Clin Physiol Funct Imaging (2014) doi: 10.1111/cpf.

12136

INVITED REVIEW

Lift weights to fight overweight

Antonio Paoli1, Tatiana Moro1 and Antonino Bianco2
1
Department of Biomedical Sciences, University of Padova, Padova, and 2Department of Sports and Exercise Science (DISMOT), University of Palermo, Palermo,
Italy

Summary

Correspondence Although resistance training (RT) has long been accepted as a means for develop-
Antonio Paoli MD, Department of Biomedical Sci-
ing and maintaining muscular strength, endurance, power and muscle mass, its
ences, The physiological Laboratory, via Marzolo,
3 – 35131 University of Padova, Padova, Italy.
beneficial relationship with health factors and chronic disease has only recently
E-mail: [email protected] been recognized in the scientific literature. Prior to 1990, resistance training was
not a part of the recommended guidelines for exercise training and rehabilitation
Accepted for publication
Received 6 November 2013;
for either the American Heart Association or the American College of Sports Med-
accepted 23 January 2014 icine (ACSM). In 1990, the ACSM recognized resistance training as a significant
component of a comprehensive fitness programme for healthy adults of all ages, a
Key words position subsequently confirmed few years after. At present, even though interest
excess postexercise oxygen consumption; exercise;
in clinical applications of RT is increasing, there are still some concerns, among
metabolism; overweight; resistance training; weight
control
physicians, about the use of this exercise methodology in weight control pro-
grammes. This review aims to explore the metabolic effects of RT and its efficacy
and feasibility in overweight subjects.

60% is expended at rest (Black et al., 1996). Despite the rec-

Introduction
ommendations of national and international health organiza-
Health organizations report a worldwide increase in the preva- tions for at least three 30-min sessions of vigorous exercise
lence of overweight and obesity (Olshansky et al., 2005). This per week, it has been calculated, as a general example, that
increase is a great source of concern considering the fact that this would increase energy demands by only ffi1000 Kcal per
obesity and in particular abdominal obesity is one of the prin- week (i.e. ffi5% of the average weekly expenditure about
ciple risk factors for cardiovascular disease, and it is strongly 20 000 Kcal per week) (Black et al., 1996). Notwithstanding
related to dyslipidaemia, hypertension, diabetes and metabolic these considerations, clinical practice and data from the litera-
syndrome (Koh-Banerjee et al., 2004). Diet and exercise are ture consistently point to the beneficial effect of exercise on
considered the main tools to control body weight and body fat loss (Jakicic & Gallagher, 2003). The only way to reconcile
fat (Paoli et al., 2008), but nevertheless the exact ‘dose’ and this apparently contradictory evidence between experimental
‘quality’ of diet (Paoli et al., 2013a,b) and exercise is still a and clinical data is to hypothesize the existence of other exer-
subject of debate (Paoli et al., 2012a,b). The correct dose and cise-related factors involved in the fat loss effect other than
quality of exercise, that is, the knowledge of how and how the simple increase in energy expenditure during exercise.
much should be suggested to patients is of importance for
clinicians and medicine practitioners. The main question about
Mechanisms of physical activity’s effects on
the effect of exercise on body weight regards the influence it
body weight control
has on energy expenditure. Overall, daily energy expenditure
may be briefly divided into three different components that Three fundamental mechanisms have been taken into consid-
can be categorized as (i) resting metabolism, (ii) thermic eration to explain the effects of physical exercise on body
effects of food and (iii) the energy expenditure of physical weight control, and it may (i) reduce hunger, (ii) improve
activity associated with exercise and non-exercise movement fitness levels and consequently might change behaviour related
(Jequier, 2002). It has been demonstrated that in Western to non-exercise activity thermogenesis such as walking and
countries, the mean ratio of daily energy expenditure and stair climbing, (Jakicic & Gallagher, 2003) (iii) exert a posi-
resting energy expenditure (REE) is 1
66; in other words, tive effect on resting metabolism. Regarding the latter, resting
only 40% of energy is expended on activity while the remaining energy expenditure (REE) is the largest component of the

© 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd 1
2 Resistance training and overweight, A. Paoli et al.

