4% (dehy- decrease required to stimulate fluid regulatory responses
dration) body mass losses do not influence plasma (204).
volume expansion or adjustments in thermal, cardio- Taken together, the potential for permissive dehydra-
vascular and perceptual responses (939). Interest- tion or restricted fluid consumption to enhance the
ingly however, sweat rate increased to a greater adaptive response to chronic heat exposure remains
extent (150 mL·h 1) following dehydrated heat accli- contentious, with minimal evidence to suggest that mod-
mation, which is somewhat surprising given the re- erate changes in hydration status influence heat accli-
stricted stimulus to induce adaptations (i.e., three mation induction (227, 941). Additional studies are
sessions separated by 48 h). therefore required to elucidate whether this practice is
Using a 5-day controlled hyperthermia (38.5 C) app- beneficial, deleterious, or even trivial to the adaptive
roach with intervals and steady-state cycling in separate process and to endurance performance. Given the
groups of endurance-trained athletes, Pethick et al. potential for a dehydration-mediated compromise in
(940) reported that euhydration (0.2% body mass loss) training intensity (i.e., lower sustained work rate) during
and dehydration (2.2%) led to similar decreases in rest- exercise-heat acclimation, consideration should be
ing core temperature (0.3 C) but failed to improve 20- given to performing higher intensity exercise at the
km time trial performance in the heat. An expansion of onset of each session, or in separate cooler sessions al-
plasma volume was observed (3.6%), however, only together, if the goal is to provide a training stimulus
when data were aggregated with a control group added based on load factors. Future studies may also seek to
after the initial experimentation. The control group exer- determine the effectiveness of dehydrated interventions
cised at 75% of maximum heart rate in 22 C, which cor- against appropriately work-matched euhydrated con-
responded to the average heart rate sustained by the trols in a crossover design approach, with a standardize
experimental groups undertaking controlled hyperther- degree of daily body mass loss and postintervention
mia heat acclimation. Accordingly, work rate was not rehydration guidelines.
matched and the manner in which the target heart rate
was achieved differed between individuals and within 6.1.8. Summary.
each training session. Of note, despite daily whole
body temperature being much lower in the control Heat acclimation is an integrative process that elicits a
group, plasma volume expansion (5.2%) was similar host of physiological adaptations impacting on ther-
to the euhydrated (4.8%) and slightly greater, albeit moregulation, fluid balance, cardiovascular function,
not significantly, than the dehydrated (1.7%) group. and metabolism. Several active and/or passive
The expansion may have originated from an increase approaches can be employed to induce these adapta-
in training load, with the authors acknowledging that tions, with regimens of over 10 days purported to opti-
training intensity and volume were greater than mize the adaptive response. Heat acclimation has
recently experienced (940). These data do not support traditionally been used to enhance performance in the
the notion that dehydrated heat acclimation enhances heat, although recent investigations have proposed
fluid regulatory processes, but rather, that training per that the benefits of chronic heat exposure may also
se may provide an adaptation stimulus beyond that contribute to improve aerobic performance in cool
imposed by heat stress and dehydration. In a recent 10- conditions. Contention remains, however, as to the
day crossover design study in which recreationally impact of exercise-heat acclimation on performance in
trained individuals exercised at a heart rate equivalent cooler environments, with the role of training per se
to 65% V_ O2max (i.e., controlled heart rate heat acclima- potentially interfering with the response. Uncertainty
tion), euhydration (0.6% body mass loss) was shown also surrounds the premise that a constant forcing
to be more beneficial than dehydration (2.9% body function throughout the heat acclimation process

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 PÉRIARD ET AL.

allows for maintaining the expansion of plasma vol- 6.2.1.1. INTERNAL COOLING AND THERMAL RESPONSES.
ume and whether permissive dehydration enhances Cold beverages have a recommended temperature
fluid regulatory processes. between 10 C and 24 C (734, 755), whereas ice slurry
beverages (<0 C) consist of millions of very small ice
6.2. Cooling particles submerged in a liquid. The small particle size of
the ice slurry provides a larger surface area for heat
Exercise performance in the heat is impaired due to the transfer, with additional energy required to phase
complex interplay between increases in thermal strain change from ice to water (334 kJ·kg 1) (948). This phase
(i.e., core and skin temperature), thermal perception (i.e., change is threefold larger than that of warming cold
sensation and (dis)comfort), fluid disturbances (i.e., dehy- water to mean body temperature, which underlines the
dration), and cardiovascular, CNS, and skeletal muscle effectiveness of ice at providing a greater heat sink.
function (see sect. 4). Over the past decades, different Furthermore, the liquid of iced beverages allows heat
cooling techniques have been developed with the aim transfer via conduction by facilitating contact between
of offsetting exercise-induced increases in core body the ice particles and body tissue of the digestive tract
temperature and improve thermal perception. Cooling (i.e., mouth, esophagus, stomach, and gut). Hence, inges-
interventions can increase heat storage capacity before tion of cold or iced beverages can directly influence core
exercise (i.e., precooling) and attenuate the increase in temperature, as energy is required to warm the
core body temperature during exercise (i.e., per-cool- ingested fluids to body temperature, resulting in a
ing). Meta-analyses have shown that cooling interven- lower core body temperature (948). Thermal comfort
tions can successfully improve aerobic exercise per- and thermal sensation are also improved (949, 950),
formance in the heat (942–945), but their effectiveness as the cold/iced beverages stimulate thermoreceptors
is highly variable across techniques and study protocols. in the mouth and gut (574, 951). An additional benefit
Performance benefits from cooling appear to be the of internal cooling techniques is their contribution to
greatest during exercise in high ambient temperatures hydration status before and/or during exercise. In con-
(>30 C) and/or conditions in which prolonged exercise trast, skin temperature is only slightly affected follow-
is performed (945). The current section summarizes the ing internal cooling strategies, with minor reductions
characteristics of available cooling techniques, dis- due to vasoconstriction.
cusses the principal underlying mechanism(s) under- Although ice slurry ingesting can effectively lower
pinning their effectiveness, and reviews the (dis) core temperature, some studies suggest that evapo-
advantages associated with their use in practice. rative heat loss is attenuated during the initial phase
Subsequently, the optimal application of pre- and per- of exercise in hot (33 C) and dry (24% RH) ambient
cooling interventions is examined, followed by a com- conditions (949, 952), which may contribute to accel-
parison of the benefits of various cooling interventions erate exercise-induced elevations in core body tem-
for different types of activities (i.e., sprint vs. intermit- perature. Furth-ermore, consumption of large
tent vs. endurance exercise). Finally, methodological volumes of ice beverages may induce physical com-
and practical considerations are addressed to enable plaints such as gastrointestinal distress, nausea, and/
the translation of findings from laboratory studies to or “brain freeze”/headache. It is, therefore, recom-
real-world application. mended to practice internal cooling strategies during
training sessions and simulated competition to deter-
6.2.1. Cooling techniques. mine the optimal volume and beverage temperature
tolerated by individual athletes. In addition to the
Cooling techniques can be divided into internal and ingestion of cold fluids, several studies have
external cooling (TABLE 7). Internal cooling aims to alle- explored the possibility to influence internal (i.e.,
viate thermal strain due to lowering core body tempera- mouth and gut) thermal perception as a strategy to
ture and creating a heat sink via cold fluid or ice improve exercise performance. As such, menthol has
ingestion. External cooling techniques, such as cooling been used as a mouth rinse (953) or additive to exist-
garments, cold water immersion, or fanning, aim to ing cooled beverages (954). Menthol is known to
reduce thermal strain via an increase in the core-to-skin induce a sensation of freshness, coolness, and nasal
temperature gradient and an improved thermal percep- patency via stimulation of the transient receptor
tion. Internal and external cooling techniques can be potential melastatin 8 channel (955), which serves as
used in isolation but also in conjunction as the attenua- a cold receptor (956). The high density of cold-sensi-
tion of heat strain with a combination of techniques may tive thermoreceptors on the tongue and mucous
induce a greater net effect, both physiologically and per- membranes of the oropharyngeal cavity, therefore,
ceptually (946, 947). induce a larger effect compared with a similar dose

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 EXERCISE UNDER HEAT STRESS

Table 7. Classification and characteristics of distinct cooling techniques

Cooling Technique Examples Precooling Per-Cooling Key Advantages Potential Disadvantages

External Cooling

Cooling garments Cooling vest   Most effective per-cooling strat- Additional weight may hamper
Ice vest egy use for per-cooling
Cooling packs Available in different types and Large differences in cooling
Ice towel sizes time and rate across gar-
Neck collar Garments can be adjusted to ments
sport type Sport rules and regulations may
Phase change materials can be prohibit use during
adjusted to melting-point spe- competition
cific cooling temperatures
(i.e., 6 C, 15 C, 21 C)
Easy to apply and implement

Cold water immersion Whole body immersion  Most effective precooling strat- Difficult to implement in field-
Partial water immersion egy based settings
Covers a large part of the body Special equipment is needed
(e.g., bath, ice)
May lower muscle temperature
below optimal physiological
state

Fan use (Cold) air fanning  Easy to apply and implement Only applicable to static condi-
Water spray 1 fanning tions
Less effective in humid environ-
ments
Electricity or batteries required

Menthol cooling Cream  Easy to apply and implement High concentrations may induce
Gel adverse health effects (i.e.,
Spray skin irritation)
Limited to no effect on perform-
ance outcomes
Effect only perceptual, no cool-
ing power provided

Internal Cooling

Cold/iced beverage Cold water ingestion   Direct effect on core body tem- Potential gastrointestinal
ingestion Ice slurry ingestion perature discomfort
Contributes to maintain fluid bal-
ance
Easy to apply and implement

Menthol cooling Beverage   Can easily be added to cold Unknown

Mouth rinse water or ice slush ingestion

on the trunk (957). Menthol mouth rinsing has been temperature) was ingested without menthol additives
shown to improve running (953) and cycling (958) (959). Hence, the application of menthol as a percep-
performance in the heat, in conjunction with lower tual internal cooling strategy can improve athletic
ratings of perceived exertion. In addition, a larger performance and thermal sensation (960, 961).
expired air volume was reported in the menthol con-
dition, suggesting that menthol may induce a greater 6.2.1.2. EXTERNAL COOLING AND THERMAL RESPONSES.
drive to breathe or lower airway resistance. Further Cooling garments and cold water immersion aim to
studies are warranted to clarify the underlying mech- lower heat strain and attenuate the rise in core tem-
anisms of improved exercise in the heat following perature by increasing heat transfer from the core to
menthol mouth rinsing. A 3 C menthol aromized bev- the periphery (962). This is achieved by reducing skin
erage improved 20-km time trial performance in the temperature and increasing the core-to-skin tempera-
heat (30.7 C, 78% RH) by 9% compared with a control ture gradient. A large body surface area is needed to
condition in which the same beverage (volume and achieve sufficient heat transfer, so cooling garments