daily energy budget and, consequently, any increase in REE in control. Even though the beneficial effect on health and
response to exercise could potentially have a great impact on weight control of a 24-h increase in metabolism is evident
health promotion and weight control. Even though there is (Hunter et al., 2000), the optimal amount and type of exercise
considerable individual variation in REE, it is well established routine remains to be established. We recently discussed that
that fat-free mass (lean body mass) is the main factor that resistance training should be investigated more thoroughly
influences REE, accounting for 50–70% of the individual vari- and rigorously by taking into account the variables involved
ation (Westerterp et al., 1992; Zhang et al., 2002). There is a including (i) muscle action used, (ii) type of resistance used,
linear relationship between lean body mass and resting energy (iii) volume (total number of sets and repetitions), (iv) exer-
metabolism but with broad interindividual variance (Wang cises selected and workout structure (e.g. the number of mus-
et al., 2000; Muller et al., 2002). It is evident that muscle mass cle groups trained), (v) the sequence of exercise performance,
represents the majority (88%) of metabolically active fat-free (vi) rest intervals between sets, (vii) repetition velocity and
mass (FFM) with the metabolically active organs representing (viii) training frequency (Paoli, 2012; Paoli & Bianco, 2012;
only 12% of FFM, but while the former provides an energy Paoli et al., 2012a,b). It can be argued that, as Knuttgen
expenditure of approximately only 15 Kcal kg1 per day, the asserted, if EPOC increased exponentially as a function of
energy expenditure of the latter is 468 Kcal kg1 per day. exercise intensity, whereas it increased linearly as a function
Thus, muscle accounts for only a minor part (less than 20%) of exercise duration (Knuttgen, 2007), a high-intensity resis-
of total daily energy expenditure. Nevertheless, many human tance training programme could affect positively resting
studies with long-term exercise protocols, separating the metabolism. Thus, RT could act through two different ways:
effects of training and nutrition, have demonstrated that the increase in lean body mass (chronic/long-term effect) and
positive effect of training on REE is mainly mediated by transient increase in metabolism (EPOC). In fact, there are
the increase in free fat mass (i.e. muscle) (Byrne & Wilmore, several reports that weight training may require more recovery
2001). Interestingly, these studies also found that the combi- energy and a longer duration EPOC (Haddock & Wilkin,
nation of endurance and resistance training leads to an overall 2006) compared with endurance training. Despite this, there
decrease in REE (Westerterp et al., 1992; Byrne & Wilmore, are surprisingly few studies published on the specific influence
2001), but that this exercise-related decrease was evident with of high-intensity resistance training on metabolism.
endurance training, while a net increase in REE was found after
RT (Hunter et al., 2008). These results explain why in recent
Effects of exercise intensity on weight control
years there has been a lot of interest in the specific effects of
RT on weight control, and it is also the case that resistance Some studies reported that higher-intensity resistance exercise
training (RT) has only been incorporated recently as an generates greater EPOC than lower-intensity resistance exercise
important component of exercise protocols for weight control (Haltom et al., 1999; Thornton & Potteiger, 2002), and the
in some guidelines (Kraemer & Ratamess, 2005; Donnelly reason for this greater EPOC could be attributed to a greater
et al., 2009). perturbation of energy homeostasis (Melanson et al., 2002,
2005; Schuenke et al., 2002). In this regard, we recently dem-
onstrated that a high-intensity resistance training programme
Resistance training and metabolism
can induce a greater EPOC in the 24 h after the training ses-
Resistance training acts in a substantially different way com- sion (Paoli et al., 2012a,b) (Fig.1) and that this kind of RT,
pared with endurance training (ET), and it increases muscle mixed with a high-intensity endurance interval training, can
mass in the long term (Paoli et al., 2010, 2013a,b) but also improve body composition and blood lipids (Paoli et al.,
increases excess postexercise oxygen consumption (EPOC) 2013a,b). It is clear that the intensity of exercise is a keystone
immediately after the training session (Schuenke et al., 2002). of postexercise energy expenditure not only in endurance
In 1984, Gaesser and Brooks defined the recovery period in exercise such as cycling (Little et al., 2010) but also in resis-
which an increase in oxygen uptake is observed as ‘excess tance training. The mechanisms underlying these effects are
postexercise oxygen consumption’ (EPOC). EPOC can be not still clear, but we can raise some hypotheses:
divided into two phases: short term (due to the so-called oxy- 1) the greater increase in blood lactate (which is evidence of a
gen debt or fast component of excess postexercise oxygen major metabolic stress derived from high-intensity resistance
consumption) and long term (slow component of excess post- training and may reflect the utilization of lactate as fuel in the
exercise oxygen consumption due to various mechanisms not aerobic pathway) imposes an increase in postexercise energy
yet completely understood but most likely linked to the resto- expenditure (Binzen et al., 2001). Lactate removal, though,
ration of homeostasis). As a matter of fact, after intense or may only be part of the process, in fact, if lactate is infused
prolonged exercise, oxygen consumption remains increased during the postexercise period, it does not elicit a further
for several hours and is referred to as the slow component of increase in EPOC (Barnard & Foss, 1969). However, lactate
excess postexercise oxygen consumption (EPOC). This elevated may explain, together with an increase in body temperature
postexercise metabolism plays a part in the energy cost of (Gaesser & Brooks, 1984), only the short-term component of
exercise and in the overall effect of exercise in body weight EPOC;