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 PÉRIARD ET AL.

typically target the torso (24% of body surface area) very cold water (i.e., <5 C due to the after drop effect)
(70), whereas cold water immersion to the upper chest (972). A potential caveat of cold water immersion is the
targets 90% of the body. The decrease in skin tem- reduction of muscle temperature leading to reductions in
perature with external cooling is also associated with muscle power, force and velocity (973), and a loss of dex-
a reduction in cutaneous blood flow (963), which terity (974). Thus application of local or whole body cold
allows for central blood volume to be better main- water immersion should be dependent on the type of
tained, thus attenuating cardiovascular strain and con- exercise that needs to be delivered.
tributing to improve exercise performance in the heat. Increasing airflow using a fan can enhance heat loss
Examples of cooling garments include cooling vests via convection and evaporation during exercise in the
(5–10 C) and ice vests (0 C), but local cooling interven- heat. Indeed, a curvilinear relationship was found
tions can also be used such as cooling collars or ice tow- between wind speed and heat storage in cyclists
els. Cooling garments need to be activated in a freezer, (FIGURE 24) (315). Increases in wind speed were associ-
refrigerator, or ice water before their use. Reductions in ated with a lower heat storage, with a plateau occurring
core body temperature, skin temperature, and heart rate beyond a wind speed of 25 km·h 1. Reductions in core
have been reported following the use of most, but not all, and skin temperature, sweat rate, and heart rate have
commercially available cooling garments during precool- been found with increasing air velocities when exercis-
ing (942, 964). The absolute cooling capacity of the spe- ing at a constant work rate (315, 975), whereas thermal
cific garment is key, in combination with the body surface sensation is improved (976). Furthermore, an improved
being covered (as large as possible), appropriateness of exercise performance was found at higher air velocities
the fit to the user (to allow conduction of heat), and the (315, 975). Adding water spray or skin wetting to fanning
wear time or time that the cooling effects last (preferably may further enhance heat dissipation (i.e., evaporation)
>20 min). The use of cooling garments during exercise (977), especially in hot and dry environments. It is impor-
(per-cooling) may not lower core temperature per se tant to note that the benefits of increasing airflow only
(942), but the preservation of a large core-to-skin temper- pertain to exercise in the laboratory or work performed
ature gradient may be beneficial to enhance performance in an indoor setting, as airflow cannot be artificially influ-
and attenuate the rate of rise in core temperature. enced during outdoor competition.
Neck cooling and head cooling are limited by their External menthol application involves spraying a solu-
small body surface area (1% and 8%, respectively (70)), tion on the skin or clothing, or applying a cream or gel to
so cooling garments covering these body sites do not the skin. External menthol application does not affect
impact on physiological parameters such as core body core and skin temperature but improves thermal sensa-
temperature and heart rate (965). On the other hand, tion similarly to internal menthol cooling (960). Some
cooling the neck and head can reduce skin temperature (978, 979), but not all (980, 981), studies suggest that
and disproportionally improve thermal sensation and high menthol concentrations (>1%) may induce undesir-
thermal comfort via stimulation of the thermoreceptors able effects, such as vasoconstriction, reduced skin
(966). Some studies have reported that per-cooling with blood flow, delayed onset of sweating, and a greater
neck and head garments can improve self-paced and
constant work rate exercise performance in the heat 100
under laboratory conditions (967–969).
Heat storage (W·m-2·h-1)

Local and whole body cold water immersion are effec-

75
tive strategies to extract heat from the body during pre-
and/or postcooling (942, 970). Water temperatures of 15
to 25 C are typically adopted, but lower temperatures 50

may be applied for postcooling. Very cold water immer-

sion of a large body area may be perceived as uncomfort- 25
able, which may reduce exposure time and impact.
Although colder water was believed to induce greater
0
physiological changes over a longer period of time, 0 10 20 30 40 50
severe skin vasoconstriction may prevent core body tem- Wind speed (km·h-1)
perature from decreasing during cold water immersion.
FIGURE 24. Calculated heat storage expressed per hour during
Indeed, a recent study found similar cooling rates using exercise at 60% of peak power output at different air velocities.
14 C and 26 C water due to an attenuated vasoconstric- 1
Heat storage at 0 km·h was significantly different from all other
tor drive at 26 C (971). Nevertheless, the mixture of warm 1
conditions, whereas the 10 km·h condition was only higher com-
1
“central blood” with cool “peripheral blood” will reduce pared with the 50 km·h condition. Redrawn with permission from
Saunders et al. (315).
core body temperature after termination of immersion in

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 EXERCISE UNDER HEAT STRESS

increase in core temperature. A recent meta-analysis suggest that whole body vigorous cooling is superior to
reported a lack of performance benefits for external localized and/or less vigorous cooling techniques at
menthol cooling (960), but large differences were found improving exercise performance in the heat.
across studies. Future studies are warranted to assess
whether a specific dose, application technique (e.g., 6.2.2.2. PER-COOLING. Per-cooling interventions aim to
spray versus cream versus gel) and location of menthol attenuate the increase in core temperature during exer-
application may improve performance. cise. The relevance of per-cooling is reinforced by the
fact that the benefits of precooling interventions typically
6.2.2. Cooling and performance. fade 25 min after the onset of exercise (996). Beyond
this time point, core temperature does not differ any
6.2.2.1. PRECOOLING. Precooling interventions aim to more between the precooling and control condition
lower thermal strain before exercise, using internal and/ (989, 997, 998), suggesting that the benefits of precool-
or external cooling strategies. Precooling-induced red- ing are predominantly derived during the early phase of
uctions in core temperature lead to an increased heat endurance exercise. Furthermore, exercise intensity
storage capacity (942). The application of precooling is (i.e., work rate), and therefore heat production and ther-
not a novel approach. Initial studies, published 65 to 85 yr mal strain, are much higher during exercise as com-
ago, investigated the effects of cooling on cardiovascular pared with warming-up, emphasizing a potential larger
dynamics, oxygen uptake, and heat exposure tolerance ergogenic benefit of per-cooling versus precooling. On
time (982–984), mainly from an occupational health per- the other hand, not all cooling techniques (i.e., cold
spective. Studies published in the late 1970s and early water immersion) can be applied for per-cooling due to
1980s were the first to assess the impact of precooling on practical (i.e., accessibility, additional mass, and power
exercise performance using cold water swimming (13– cord) or regulatory limitations during competition (999).
15 C) and cold air exposure (0 C) (985–987). Cold water Several systematic reviews and meta-analyses have
swimming did not improve time to exhaustion and assessed the performance benefits of per-cooling (943,
V_ O2max, but this may have resulted from extreme cooling 995, 1000–1003). Although there is consensus that per-
as some participants became hypothermic (985). Cold air cooling interventions improve performance in the heat,
exposure did improve time to exhaustion (987) and work the effects differ across study designs and cooling tech-
rate (986) during cycling exercise in mild ambient condi- niques. For example, there is debate as to whether per-
tions (18 C). From the mid-1990s onwards, many studies cooling improves time to exhaustion, as systematic
evaluated the physiological and psychological benefits of reviews and meta-analysis reported inconsistent out-
precooling and found that whole body cooling [i.e., cold comes (1002, 1003). Ruddock et al. (1002) only included
water immersion (949, 988), and cold air exposure (986, cooling techniques that would be practical for athletes
987, 989)], partial body cooling [i.e., cooling vests (990, to use during competition. Four studies were included,
991), and cooling packs (992, 993)] and internal cooling encompassing neck cooling, palm cooling, and cold fluid
techniques [i.e., cold water and ice slurry ingestion (949, ingestion, but no clear performance benefit was found.
964, 994)] were effective at increasing endurance per- In contrast, Stevens et al. (1003) adopted less strict inclu-
formance in the heat. sion criteria and pooled findings from nine per-cooling
The magnitude of performance improvement follow- studies, including cold fluid ingestion, fanning and water
ing precooling is highly variable and depends on the 1) spraying, menthol mouth rinsing, cooling garments,
exercise protocol (i.e., constant work rate vs. self-paced neck cooling, and palm cooling. The authors reported
exercise), 2) nature of the exercise performed (i.e., sprint that only one of nine studies found no performance
vs. intermittent vs. endurance), 3) cooling dose provided improvement, so concluded that per-cooling could
(i.e., cooling intensity and duration and body surface effectively improve time to exhaustion. Self-paced exer-
area covered), 4) perceived reductions in heat strain, cise protocols such as time trials may be more suitable
and 5) ambient conditions (i.e., compensability of the to assess the benefits of per-cooling, given their better
environment) (942, 970). Several meta-analyses have reliability and ecological validity (1004). Indeed, per-cool-
summarized the benefits of precooling on exercise per- ing was found to be effective during self-paced exercise
formance (942–945). The most recent overview identi- studies in all systematic reviews and meta-analyses
fied data from 45 experimental trials (995). Precooling (1002, 1003). These findings reinforce the performance
improved exercise in the heat in all but two trials, with an benefits of per-cooling during competition.
average performance enhancement of 4.7%. Cooling A recent study quantified the ergogenic effects of
technique-specific improvements varied from 2.0% to per-cooling among 270 athletes from 26 studies. It
7.1%, with cold water immersion being the most effective was observed that exercise performance improved by
precooling strategy (FIGURE 25). These findings 5.3% (995). Cooling technique-specific improvements

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 PÉRIARD ET AL.