© 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd
 Resistance training and overweight, A. Paoli et al. 3

2) an increase in b-adrenergic system activity (Hunter et al., component of EPOC as it is an index that the organism is
2006); using fatty acids rather than glycogen to satisfy the energy
3) hormonal variations: in response to exercise-induced cost of exercise (Bahr et al., 1990) and seems to be a compen-
trauma, an increase in metabolic hormonal concentration is satory sparing of glycogen after any kind of resistance training
seen (e.g. cortisol, catecholamines and thyroid hormone), (Poehlman & Melby, 1998).
which could increase metabolism (Schuenke et al., 2002); Several causes could explain the RER lowering after resis-
4) the increased protein resynthesis due to postexercise muscle tance training (see Fig. 2):
damage is energy expensive (approximately 20% increase in 1) glucose metabolic pathways are directed to replenish glyco-
resting metabolism) (MacDougall et al., 1995) and could con- gen stores first instead of being used for energy supply. This
tribute to greater EPOC after high-intensity resistance training means that glucose and all gluconeogenic precursors will be
(Binzen et al., 2001; Gasier et al., 2012); spared from further oxidation and will be converted to glu-
cose and glycogen, so lipids become the preferred oxidation
Moreover, an important effect of high-intensity exercise is
substrate (Borsheim & Bahr, 2003);
the improvement in utilization of fatty acids instead of glucose
2) the AMP kinases/acetyl CoA carboxylase (AMPK/ACC)
that could lead to a getter utilization of fat stores. This effect
pathway. It has been demonstrated that intense exercise
can be highlighted by a decrease in respiratory exchange ratio
increases AMPK (Gibala, 2009); thus, AMPK can phosphory-
(RER). The respiratory exchange ratio (i.e. the ratio between
late ACC, decreasing its activity; the decreased ACC activity
CO2 expired and O2 consumed) is a good way to identify the
leads to a decrease in the rate of the synthesis of malonyl
origin of energy substrates: when RER is close to 0
7, it
CoA, and consequently, there is a release of inhibition of
means that the major energy source is lipids, while when the
carnitine palmitoyltransferase I (CPT1) activity leading to an
ratio is near 1, carbohydrates are the main source of energy.
increase in lipid oxidation (Winder, 2001);
It is clear that an improvement in fat oxidation can help
3) an increase in atrial natriuretic peptide (ANP) stimulated by
weight control. Fasting or very low carbohydrate diet can lead
exercise could play a role in the increased rate of lipid oxida-
to a decrease in RER (Paoli et al., 2012a,b, 2013a,b), but also
tion; production of ANP is related to the intensity of exercise
training can have the same result (Paoli et al., 2011, 2012a,b).
(Moro et al., 2008; de Almeida et al., 2012), it has been dem-
The increase in the rate of fatty acid oxidation (i.e. the reduc-
onstrated that ANP increases lipolysis (Souza et al., 2011), and
tion in RER) indicates that triacylglycerol/fatty acid cycling is
this pathway appears to be more suitable than the increase in
an important supporter of the energy cost in the prolonged

Figure 1 Changes in resting energy expendi-

ture (REE) and respiratory exchange ratio
(RER) at basal condition and 22 h after a ses-
sion of traditional resistance training or
high-intensity interval resistance training.
** P<0.005. (Modified from Paoli et al.,
2012b)

Figure 2 Factors involved in resistance train-

ing effects on weight control.