20
Pre-cooling

16
Performance benefit (%)

12

0
FIGURE 25. Relative performance improvements for
Cold water Mixed method Cold water Cooling packs Cooling vest pre-cooling (top) and per-cooling (lower panel) interven-
immersion cooling ingestion
tions during exercise in the heat. The dashed line repre-
sents the average performance benefit for pre-cooling
20 (4.7 6 4.7%) and per-cooling (5.3 6 6.5%). Cooling strat-
Per-cooling egy-specific data are presented as average 6 SD and
extracted from Bongers et al. (995).
16
Performance benefit (%)

12

0
Cooling vest Fanning & Cold water Cooling packs Menthol
water spraying ingestion cooling

varied from 3.2% to 11.9%, with the use of cooling/ice 6.2.2.3. MAGNITUDE OF PERFORMANCE BENEFIT. The
vests being the most effective per-cooling strategy benefits of cooling are not uniform across athletes
(FIGURE 25). Previous studies also assessed the engaging in different types of activities and sports.
effects of per-cooling on psychological and physio- Based on the relative isometric and isotonic compo-
logical outcomes, demonstrating improved ratings of nents of exercise, athletes can be classified as endur-
perceived exertion, thermal perception, and skin tem- ance (e.g., running, cycling, race walking, triathlon),
perature (1003), but no effect on peak core tempera- intermittent (e.g., field hockey, football, tennis, beach
ture, heart rate, and sweat rate (942, 1003). Few volleyball), power (e.g., sprint, BMX), or skill (e.g., sailing,
studies have assesed the combined effects of pre- archery). In general, endurance athletes seem to benefit
cooling and per-cooling to explore whether the most from cooling (995). Meta-analyses have shown that
effects are superior to the use of a single cooling precooling induces greater improvements in exercise
strategy. Exercise performance improved by 5.6% performance in endurance athletes than intermittent ath-
(range: 1.7% to 123%) in the combination condition letes (944, 945). Likewise, per-cooling interventions
but did not differ from the independent application of induce greater benefits during aerobic compared with
precooling or per-cooling (943). A potential explana- anaerobic exercise, with cold beverage ingestion and
tion for the lack of difference may relate to the dura- external cooling providing the greatest benefits for aero-
tion of the exercise protocols that were used (<1 h) in bic performance and whole body cooling garments
combination with the high frequency of cooling inter- being favorable for anaerobic exercise (1001). The differ-
ventions during exercise (i.e., cold water ingestion) ence in performance improvement between endurance
(1003). Hence, future studies should explore whether and intermittent exercise likely relates to the duration
the combination of pre- and per-cooling yield addi- and cumulative heat gain occurring during exercise. As
tional benefits for endurance exercise lasting >1 h in a thermal strain is often greater in endurance versus inter-
sport-specific context. mittent exercise, the window for improvement is likely

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 EXERCISE UNDER HEAT STRESS

larger. Nevertheless, it is important to reiterate that both limitations may hamper translation to field conditions on
endurance (6.4%) and intermittent athletes (3.0%) have several levels. First, the translation of findings from ama-
been shown to benefit from cooling interventions (995). teur to professional athletes may be associated with
Power athletes (e.g., sprinters, jumpers) do not benefit lower benefits as the window for improvement is smaller
from cooling, and exercise performance may even be given their greater aerobic fitness. On the other hand,
deteriorated following precooling (944, 945). The lack of no clear association between fitness (i.e., V_ O2max) and
cooling benefits in such athletes is multifactorial. First, the effects of precooling on performance have been
exercise duration is short (typically <1 min), so the impact identified (945). Second, cooling benefits may be differ-
of thermal strain is unlikely to limit performance. Second, ent for veteran compared with young athletes, as exer-
it is methodologically difficult to provide evidence for cise performance, and thus heat production, declines
small improvements (i.e., <1 s) in sprint performance, as with advancing age (1014), whereas thermal sensation
a large sample size and specific (high-resolution) mea- and perception is impaired (86). Third, most meta-analy-
surement equipment are needed. Third, muscle tempera- ses aggregate data independently of exercise protocols,
ture is a key determinant for skeletal muscle contractility, which induces heterogeneity to the overall effect of
anaerobic metabolism, and sprint performance (466, 467, cooling, such that the benefits of cooling in specific set-
1005). Cooling interventions may (in)directly impact mus- tings (i.e., activity, exposure time, exercise intensity) may
cle temperature and attenuate performance in power ath- be either over or underestimated. Fourth, the perform-
letes. As such, cooling interventions are not recomm- ance benefits of cooling are less clear in temperate am-
ended for power athletes. bient conditions (945) and largely unknown in cool
The benefits of cooling in skill-based sports are less temperatures. Of note, even in 10.5 C conditions a high
well studied, despite the presence of elevated thermal proportion (15%) of amateur runners experienced hyper-
strain in some sports (1006). Mixed outcomes have been thermia (core temperature >40 C) during a 15-km road
reported in studies assessing the impact of cooling inter- race (1015). Fifth, the interplay between ambient temper-
ventions on psychological and cognitive outcomes. For ature, absolute humidity, solar radiation, and wind speed
example, cold pack application to the head improved is highly dynamic in field conditions and thus not compa-
working memory and rapid visual processing following rable with most ambient conditions adopted in labora-
passive heating but had no effect on pattern recognition tory studies (i.e., high temperature, moderate humidity,
memory (1007). Another study reported that application no solar radiation, and low wind speed). The typically
of cold packs to the head preserved working memory low airflow provided during laboratory-based studies
capacity but not visual memory in the heat (435). Other appears to be particularly influential and lead to an over-
studies showed no benefit of cooling interventions on estimation of the ergogenic benefits of precooling. For
cognitive capacity (1008) or only in specific subdomains example, Morrison et al. (1016) demonstrated that com-
(1009, 1010). These inconsistent outcomes suggest that bining cool water immersion (24 C) precooling with an
the effect of cooling on cognitive function is dependent airflow of 4.8 m·s 1 during exercise in warm conditions
on the intervention (i.e., timing, type, frequency, and du- (30 C) did not enhance performance or decrease ther-
ration of cooling) (1011), type of task (1012), and the factor mal and cardiovascular strain more than providing air-
investigated (e.g., cognitive tasks, working memory, vis- flow alone. Additional studies are therefore warranted
ual memory, executive function, and auditory function) to validate the performance benefits of pre- and per-
(1013). More research is needed to determine which type cooling under realistic ambient conditions, including
(pre- vs. per-cooling) and technique (i.e., internal versus appropriate airflow. Sixth, it is unknown how heat accli-
external) of cooling can be beneficial to skill-based mation status impacts the benefits of cooling strategies
athletes. during exercise in the heat. Seventh, sex differences in
body characteristics and exercise-induced increases in
6.2.3. From laboratory to field conditions. core temperature and sweat rate may contribute to dis-
tinct benefits of specific cooling strategies in male ver-
Most studies assessing the benefits of cooling interven- sus female athletes (83, 1017). Taken together, these
tions have been performed in laboratory conditions restrictions indicate that laboratory findings cannot be
using moderately to well-trained young individuals. A directly extrapolated to field conditions, as certain cool-
large variety of experimental protocols have been used ing techniques and protocols may not be as effective as
to assess performance benefits (e.g., time to exhaustion initially demonstrated. Future studies should therefore
and self-paced exercise) in different modes of exercise further examine the implementation of cooling strategies
(e.g., cycling and running), with most studies performed in field conditions.
in hot ambient conditions (>30 C). The large majority of Recent studies have evaluated the use of cooling
studies only included young men. These study interventions by elite athletes competing in World

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 PÉRIARD ET AL.

Championship events under hot and humid ambient 6.3. Hyperhydration

conditions. During the 2015 International Association
of Athletics Federations World Championships in Hydration status can be severely affected during exer-
Beijing (China), 307 athletes from 5 event categories cise in the heat, so it is recommended that athletes
(i.e., field, sprints, middle distance, long distance and undertake exercise in a euhydrated state to optimize
decathlon/heptathlon) participated in a survey (1018). performance (181, 1020). To reduce net fluid loss and
Only 52.4% of the participants reported that they offset the deleterious effects of dehydration on per-
planned on using at least one precooling strategy, formance in the heat, preloading or preexercise
10.4% planned on using two strategies and 4.9% three hyperhydration has been explored as a mitigation
strategies. Male athletes (52%) and those competing strategy. In this section the effects of four hyperhy-
in middle distance races (70.3%) more often applied dration strategies will be evaluated: water, glycerol,
cooling strategies. A similar study was performed with sodium, and creatine.
69 professional cyclists before the 2016 Union
Cycliste Internationale World Championships in Doha 6.3.1. Water loading.
(Qatar) (1019). Almost all cyclists planned some form of
precooling before the individual or team time trial The first study to examine the effects of hyperhydration
(96.4% and 98.6%, respectively). Although 74% of par- using water dates back to 1965. Soldiers drinking 2 liters
ticipants indicated that they would precool before the of 24 C water before 90 min of walking in the heat
road race, a large difference in the use of precooling (49 C, 15% RH) demonstrated a lower end-exercise rec-
was found between male (57%) and female (96%) tal temperature (0.3 C) and 2.5% increase in sweat
cyclists. Findings from these two studies highlight the rate compared with those not hyperhydrating (1021). The
heterogeneity in the use of cooling strategies by pro- authors concluded that “overhydration is beneficial to
fessional athletes. Whereas only half of track and field men working in the heat.” However, there are two main
athletes used prearranged precooling strategies, limitations in this study. First, hyperhydration was not
almost all cyclists planned on using a precooling strat- compared with euhydration, as the soldiers in the con-
egy ahead of the time trial. Differences in education trol condition were 1% hypohydrated. It has been sug-
on the (perceived) benefits of cooling, but also avail- gested that the higher rectal temperature in the control
able resources and the type of sport (e.g., sprinters vs. condition compared with the hyperhydration condition
endurance athletes), may have contributed to these may have been the result of the slight hypohydration,
differences. Given the increasing evidence regarding rather than the positive effects of hyperhydration (601).
the performance benefits of cooling, a further Second, the low temperature of the drinking water may
increase of the prevalence of cooling strategies dur- have provided a precooling effect, such that the benefi-
ing competition in hot and humid environments is cial effects were not linked to hyperhydration per se, but
expected. Whether similar trends are applicable to to precooling (see sect. 6.2). To exclude the role of pre-
the use of per-cooling is currently unknown and cooling, water of 37 C should be consumed to achieve
should be explored in future studies. hyperhydration. Two studies did so in temperate condi-
tions (23 C, 50% RH). In one study participants drank
6.2.4. Summary. 2.1 liters of 37 C water 60 min before 45 min of constant
rate exercise (1022) and in the other study 2.5– 3.0 liters
Cooling interventions improve exercise performance in of water before 70 min of exercise (600). Both studies
the heat. There is a large variety of cooling techniques observed a lower end-exercise rectal temperature of
available, and a selection can be made based on the 0.2 C with hyperhydration compared with euhydration
effectiveness, feasibility, and sport-specific regulations but no differences in sweat rate. These data indicate
that apply during competition. Precooling and per-cool- that hyperhydration using water at a temperature similar
ing solutions appear equally effective, but their combina- to body temperature in amounts of 2 liters leads to a
tion does not lead to further synergy. The benefits of slightly lower body core temperature during exercise.
cooling are also different across activities and sports. However, it is difficult to consume such large volumes of
Endurance and intermitting athletes benefit most, fluid in the hours preceding exercise; therefore, it is rec-
whereas power athletes and sprinters do not benefit at ommended that protocols be practiced to determine
all. The benefits of cooling for skill-based sports are less their effectiveness and potential side effects including
clear and should be further investigated. There is also a gastrointestinal discomfort and headaches (304).
need to evaluate the benefits of cooling in elite athletes, The observations in the previous paragraph raise the
as current evidence is entirely based on observations in question regarding how body core temperature can be
moderate to highly trained athletes. lower following hyperhydration when sweat rate is not

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 EXERCISE UNDER HEAT STRESS

increased. The answer may lie with a study in which preloaded with intravenous fluids (1023, 1026).
blood volume was manipulated before exercise in the Moreover, intravenous fluid use in Olympic sports must
heat (602). In this study, participants received an infu- comply with the World Anti-Doping Code and may
sion of isotonic serum albumin to increase blood volume require a therapeutic use exemptions to be granted with
by 7.9%. During 30 min of cycling in the heat (40 C, 30% appropriate clinical justification (1027). Therefore, the
RH) at 65–70% V_ O2max, mean esophageal temperature focus in this section is on oral hyperhydration, as most
was 0.11 C lower following infusion and sweat rate was athletes are unlikely to use intravenous methods.
unaffected, which is in line with previous observations in
temperate conditions (600, 1022). During hypervolemic 6.3.2. Glycerol.
exercise, blood volume decreased to a larger extent
than in the control condition (541 vs. 421 mL) (602). The Glycerol, a 3-carbon alcohol metabolite, is an endoge-
authors suggested that the expansion of blood volume nous substance distributed across the body at low
was linked to a reduction in vasomotor tone (i.e., concentrations (0.05–0.3 mmol·L 1) (1028). Glycerol
reduced vasoconstrictor activity), leading to a smaller enhances fluid retention so it can be used to increase
net reabsorption of fluid from inactive tissues and total body water content. This was first shown in
greater filtration in active muscles. The reduction in vas- humans in 1987 (1029). Glycerol-induced hyperhydra-
omotor tone was associated with greater skin blood tion was on the World Anti-Doping Agency Prohibited
flow when hyperhydrated in the heat and thus lower List until January 2018, but athletes are now free to
body core temperature due to enhanced dry heat loss use it for hyperhydration. Elevations of glycerol levels
(602). Skin temperature recordings during hyperhydra- can be achieved using venous infusion or fluid inges-
tion failed to demonstrate a difference with those of con- tion. Venous infusion increases the blood osmolality
trol conditions (600, 1022), indicating that additional faster than the coingestion of water and dissolved
research is required to confirm this hypothesis. If wet glycerol, but has obvious practical limitations such as
and dry heat loss is not changing due to hyperhydration being more invasive. The effectiveness of glycerol for
and core temperature shows a slower increase, the retaining water depends on the timing, dose and
extra body volume may act as a heat sink. However, amount of fluid ingested (1028).
assuming a specific heat for the human body of There are two pathways via which glycerol is sug-
3.47 kJ·kg 1· C 1 and a body mass of 70 kg, calculations gested to increase water retention and total body water.
indicate a similar heat gain of 2 C without predrinking First, glycerol attenuates the decrement in antidiuretic
and a gain of 1.95 C after hyperhydrating with 2 liters. hormone that is observed due to water loading by
Therefore, the increased heat sink only partially explains increasing plasma osmolality (1030). Thus water secre-
the reduction in body core temperature observed with tion is lower following hyperhydration. Second, glycerol
hyperhydration. Along with the fluid shifts occurring may have a direct effect on the kidneys as it is reab-
within the central circulation during hyperhydrated exer- sorbed in the proximal and distal tubules, which induces
cise, fluid regulation within the bladder occurs in an osmotic drive for the reabsorption of water. Glycerol
response to activation of the RAAS to maintain homeo- can maintain this gradient for a relatively long period
stasis and excrete excess fluids (see sects. 3.1 and 3.2). because it has a slow metabolism and is thus slowly
However, it has been reported that after 45 min of exer- excreted through urine, ultimately leading to higher
cise, 65% of the ingested water is still present in the water reabsorption (1031).
central circulation and the remaining volume in the blad- Several studies have investigated the effects of glyc-
der (1022). erol induced hyperhydration during exercise in the heat.
In summary, drinking 2 liters of water before exer- One of the first studies used a constant work rate (60%
cise in the heat seems to slightly lower body core tem- V_ O2max) protocol in hot/dry conditions (42 C, 25% RH)
perature during exercise without affecting sweat rate. and observed a lower rise in rectal temperature and
Hyperhydrating with water may be ineffective, however, enhanced sweat rate after ingestion of 1 g·kg 1 body
as a rapid decrease in aldosterone concentration will mass of glycerol with 21.4 mL·kg 1 of water, compared
signal the kidneys to excrete excess water in the form of with no glycerol (1032). In the subsequent decade, stud-
dilute urine. Therefore, the coingestion of an osmotically ies investigating the effects of glycerol-induced hyperhy-
active agent like sodium, glycerol, or creatine can assist dration (1033–1038) observed considerably different
with fluid retention (304). Next to oral ingestion of outcomes across various types of exercise in the heat.
osmotically active agents, intravenous infusion of colloid TABLE 8 summarizes the protocols and results of these
(1023) or crystalloid (1024) solutions is used for plasma studies, all of which adopted a crossover design and
volume expansion before exercise (1025). However, no provided a similar amount of water in the control trial to
differences are observed in thermal strain when that of glycerol in the experimental hyperhydration trial.

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 PÉRIARD ET AL.

The glycerol ingestion protocols showed small differen- how does sodium preloading affect thermal strain and
ces in thermal strain and performance across studies, performance in the heat. Several studies were performed
with most ingestion rates commensurate with recent to explore the effect of sodium hyperhydration on per-
suggestions of a glycerol dose of 1.2 g·kg 1 body mass formance in the heat (TABLE 9), all of which were con-
with a fluid volume of 26 mL·kg 1 body mass per hour ducted following those with glycerol.
(1039, 1040). Sims et al. (1044) investigated the extent to which so-
Latzka et al. (1035) observed no differences in thermal dium intake (164 vs. 10 mmol·L 1 sodium) before exercise
strain with and without glycerol induced hyperhydration in the heat (32 C, 50% RH) influenced exercise capacity
in compensable (1035) and uncompensable (1036) heat in eight males (1043) and 13 females. In males, plasma
stress, although performance was enhanced with glyc- volume increased by 4.5% after high sodium intake and
erol induced hyperhydration in uncompensable heat was unchanged following low sodium intake. Time to
stress (1036). In their review, Latzka and Sawka (1041) exhaustion was improved by 25% and end-exercise rec-
concluded that there appeared to be no thermoregula- tal temperature lower by 0.4 C in the high sodium group
tory or performance benefit from hyperhydration when (1043). In females, all in the luteal phase, plasma volume
euhydration was maintained during exercise and that increased by 4.4% after high sodium intake and was
glycerol induced hyperhydration was not better than unchanged with low sodium intake. Time to exhaustion
water hyperhydration for a given hydration status at the increased by 26% but end-exercise rectal temperature
start of exercise. Others have also reported no differ- did not differ (after recalculation of the raw data pro-
ence in performance between glycerol and water- vided in the study) (1044). Sweat rate was slightly
induced hyperhydration during mountain bike racing lower for the high sodium condition in females relative
(1038) and self-paced exercise in the heat (1037). These to low sodium intake and did not differ between con-
findings are in contrast with reports of improved per- ditions in males. Based on these results, the authors
formance during cycling time trials following glycerol- suggested that additional sodium intake before exer-
induced hyperhydration (1033, 1034) and a lower rectal cise may enhance performance. In contrast, however,
temperature (0.4 C) (1033), which may have contributed drinking a sodium solution of 130 mmol·L 1 sodium in
to enhance performance. A meta-analysis assessing the 26 mL·kg 1 water before exercise did not result in per-
effects of glycerol-induced hyperhydration during exer- formance enhancement during an 18-km treadmill run
cise in the heat was published by Goulet et al. (1031), but in 28 C, although heart rate (5 beats·min 1) and
this review included only four studies (1033, 1034, 1037, end-exercise rectal temperature (0.3 C) were lower
1038). The authors excluded the work of Latzka et al. (1046).
(1035, 1036) since it did not meet their inclusion criteria Two studies investigated the effect of sodium on
and included a study that was not performed in the heat time trial performance after 2 h of dehydrating exer-
(685). The analysis was performed for hyperhydration cise at 63% V_ O2max (1047) or 1 h at 50% of the maxi-
studies in temperate and hot conditions and it mum power output (1048). The first study showed that
was concluded that glycerol-induced hyperhydration sodium concentrations of 164 and 82 mmol·L 1 simi-
improved fluid retention by 50% relative to water- larly increased plasma volume and improved time trial
induced hyperhydration. This was associated with a performance compared with no sodium during pre-
6.2% improvement in endurance performance. In sum- loading, although this study showed no reduction in
mary, adding glycerol to water for hyperhydration pur- core temperature or increase in sweat rate (1047). The
poses results in greater water retention. However, the positive effects of sodium preloading on performance
benefits of glycerol hyperhydration for reducing thermal were also demonstrated in the second study in which
strain and improving performance are equivocal and participants consumed 60 mg·kg 1 body mass of salt
more research with sufficient statistical power is (1 g of salt = 390 mg of sodium) with 2 mL·kg 1 of water
required to clarify the effect of glycerol hyperhydration. before 60 min of submaximal exercise, followed by a
cycling time trial in 30 C (1048). Participants drank ad
6.3.3. Sodium. libitum during submaximal exercise and ingested
much more water following salt preloading (1,830 vs.
Most of the early work showing that adding sodium to a 815 mL for placebo and 782 mL for no treatment).
drink increases plasma volume was performed by NASA Water retention increased with salt intake (815 vs.
before the turn of the century (1042). Although sodium 244 mL and 148 mL, respectively). Time trial perform-
expands plasma volume in combination with water intake ance was also improved, while sweat rate did not
due to its osmotic effect, it is also suggested that large differ.
concentrations of the sodium ions in the plasma may Sodium has also been ingested in combination with
reduce sweat rate (621). As such, the question becomes citrate instead of chloride (1045), which was found to