© 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd
4 Resistance training and overweight, A. Paoli et al.

catecholamines that have a very short half-life and appears not 2009; Ibanez et al., 2010; Idoate et al., 2011; Kreider et al.,
to be related to lipolysis after RT (Ormsbee et al., 2009); 2011; Thornton et al., 2011; Willis et al., 2012). More
4) growth hormone increase also could explain a part of the recently, our group has demonstrated the safety and feasibil-
increase in lipid oxidation; it was demonstrated by Bottaro ity, after a familiarization period, of high-intensity resistance
et al. et al. (Bottaro et al., 2009) that intense exercise with training in sedentary and overweight subjects (Paoli et al.,
incomplete recovery might stimulate GH production in a 2010, 2013a,b)
significant manner;
5) there is some new evidence that suggests how some cyto-
Conclusions
kines and other peptides (myokines) that are produced and
released by muscle fibres can exert autocrine, paracrine or Taken together, these recent findings suggest that resistance
endocrine effects that might influence the metabolic effect of training could positively affect body composition and that it
exercise (Pedersen, 2011). A recent paper describes a new could usefully be included in lifestyle weight control pro-
polypeptide hormone, irisin, which is regulated by PGC1-a; it grammes. In our opinion, the general medicine practitioner
is secreted from muscle into the bloodstream and may activate should become familiar with this kind of training and its met-
thermogenic mechanisms in adipose tissue – this might also abolic effects in order to recommend it to patients with
play a role in short time reported to lower RER (Bostrom weight problems.
et al., 2012).
Some concerns could be raised about the feasibility of RT Acknowledgments
and in particular high-intensity RT in unfit overweight sub-
The authors thank Keith Grimaldi for improving English
jects (LaForgia et al., 2006), but there is experimental evi-
language of this article. The authors have no disclosures and
dence supporting the suitability of RT in such individuals
no conflict of interests.
(Sothern et al., 2000; Bouchard et al., 2009; McGuigan et al.,