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Table 8. Summarized methods and results of studies investigating the effect of glycerol-induced hyperhydration on
thermal strain and performance in the heat
Preexercise Environmental Core Skin
Sample Water, mL·kg 1/ Plasma Sweat Rate, Performance
Study Ingestion Exercise Protocol Conditions, 8C, Temperature, Temperature,
Size Glycerol, g·kg 1 Volume, % L·h-1 (G/C) (G/C)
Time, min %RH 8C (G/C) 8C (G/C)

Lyons et al. (1032) 6 21.4/1.0 150 90 min at 60% 42/25 0.7 37.4/38.1 0.97/0.75
V_ O2max

Latzka et al. (1035) 8 25.2/1.2 (LBM) 60 120 min at 45% 35/45 0.0 38.6/38.6 0.94/0.95 35.5/35.4
V_ O2max

Latzka et al. (1036) 8 29.1/1.2 (LBM) 60 30 min at 55% 35/45 0.1 38.8/38.7 1.26/1.09 37.6/37.4 33.8/29.5 min
V_ O2max

Hitchins et al. (1034) 8 22.0/1.0 150 60 min at 60% 32/60 0.8 38.9/39.0 1.92/1.85 33.2/33.2 472/450 kJ
V_ O2max

Anderson et al. (1033) 6 20.0/1.0 120 90 min at 98% LT 35/30 0.8 38.7/39.1 252/240 kJ

Marino et al. (1037) 7 21.0/1.2 150 60-min time trial 35/63 0.2 38.8/39.0 1.72/1.15 33.7/34.0 Equal distance

Wingo et al. (1038) 12 28.0/1.0 48-km mountain WBGT 28 0.1 38.5/38.0 1.42/1.44 No time
bike race difference

C, control; G, glycerol; LBM, lean body mass; LT, lactate threshold; WBGT, wet-bulb-globe temperature; RH, relative humidity. P < 0.05, significant different from control.

induce a 3.6% increase in plasma volume but no increased by 10 to 40% through the use of creatine sup-
reduction of thermal strain during prolonged cycling. plements, depending on initial total creatine levels
The taste of salt drinks is often not pleasant, and salt (1050). The primary role of creatine is the resynthesis
tablets as an alternative have been investigated with of ATP via the creatine kinase reaction. Thus creatine
regards to fluid retention capacity. Savoie et al. (1049) is important for short duration exercise performance
reported that a salt solution provided better fluid and has been shown to improve sprint performance in
retention than tablets with equal concentrations of so- the heat when used as a supplement (1051). As such,
dium, probably due to the time it takes the tablets to there has been a limited focus in the literature on the
dissolve in the stomach. Sodium supplementation use of creatine to enhance endurance exercise per-
may be required during prolonged exercise to attenu- formance (1052). However, creatine ingestion has
ate hyponatremia when large volumes of fluid are been shown to have a positive effect on body water
consumed. It must be acknowledged, however, that retention (1053). The increased fluid retention associ-
salt or sodium supplementation cannot prevent exer- ated with creatine loading has been attributed to os-
cise-associated hyponatremia when persistent and motic effects resulting in cell swelling and increased
excessive fluid intake produces volume overload protein synthesis (1054). Creatine supplementation of
(267) (see sect. 3.4). In summary, intake of high con- at least 5 days is needed for increasing body mass (1–
centration sodium drinks (>82 mmol·L 1) with a vol- 3 kg) and total body water (1050). In contrast to so-
ume of at least 10 mL·kg 1 or of salt capsules (60 mg dium and glycerol supplementation, creatine has no
salt·kg 1 body mass) with concomitant ad libitum effect on renal responses (1051).
water intake before exercise lead to increased plasma Based on these observations, a study was performed
volume. Rectal temperature at the end of exercise has to investigate the effects of creatine supplementation on
been shown to be lower in some studies with sodium exercise capacity in the heat with the experimental
preloading, although none demonstrated an increase group ingesting 22.8 g of creatine with a glucose poly-
in sweat rate. Most studies observed an increased mer every day for 7 days, whereas the control group
performance in the heat. only ingested the glucose polymer (1055). Total body
water increased by 1.5% in the experimental group and
6.3.4. Creatine. no changes were noted in the control group. No differ-
ences were observed in time to exhaustion between the
Creatine is a nonessential dietary compound synthe- experimental and control groups after creatine inges-
sized in the liver and pancreas, and mainly stored in tion. Interestingly, there was considerable variation in
the muscles (1050). Creatine muscle storage can be the amount of creatine absorbed across participants,

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Table 9. Summarized methods and results of studies investigating the effect of sodium-induced hyperhydration on
thermal strain and performance in the heat
Preexercise Environmental Plasma Core Skin
Sample Protocol Control Water/ Sweat Rate, Performance
Study Ingestion Exercise Protocol Conditions, 8C, Volume/Body Temperature, Temperature,
Size Water/Sodium Sodium L·h-1 (S/C) (S/C)
Time, min %RH Mass, % 8C (S/C) 8C (S/C)

Sims et al. 8 10/164 10/10 105 70% V_ O2max to 32, 50 4.5 PV 38.9/39.3 1.6/1.9 57.9/46.4 min
(1043) exhaustion

Sims et al. 13 10/164 10/10 105 70% V_ O2max to 32, 50 4.4 PV 39.0/39.1† 1.3/1.7 98.8/78.7 min
(1044) exhaustion

Nelson et al. 12 12/170 Gatorade 100 15% >VT for 31, 64 3.6 PV 38.7/38.7 0.5/0.5
(1045) 62 min

Gigou (1046) 6 26/130 No sodium 110 18-km time trial run 28, 28 1.3 BM 39.4/39.7 1.9/1.9 85.3/85.6 min

Hamouti et al. 10 10/164 10/82 90 171-kJ time trial 33, 30 2.1 PV 38.8/38.8 1.4/1.4 34.4/34.4 No difference
(1047)

Hamouti et al. 10 10/164 No sodium 90 171-kJ time trial 33, 30 4.5 PV 38.8/39.1 1.4/1.4 34.4/34/6 289/269 W
(1047)

Morris et al. 7 2/60 salt No treatment 180 200-kJ time trial 30, 18-20 0.9 BM 37.4/37.6 Similar (no data) 773/872 s
(1048)

Morris et al. 7 2/60 salt Aspartame 180 200-kJ time trial 30, 18-20 0.8 BM 37.4/37.3 Similar (no data) 773/851 s
(1048)

Only studies with 6 or more participants included. BM, body mass; C, control, S, sodium; VT, ventilatory threshold; W, water. Water is in mL·kg 1, sodium is in mmol·L 1, and salt is in mgmL·kg 1, where 1 g

†
equals 0.39 g sodium. P < 0.05, significantly different from control. After recalculation of the raw data in the study.

with those absorbing more creatine demonstrating an benefits and whether these may differ between con-
improvement in time to exhaustion. The experimental stant work rate and self-paced exercise protocols.
group also had lower sweat rates (0.3 L·h 1) and lower
end-exercise rectal temperatures (0.4 C) compared with 6.3.5. Combinations of glycerol, sodium, and
the control group. The authors suggested that the lower creatine.
increase in rectal temperature and improvement in per-
formance may be related to the 1.5% extra body volume Several studies have examined the use of a combination
and concomitant increased heat storage capacity after of different hyperhydrating agents. For example, Savoie
creatine ingestion. However, as shown in sect. 6.3.1, the et al. (1049) reported that sodium and glycerol hyperhy-
effect of this increased heat capacity is <0.1 C for mean dration have similar beneficial thermoregulatory effects
body temperature and thus does not give a suitable ex- during exercise. However, the combination of glycerol
planation for the observations. (1.4 g·kg 1 fat free mass) and sodium (7.5 g·L 1 of table
In a separate study, participants ingested 21.6 g of cre- salt) dissolved in water (30 mL·kg 1 fat free mass) led
atine monohydrate or a placebo for 7 days before a to significantly greater fluid retention (1.4 liters) com-
90-min heat tolerance test that started after the par- pared with sodium (1.1 liters) or glycerol (0.7 liters) alone
ticipants lost 2% of their body weight due to exercise (1039). These findings suggest that the combination of
in the heat (1056). The authors reported no differen- sodium and glycerol is more effective at retaining fluid
ces in rectal temperature and sweat rate between than each component separately.
conditions, indicating that short-term creatine sup- The combined effects of creatine and glycerol sup-
plementation did not influence thermoregulatory plementation were investigated to determine their
responses in hypohydrated individuals. Given the effects on physiological variables during 40 min of con-
conflicting outcomes of creatine ingestion in these stant-load exercise at 63% of maximum work rate and
two studies, no firm conclusions on the effects of cre- performance during a subsequent 16.1-km time trial in
atine on thermoregulation during exercise in the heat the heat (30 C) using four experimental conditions: pla-
can be drawn. Additional research is warranted to cebo, creatine, glycerol and the combination of creatine
explore potential performance and thermoregulatory and glycerol (1057). Two daily doses of glucose (i.e.,

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 EXERCISE UNDER HEAT STRESS

placebo: 11.4 g), creatine (11.4 g), glycerol (1 g.kg 1 body 7. CONCLUSIONS
mass), and creatine and glycerol combined were taken
for 7 days. Glycerol increased total body water by The last decade has been the warmest on record and
0.50 liters, creatine by 0.63 liters and the combination of part of a persistent long-term trend. Along with an
the two by 0.87 liters compared with placebo. Creatine increase in the incidence and severity of heat waves,
and the combination of creatine and glycerol signifi- this trend places both elite and recreational athletes of
cantly attenuated heart rate, rectal temperature, and all ages at greater risk of exertional heat illness and pro-
perceived exertion during constant rate exercise, but no vides sporting organizations with increasing logistical
regimen influenced time trial performance. It has also constraints when preparing for an event. Although
been shown that the beneficial effects of creatine and humans are capable of regulating body core tempera-
glycerol combined on attenuating the increases in heart ture within a narrow range in a variety of scenarios, exer-
rate and rectal temperature are confined to exercise cise under heat stress provides a unique and
performed in hot (35 C) but not cold (10 C) conditions integrative challenge to physiological function. The
(1058). The high amounts of water retained by the com- factors that constitute the thermal environment deter-
bined ingestion of creatine and glycerol and the slower mine the compensability of a setting and whether
increase in body core temperature are linked to the cre- thermoregulatory responses can maintain heat bal-
atine-induced increase in intracellular water and simulta- ance. Under heat stress, endurance exercise capacity
neous increase of extracellular water due to glycerol, and performance are impaired as heat gain often
but the exact mechanisms remain to be elucidated exceeds heat loss. This impairment is primarily medi-
(1057). ated by hyperthermia-induced adjustments in cardio-
vascular, central nervous system, and skeletal muscle
6.3.6. Summary. function. Failure or inability to replenish excessive
Hyperhydration using water alone or coingested with body water loss leads to a reduction in blood (plasma)
sodium, glycerol or creatine increases body water volume and increase in osmolality that compromises
content and thus the potential for preserving fluid ho- thermoregulatory capacity and further exacerbates
meostasis for longer during exercise. The increase in the rise in thermal strain, precipitating the develop-
plasma volume secondary to volume loading is par- ment of fatigue. The decision to discontinue exercise
ticularly important when exercise is performed in the at a constant work rate or reduce self-paced exercise
heat as it may aid with heat dissipation. Drinking work rate in the heat, with or without hypohydration,
2 liters of water at or below body temperature in occurs across a spectrum of physiological and per-
the hours before exercise in the heat may slightly ceptual responses. These responses are specific to
attenuate the rise in body core temperature, without the exercise being undertaken, intensity of effort, pre-
affecting sweat rate. The ingestion of glycerol with vailing ambient conditions, contextual parameters,
water before exercise in the heat appears to increase and individual expectations. Given the controversy
fluid retention and has been shown to increase sweat regarding how best to hydrate during exercise, similar
rate and lower end-exercise body core temperature factors should be considered when deciding on which
and seems to enhance exercise capacity (i.e., con- hydration approach to utilize. Factors to consider
stant work rate), but not exercise performance (i.e., include the intensity and duration of the exercise task,
self-paced). Most studies in which sodium was ambient conditions, availability of fluids, and fluid
ingested before exercise showed enhanced exercise needs.
capacity but mixed results regarding exercise per- Several strategies may be adopted to mitigate the
formance. Some studies showed an attenuated rise deleterious influence of heat stress. For example,
in body core temperature, but no study showed any heat acclimation elicits physiological adaptations that
change in sweat rate. Only two studies were identi- enhance thermoregulation, fluid balance, cardiovascular
fied in which creatine was used to hyperhydrate function, and metabolism, all of which contribute to
before exercise in the heat and reported conflicting enhance performance in the heat. A variety of active
findings. Since the effects of hyperhydration on ther- and/or passive approaches can be employed to induce
mal strain and exercise capacity and performance in adaptations, with regimens of 10–14 days proposed to
the heat depend on many factors like the amount of optimize responses. Pre- and per-cooling techniques
fluid ingested, the exercise task, ambient conditions, may also enhance endurance performance in the heat.
and concentration of coingested sodium, glycerol, These techniques are based on either internal (e.g., ice-
and creatine, the available studies currently only pro- slurry ingestion) or external (e.g., cold water immersion)
vide a first step toward a better understanding of the cooling, with the selection of an appropriate technique
complex interactions. determined by its effectiveness, feasibility, and event-

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 PÉRIARD ET AL.

specific compatibility. Hyperhydration using water or Hyperthermia with and without dehydration reduces
coingested with sodium, glycerol, or creatine increases exercise capacity and performance through several inte-
body water content and has been suggested to pre- grative pathways involving alterations in cardiovascular
serve fluid homeostasis for longer during exercise in the function (i.e., skeletal muscle blood flow and metabo-
heat. While some of these approaches have been lism), adjustments in central neural drive (i.e., voluntary
reported to provide benefits (e.g., attenuated rise in muscle activation), and intensification of perceptual
core temperature and enhanced exercise capacity), strain (i.e., exertion, thermal discomfort, thirst). The
there appears to be a requirement for further perform- increase in thermal strain and compromise in hydration
ance and mechanistic studies. status that occur during prolonged exercise in the heat
without adequate fluid replacement provide a significant
7.1. Contemporary Controversies and Avenues of hemodynamic challenge that progressively reduces
Research V_ O2max. Although the reduction in maximal aerobic
power represents a primary determinant in fatigue de-
The impact of heat stress on exercise performance velopment, the decision to volitionally terminate exer-
and physiological responses has been extensively cise (i.e., V_ O2max test or constant work rate exercise) or
investigated, as have strategies to mitigate the dele- reduce work rate (i.e., time trial exercise) remains task
terious effects of hyperthermia and dehydration. specific and occurs across a continuum of physiological
Nevertheless, several aspects of these areas of and perceptual endpoints. As such, recognizing the
research remain under debate. This section highlights nuances associated with impairments in aerobic exer-
the main areas of contention and controversy, as well cise under heat stress and appropriately contextualizing
as avenues of research that warrant further investiga- the impact of hyperthermia and dehydration are
tion and elucidation. Traditionally, thermoregulation required to further advance our understanding of fatigue
at rest and during exercise in the heat is described development.
using the model of a central integrator of peripheral A compromise in hydration status is well recognized
and central thermal inputs that activates thermoeffec- as a factor exacerbating fatigue development during
tor responses (e.g., vasoconstriction and sweating) aerobic exercise in the heat. However, the precise body
when core temperature is displaced beyond a certain water deficit associated with impaired endurance exer-
point. This simple model has been challenged, how- cise remains contentious, as it relates to several factors,
ever, and more complex models involving several including the nature of the exercise task (i.e., constant
integrators and other afferent signals (e.g., heat flux) work rate vs. self-paced) and whether initiated in a state
should be considered. of hypohydration, or if dehydration is induced. A further
Exercise in the heat is associated with an point of contention relates to the optimal approach used
increased risk of EHI, particularly in uncompensable to hydrate during exercise: drink ad libitum or plan to
conditions. Exertional heat stroke is a life-threatening drink. This debate is nuanced and influenced by the in-
condition and often affects athletes that previously tensity and duration of exercise, environmental condi-
performed exercise at a similar intensity and duration tions, and context (e.g., indoors or outdoors) in which
under comparable environmental conditions, without exercise is undertaken, along with a host of personal
experiencing any problems or complaints. Although factors (e.g., experience, fitness, and acclimation status).
several risk factors have been identified, there Thus, to further elucidate the impact of a loss in body
remains a need for the development and validation water on performance and the approach utilized to
of algorithms to estimate person-specific risk calcula- hydrate, the factors described above should be well
tions of EHI during exercise in the heat. Novel controlled and research conclusions appropriately con-
approaches such as (big) data science and deep textualized.
learning may be adopted in addition to traditional Heat acclimation adaptations improve thermoregu-
studies utilizing thermophysiological and epidemio- latory capacity and fluid balance and enhance exer-
logical assessments. Technological developments to cise capacity and performance in the heat. However,
allow affordable measurement of real-time insight contention remains regarding the enhancement of
into core temperature may also aid in assessing the performance in cool conditions following heat accli-
risk for heat stroke using wearables, as such meas- mation and the precise mechanisms mediating this
urements are currently largely restricted to the sci- potential improvement. Further research is therefore
ence domain. Furthermore, the involvement of required to elucidate if heat adaptations are beneficial
genetics should be further explored as an increasing to exercise performed in cooler conditions and the
number of studies suggest a role for inherited factors pathways via which this occurs. Additional research is
(1059–1061). also needed to clarify whether blood/plasma volume

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 EXERCISE UNDER HEAT STRESS

expansion is maintained during the adaptive process publications. This applies not only for determining
(i.e., time course of expansion and retention) by ensur- the influence of cooling strategies but also for eluci-
ing a constant thermal impulse. The potential for per- dating the acute and chronic effects of heat stress
missive dehydration, or restricted fluid consumption, and hypohydration.
to enhance the adaptive response (i.e., plasma vol- Hyperhydration before exercise in the heat has
ume expansion) by further challenging fluid regulatory been investigated as a compensatory mechanism to
responses also warrants additional research. There is offset the detrimental effects of dehydration. Although
also a need for research that bridges the gap between hyperhydration using intravenous fluids has been
long-term (30 to 60 days) animal-based mechanistic reported in some sports, strong evidence of its benefi-
(i.e., genomic responses, molecular signaling, and epi- cial effects on thermal strain and performance is lack-
genetics) research and classic shorter term (10– ing. Water hyperhydration has been shown to lower
14 days) human physiological heat acclimation under- the rate of increase in body core temperature during
taken in sport, occupational, and military settings. exercise in the heat, but the temperature of the
Investigating the molecular and cellular responses ingested water plays a role in this that requires clarifi-
associated with the heat acclimation phenotype will cation. Adding glycerol, sodium, and/or creatine to
lead to a better understanding of what drives the ingested water increases water retention, but does
adaptive process. not necessarily reduce thermal strain and increase
Pre- and per-cooling improve exercise performance in sweat loss. The direct effect of sodium on the sweat
the heat. However, a large variability in the effect of dif- gland may play a role that requires elucidation. The
ferent strategies is observed across studies, highlighting extent to which intracellular or extracellular fluids are
the need for individual person data meta-analyses to affected by the osmotically active agents should also
elucidate the influence of personal factors (i.e., age, be further examined. Hyperhydration seems to be
sex, and training status), ambient conditions (i.e., air more beneficial for time to exhaustion than self-paced
temperature, wind speed, and humidity) and exercise exercise, although more work is required to delineate
characteristics (i.e., intensity, duration, and protocol) on the specific effects of hyperhydration on various exer-
the magnitude of cooling benefits. Such an approach has cise protocols.
sufficient statistical power to answer these relevant ques-
tions, as it is often not feasible to conduct subanalyses in
a single study due to the limited sample size. To facili- APPENDIX A
tate such initiatives, it is recommended to present
individual data beyond aggregated outcome meas- TABLES A1, A2, A3, and A4 provide protocol details of the
ures (e.g., mean, median, and effect size) in future studies in TABLES 2–5.

Table A1. Constant work rate studies with dehydration

Environmental
Dehydration, %body
Study Sample Size Exercise Protocol Conditions, 8C, %RH, Performance Outcome
mass
m·s-1

de Melo-Marins et al. (673) 11 Cycling: 70% V_ O2max to 34.0, 40.0, – EU: 0.2 6 0.4 EU: 38.0 6 9.0 min
exhaustion DE1: 1.0 6 0.5 DE1: 37.0 6 8.0 min
DE2: 1.3 6 0.6 DE2: 37.0 6 9.0 min

Fallowfield et al. (672) 8 Running: 70% V_ O2max to 20.0, –, – EU: 0.8 EU: 103.0 6 35.1 min
exhaustion DE: 2.0 DE: 77.7 6 21.8 min

Marino et al. (674) 8 Cycling: 70% peak 31.3, 63.3, – EU: 0.2 6 0.1 EU: 41.2 6 17.1 min
power output to DE1: 1.0 6 0.4 DE1: 40.6 6 14.0 min
exhaustion DE2: 1.7 6 0.5 DE2: 32.5 6 16.3 min

Maughan et al. (671) 6 Cycling: 70% V_ O2max to Temperate EU: 0.7 EU: 76.2 6 22.3 min
exhaustion DE: 1.8 DE: 70.2 6 20.3 min

McConell et al. (670) 7 Cycling: 69% V_ O2peak for 21.3, 43.0, – EU: 0.1 6 0.1 EU: 328.0 6 246.1 s
2 h 1 90% V_ O2peak to DE1: 1.8 6 0.1 DE1: 248.0 6 283.1 s
exhaustion DE2: 3.2 6 0.1 DE2: 171.0 6 198.4 s

Protocol details are from TABLE 2. RH, relative humidity; DE, dehydration; EU, euhydration. P < 0.05, significantly different from EU.

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Table A2. Constant work rate studies with hypohydration

Environmental
Sample Hypohydration Hypohydration, % Performance
Study Exercise Protocol Conditions, 8C,
Size Protocol body mass Outcome
%RH, m·s 1

Baker et al. 8 Running: 2-h intermit- Running: 85% V_ O2max 30.0, 40.0, – EU: 0.0 EU: 21.0 min
(668) tent 70% V_ O2max exhaustion run HY1: 2.0 HY1: 14.0 min
HY2: 3.3 HY2: 8.0 min

Cheung and 15 Walking: 4.5-6.0 km·h 1, Walking: 3.5 km·h 1, 0% 40.0, 30.0, – Moderate Fitness-Pre Moderate fitness-Pre
McLellan (677) 3–7% gradient until gradient in protective EU: 0.0 6 0.0 EU: 98.6 6 19.6 min
2.5% body mass loss, clothing to HY: 2.8 6 0.9 HY: 78.3 6 16.9 min
15 h before exercise exhaustion Moderate Fitness-Post Moderate Fitness-
protocol EU: 0.1 6 1.2 Post
HY: 2.6 6 0.6 EU: 101.4 6 11.4 min
High Fitness-Pre HY: 80.6 6 18.0 min
EU: 0.0 6 0.0 High Fitness-Pre
HY: 2.0 6 0.5 EU: 114.5 6 27.4 min
High Fitness-Post HY: 100.9 6 20.4 min
EU: 0.0 6 0.7 High Fitness-Post
HY: 1.9 6 0.8 EU: 115.6 6 18.4 min
HY: 110.5 6 29.7 min

Cheung and 8 Walking: 5 km·h 1 5–7% Light walking: 40.0, 30.0, – Light Exercise Light Exercise
McLellan (678) gradient until 2.5% 3.5 km·h 1, 0% gradi- EU: 0.0 6 0.0 EU: 106.5 6 22.1 min
body mass loss, 15 h ent in protective HY: 2.2 6 1.0 HY: 87.1 6 14.2 min
before exercise clothingHeavy walk- Heavy Exercise Heavy Exercise
protocol ing: 4.8 km·h 1, 4% EU: 0.0 6 0.0 EU: 59.7 6 9.5 min
gradient in protective HY: 2.2 6 0.9 HY: 53.3 6 8.9 min
clothing to
exhaustion

Cheung and 15 Walking: 4.5– Walking on motorized 40.0, 30.0, – Training Group-Pre Training Group-Pre
McLellan 5.5 km·h 1, 3–6% gra- (speed not men- EU: 0.0 6 0.0 EU: 93.1 6 18.9 min
(368) dient until 2.5% body tioned) treadmill in HY: 2.0 6 0.4 HY: 75.8 6 14.4 min
mass loss, 15 h before protective clothing to Training Group-Post Training Group-Post
exercise protocol exhaustion EU: 0.2 6 0.5 EU: 94.0 6 16.2 min
HY: 2.1 6 0.5 HY: 80.3 6 11.7 min
Control Group-Pre Control Group-Pre
EU: 0.0 6 0.0 EU: 85.3 6 10.2 min
HY: 1.9 6 0.6 HY: 74.6 6 10.1 min
Control Group-Post Control Group-Post
EU: 10.6 6 0.9 EU: 90.9 6 11.9 min
HY: 2.2 6 0.8 HY: 79.6 6 10.3 min

Ebert et al. (675) 8 Cycling: 53% maximal Cycling: simulated hill 29.3, 36.7, 4.2 EU: 10.3 6 0.4 EU: 19.5 6 6.0 min,
aerobic power for 2 h climb (8% gradient) at HY: 2.5 6 0.5 313 6 28 W
88% maximal aerobic HY: 13.9 6 5.5 min,
power to exhaustion 308 6 28 W

Walsh et al. 6 Cycling: 70% V_ O2peak Cycling: 90% V_ O2peak to 32.0, 60.0, 0.8 EU: 0.2 EU: 9.8 6 3.9 min
(676) for 1 h exhaustion HY: 1.8 HY: 6.8 6 3.0 min

Protocol details are from TABLE 3. RH, relative humidity; EU, euhydration; HY, hypohydration. P < 0.05, significantly different from EU.

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 EXERCISE UNDER HEAT STRESS

Table A3. Self-paced exercise studies with dehydration

Environmental
Sample Dehydration, %
Study Exercise Protocol Conditions, 8C, %RH, Performance Outcome
Size body mass
m·s 1

Adams et al. (690) 7 Cycling: 2 h at 55% 35.0, 30.0, 4.5 EU: 0.2 6 0.6 EU: 295 6 29 W, 12.9 6 0.8 min
V_ O2peak 1 5-km time DE: 2.2 6 0.4 DE: 276 6 29 W, 13.5 6 1.0 min
trial

Bachle et al. (679) 10 Cycling: 1-h time trial 20.6, 72.1, – EU: 10.8 EU: 127 W
DE: 1.0 DE: 123 W

Backx et al. (681) 8 Cycling: 1-h time trial 20.0, 70.0, 0.3 EU: 0.7 EU: 43.1 6 2.1 km, 291 6 35 W
DE1: 1.3 DE1: 43.0 6 2.3 km, 290 6 39 W
DE2: 1.7 DE2: 43.2 6 2.5 km, 295 6 42 W

Bardis et al. (683) 10 Cycling: 1 h at 70-75% 29.0, –, 1.0 EU: 1.4 6 0.3 EU: 16.6 6 2.3 min
HRmax 1 5-km outdoor DE: 2.2 6 0.2 DE: 17.6 6 2.9 min
hill climb

Bardis et al. (687) 10 Cycling: 3  (5 km at 31.6, –, – EU: 0.5 6 0.3 EU: 30.2 6 2.4 km.h 1
1
50% peak power DE: 1.8 6 0.7 DE: 28.8 6 2.6 km.h
output 1 5-km time
trial)

Below et al. (669) 8 Cycling: 50 min at 80% 31.2, 54.0, 3.5 EU: 0.5 EU: 10.2 6 0.8 min, 276 6 17 W
V_ O2max 1 10-min DE: 1.9 DE: 10.9 6 0.9 min, 258 6 17 W
time trial

Daries et al. (685) 8 Running: 90 min at 65% 25.0, 55.0, 3.6–4.2 EU: 1.3 EU: 15.4 6 1.4 km.h 1
V_ O2max 1 30-min time DE1: 2.6 DE1: 15.6 6 1.1 km.h 1
trial DE2: 3.2 DE2: 15.8 6 0.9 km.h 1

Dion et al. (691) 10 Running: 21.1-km time 30.2, 42.0, 3.9 EU: 1.3 EU: 89.6 6 7.7 min, 14.2 6 1.2 km.h 1

trial DE: 3.1 DE: 89.8 6 7.7 min, 14.2 6 1.2 km.h 1

Dugas et al. (688) 6 Cycling: 80-km time trial 33.0, 50.0, 9.0–11.0 EU: 0.5 EU: 125.4 6 5.8 min, 207 6 25 W
DE1: 1.9 DE1: 126.1 6 4.8 min, 205 6 18 W
DE2: 2.1 DE2: 124.2 6 5.8 min, 214 6 24 W
DE3: 2.9 DE3: 129.9 6 6.1 min, 190 6 20 W
DE4: 3.9 DE4: 129.4 6 8.1 min, 194 6 26 W
DE5: 4.3 DE4: 128.3 6 6.3 min, 196 6 25 W

Hillman et al. (686) 7 Cycling: 90 min at 95% 23.0, –, –33.9, –, – EU1: 0.1 6 0.5 EU1: 282 6 37 W
of lactate DE1: 3.0 6 0.8 DE1: 268 6 32 W
threshold 1 5-km time EU2: 0.2 6 0.5 EU2: 262 6 42 WD
trial DE2: 3.8 6 0.8 E2: 229 6 32 W

Kay and Marino (682) 7 Cycling: 1 h time trial 19.8, 63.3, –33.2, 63.3, – EU1: 0.1 EU1: 30.8 6 5.7 km, 217 6 40 W
DE1: 1.8 DE1: 32.6 6 6.4 km, 235 6 49 W
EU2: 0.0 EU2: 30.1 6 5.0 km, 225 6 34 W
DE2: 2.2 DE2: 30.5 6 4.8 km, 225 6 45 W

McConell et al. (680) 8 Cycling: 45 min at 80% 20.9, 41.0, – EU: 0.0 6 0.1 EU: 299 6 28 W
V_ O2peak 1 15-min time DE1: 1.0 6 0.1 DE1: 297 6 25 W
trial DE2: 1.9 6 0.0 DE2: 304 6 25 W

Perreault-Briere et al. (689) 9 Cycling: 1-h time trial 30.0, 50.0, 7.0–8.0 EU: 0.6 6 0.2 EU: 35.7 6 2.0 km, 240 6 34 W
DE1: 2.2 6 0.3 DE1: 35.8 6 2.0 km, 241 6 33 W
DE2: 2.9 6 0.4 DE2: 35.6 6 1.9 km, 237 6 31 W

Robinson et al. (684) 8 Cycling: 1-h time trial 20.0, 60.0, 3.0 EU: 10.9 EU: 42.32 6 1.6 km, 303 6 8 W
DE: 2.3 DE: 43.05 6 1.9 km, 293 6 7 W

Protocol details are from TABLE 4. RH, relative humidity; DE, dehydration; EU, euhydration. P < 0.05, significantly different from EU.

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Table A4. Self-paced exercise studies with hypohydration

Environmental
Hypohydration, %
Study Sample Size Hypohydration Protocol Exercise Protocol Conditions, 8C, % Performance Outcome
body mass
RH, m·s 1

Armstrong et al. (683) 8 Diuretic 5 h before Running: 1,500-m time 15.7, 31.8, 3.6 1,500 m 1,500 m
exercise trialRunning: 5,000-m EU: 0.0 EU: 4.7 min
time trialRunning: HY: 1.9 HY: 4.9 min5,000 m
10,000-m time trial 5,000 m EU: 18.2 min
EU: 0.0 HY: 19.5 min10,000 m
HY: 1.6 EU: 38.9 min
10,000 m HY: 41.5 min
EU: 0.0
HY: 2.1

Bardis et al. (703) 10 Cycling: 2  (25 min at Cycling: 3  5-km time EU: 32.9, –, 3.2HY: EU: 0.0 6 0.0 EU: 268 W
70 75% maximum trial 33.0, –, 3.2 HY: 1.0 6 0.1 HY: 254 W
heart rate with 5-min
rest)

Berkulo et al. (704) 12 Cycling: 45 min at 50% Cycling: 40-km time trial 35.2, 51.0, 7.0 EU: 0.0 6 0.2 EU: 70.1 6 4.1 min, 223 6 32 W
peak power output, HY1: 1.1 6 0.2 HY1: 71.2 6 4.0 min, 217 6 39 W
30-min rest HY2: 1.3 6 0.3 HY2: 69.9 6 5.6 min,
224 6 35 W

Burge et al. (667) 8 24-h fluid/food restric- Rowing: 4,200 flywheel –, –, – EU: 0.0 EU: 7.0 6 0.5 min, 294 6 20 W
tion with 1.5 liters of revolutions time trial HY: 3.1 HY: 7.4 6 0.6 min, 279 6 23 W
fluid 2 h before
exercise

Casa et al. (696) 17 22 h fluid restriction Running: 12-km time trial EU: 26.3, –, –HY: EU: 0.8 EU: 53.2 6 6.1 min
28.0, –, – HY: 2.3 HY: 55.7 6 7.5 min

Castellani et al. (701) 7 Walking: 2.5–3.0 h in Cycling: 30 min at 55% 27.5, 27.0, 0.8–1.4 EU: 0.6 6 0.5 EU: 193 6 57 W
50 C without fluid V_ O2peak 1 30 min HY: 4.0 6 0.4 HY: 168 6 65 W
replacement time trial

Cheung et al. (705) 11 Cycling: 90 min at 50% With mouth rinse: 20-km 35.0, 10.0, 3.0 With mouth rinse With mouth rinse
cycling time EU: 0.5 EU: 2172.0 6 155.0 s
trialWithout mouth HY: 2.0 HY: 2185.0 6 131.0 s
rinse: 20-km cycling Without mouth rinse Without mouth rinse
time trial EU: 0.5HY: 2.1 EU: 2180.0 6 150.0 s
HY: 2133.0 6 142.0 s

Cheuvront et al. (698) 8 3 h of passive heat Cycling: 30 min at 50% 2.0, 50.0, 2.220.0, EU1: 0.3 6 0.6 EU1: 154 6 36 W
stress in 45  C V_ O2peak1 30 min time 50.0, 1.0 HY1: 2.9 6 0.7 HY1: 150 6 35 W
trial EU2: 0.4 6 0.7 EU2: 152 6 30 W
HY2: 3.0 6 0.8 HY2: 140 6 30 W

Fleming and James (697) 10 24-h fluid Prehabituation to hypo- 22.0, –, – Prehabituation Prehabituation
restriction 1 45 min hydration: 5-km run- EU: 0.2 6 0.3 EU: 1381.0 6 237.0 s
run at 75% V_ O2peak ning time HY: 2.4 6 0.3 HY: 1459.0 6 250.0 s
trialPosthabituation to Posthabituation Posthabituation
hypohydration:5 km EU: 0.1 6 0.1 EU: 1366.0 6 211.0 s
running time HY: 2.4 6 0.1 HY: 1381.0 6 200.0 s

Funnell et al. (708) 14 Cycling: 120 min at 50% Blinded hydration:15- 31.1, 47.6, 5.9 Blinded hydration Blinded hydration
of maximal power min cycling time EU: 0.6 6 0.5 EU: 903.0 6 89.0 s
trialUnblinded HY: 3.0 6 0.5 HY: 1008.0 6 121.0 s
hydration:15-min cy- Unblinded hydration Unblinded hydration
cling time trial EU: 0.5 6 0.3 EU: 874.0 6 108.0 s
HY: 3.0 6 0.3 HY: 967.0 6 170.0 s

Continued

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 EXERCISE UNDER HEAT STRESS

Table A4.—Continued
Environmental
Hypohydration, %
Study Sample Size Hypohydration Protocol Exercise Protocol Conditions, 8C, % Performance Outcome
body mass
RH, m·s 1

James et al. (707) 7 Cycling: 155-min inter- Cycling: 15-min time trial 34.0, 50.0, 0.3–0.4 EU: 0.1 6 0.1 EU: 183 6 24 W
mittent at 50% peak HY: 2.4 6 0.2 HY: 169 6 27 W
power output

Kenefick et al. (702) 32 Walking: 3-h intermittent Cycling: 30 min at 50% 10, –, –20, –, –30, EU1: within 1.0 EU1: 221 6 41 W
at 5 km·h 1 and 4% V_ O2peak 1 15 min time –, –40, –, – HY1: 4.1 HY1: 216 6 40 W
gradient in 50  C trial EU2: within 1.0 EU2: 220 6 24 W
HY2: 4.2 HY2: 199 6 22 W
EU3: within 1.0 EU3: 220 6 23 W
HY3: 4.0 HY3: 193 6 33 W
EU4: within 1.0 EU4: 174 6 21 W
HY4: 4.1 HY4: 136 6 41 W

Logan-Sprenger et al. 9 Cycling: 90 min at 65% Cycling: time trial at 6 kJ 23.0, 32.5, – EU: 0.0 6 0.0 EU: 31.8 6 4.1 min, 266 6 19 W
(494) V_ O2peak per kg of body mass HY: 2.3 6 0.4 HY: 36.0 6 3.1 min,
250 6 19 W

Merry et al. (694) 12, Cycling: 90 min at 60% Cycling: 40 min at 70% 24.3, 50.0, 4.5 Trained Trained:EU: 20.7 km
6 trained, V_ O2peak 1 14-17 h fluid V_ O2peak 1 40-min EU: within 0.5 HY: 18.0 kmUntrained:
6 untrained restriction time trial HY: 1.5–2.0 EU: 24.9 kmHY: 23.4 km
Untrained
EU: within 0.5
HY: 1.5–2.0

Oliver et al. (669) 13 Walking: 1.5 h at 50% Running: 30-min time 19.7, 58.8, 2.0 EU: 0.6 6 0.4 EU: 6295.0 m, 12.6 km.h 1

V_ O2peak 24 h and 48 h trial HY: 3.2 6 0.5 HY: 6107.0 m, 12.2 km.h 1

before exercise
protocol

Slater et al. (692) 17 24-h fluid restriction to Rowing: 2,000-m time 21.1, 29.0, –32.4, Males MalesEU1: 398.2 6 7.4 s
4% body mass loss 1 trial 60.4, – EU1: 0.8 HY1: 400.3 6 7.4 s
partial rehydration HY1: 2.0 Females
Females EU1: 453.7 6 10.8 s
EU1: 1.7 HY1: 457.2 6 9.3 s
HY1: 1.2 Males
Males EU2: 403.0 6 6.0 s
EU2: 1.1 HY2: 403.3 6 7.8 s
HY2: 2.0 Females
Females EU2: 457.9 6 10.1 s
EU2: 1.7 HY2: 461.4 6 11.2 s
HY2: 1.1

Stearns et al. (695) 17 22-h fluid restriction Running: 12 km as 3  WBGT: 26.2 EU: 0.8 6 1.0 EU: 3191.0 6 366.0 s
4 km with 4-min rest HY: 2.1 6 1.3 HY: 3339.0 6 450.0 s

Stewart et al. (700) 7 Cycling: 2 h at 50-65% of Cycling: 5-km time trial 18.0–25.0, 20.0– EU: 0.2 EU: 7.1 6 1.3 min
peak power output 30.0, – HY: 3.8 HY: 7.3 6 1.5 min

Wall et al. (706) 10 Walking and cycling at Cycling: 25-km time trial 33.0, 40.0, 9.0 EU: 0.0 6 0.1 EU: 40.6 6 2.2 min, 249 6 27 W
60% V_ O2max HY1: 2.1 6 0.1 HY1: 40.6 6 2.1 min, 251 6 28 W
HY2: 3.0 6 0.0 HY2: 406 6 2.1 min, 253 6 30 W

Protocol details are from TABLE 5. RH, relative humidity; EU, euhydration, HY, hypohydration, WBGT, wet-bulb-globe temperature. P < 0.05, significant difference from con-
trol/euhydrated condition.

CORRESPONDENCE DISCLOSURES

riard (e-mail: [email protected]).
J. D. Pe J.D.P and T.M.H.E are scientific advisory board members for
Inuteq. J.D.P. received funding from the Coca Cola Company to
perform consultancy work after this article was first submitted.
ACKNOWLEDGMENTS AUTHOR CONTRIBUTIONS

The authors thank Harry Brown and Thomas Topham for help J.D.P., T.M.E., and H.A.D. analyzed data; J.D.P., T.M.E., and
with collating the hydration data in sect. 5.4. H.A.D. prepared figures; J.D.P., T.M.E., and H.A.D. drafted

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 PÉRIARD ET AL.

manuscript; J.D.P., T.M.E., and H.A.D. edited and revised manu- 15. Gilbert M, Busund R, Skagseth A, Nilsen PÅ, Solbø JP.
script; J.D.P., T.M.E., and H.A.D. approved final version of Resuscitation from accidental hypothermia of 13.7 C with circulatory
arrest. Lancet 355: 375–376, 2000. doi:10.1016/S0140-6736(00)
manuscript.
01021-7.

16. Racinais S, Moussay S, Nichols D, Travers G, Belfekih T,

Schumacher YO, Pe
riard JD. Core temperature up to 41.5 C during
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