References
de Almeida JC, Alves CL, de Abreu LC, Sato SP, Spiegelman BM. A PGC1-alpha-depen- augments integrative myofibrillar protein
MA, Fonseca FL, de Mello Monteiro CB, dent myokine that drives brown-fat-like synthesis. Metabolism (2012); 61: 153–156.
Vanderlei LC, Macedo H Jr, Tavares CM, development of white fat and thermogene- Gibala M. Molecular responses to high-inten-
Herrero D, Rodrigues LM, Valenti VE. sis. Nature (2012); 481: 463–468. sity interval exercise. Appl Physiol Nutr Metab
Involvement of the atrial natriuretic peptide Bottaro M, Martins B, Gentil P, Wagner D. (2009); 34: 428–432.
in cardiovascular pathophysiology and its Effects of rest duration between sets of Haddock BL, Wilkin LD. Resistance training
relationship with exercise. Int Arch Med resistance training on acute hormonal volume and post exercise energy expendi-
(2012); 5: 4. responses in trained women. J Sci Med Sport ture. Int J Sports Med (2006); 27: 143–148.
Bahr R, Hansson P, Sejersted OM. Triglycer- (2009); 12: 73–78. Haltom RW, Kraemer RR, Sloan RA, Hebert
ide/fatty acid cycling is increased after exer- Bouchard DR, Soucy L, Senechal M, Dionne EP, Frank K, Tryniecki JL. Circuit weight
cise. Metabolism (1990); 39: 993–999. IJ, Brochu M. Impact of resistance training training and its effects on excess postexer-
Barnard RJ, Foss ML. Oxygen debt: effect of with or without caloric restriction on physi- cise oxygen consumption. Med Sci Sports Exerc
beta-adrenergic blockade on the lactacid cal capacity in obese older women. Menopause (1999); 31: 1613–1618.
and alactacid components. J Appl Physiol (2009); 16: 66–72. Hunter GR, Wetzstein CJ, Fields DA, Brown
(1969); 27: 813–816. Byrne HK, Wilmore JH. The relationship of A, Bamman MM. Resistance training
Binzen CA, Swan PD, Manore MM. Postexer- mode and intensity of training on resting increases total energy expenditure and free-
cise oxygen consumption and substrate use metabolic rate in women. Int J Sport Nutr living physical activity in older adults. J Appl
after resistance exercise in women. Med Sci Exerc Metab (2001); 11: 1–14. Physiol (2000); 89: 977–984.
Sports Exerc (2001); 33: 932–938. Donnelly JE, Blair SN, Jakicic JM, Manore Hunter GR, Byrne NM, Gower BA, Sirikul B,
Black AE, Coward WA, Cole TJ, Prentice AM. MM, Rankin JW, Smith BK, American Col- Hills AP. Increased resting energy expendi-
Human energy expenditure in affluent soci- lege of Sports M. American College of ture after 40 minutes of aerobic but not
eties: an analysis of 574 doubly-labelled Sports Medicine Position Stand. Appropriate resistance exercise. Obesity (2006); 14:
water measurements. Eur J Clin Nutr (1996); physical activity intervention strategies for 2018–2025.
50: 72–92. weight loss and prevention of weight regain Hunter GR, Byrne NM, Sirikul B, Fernandez
Borsheim E, Bahr R. Effect of exercise inten- for adults. Med Sci Sports Exerc (2009); 41: JR, Zuckerman PA, Darnell BE, Gower BA.
sity, duration and mode on post-exercise 459–471. Resistance training conserves fat-free mass
oxygen consumption. Sports Med (2003); 33: Gaesser GA, Brooks GA. Metabolic bases of and resting energy expenditure following
1037–1060. excess post-exercise oxygen consumption: a weight loss. Obesity (2008); 16: 1045–
Bostrom P, Wu J, Jedrychowski MP, Korde A, review. Med Sci Sports Exerc (1984); 16: 29– 1051.
Ye L, Lo JC, Rasbach KA, Bostrom EA, Choi 43. Ibanez J, Izquierdo M, Martinez-Labari C,
JH, Long JZ, Kajimura S, Zingaretti MC, Gasier HG, Fluckey JD, Previs SF, Wiggs MP, Ortega F, Grijalba A, Forga L, Idoate F, Gar-
Vind BF, Tu H, Cinti S, Hojlund K, Gygi Riechman SE. Acute resistance exercise cia-Unciti M, Fernandez-Real JM, Gorostiaga

© 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd
 Resistance training and overweight, A. Paoli et al. 5

EM. Resistance training improves cardiovas- oxidation. Med Sci Sports Exerc (2002); 34: Interval Resistance Training (HIRT) influ-
cular risk factors in obese women despite a 1793–1800. ences resting energy expenditure and respi-
significative decrease in serum adiponectin Melanson EL, Sharp TA, Seagle HM, Donahoo ratory ratio in non-dieting individuals.
levels. Obesity (2010); 18: 535–541. WT, Grunwald GK, Peters JC, Hamilton JT, J Transl Med (2012b); 10: 237.
Idoate F, Ibanez J, Gorostiaga EM, Garcia-Un- Hill JO. Twenty-four-hour metabolic Paoli A, Pacelli QF, Moro T, Marcolin G, Neri
citi M, Martinez-Labari C, Izquierdo M. responses to resistance exercise in women. M, Battaglia G, Sergi G, Bolzetta F, Bianco
Weight-loss diet alone or combined with J Strength Cond Res (2005); 19: 61–66. A. Effects of high-intensity circuit training,
resistance training induces different regional Moro C, Pillard F, de Glisezinski I, Klimcak- low-intensity circuit training and endurance
visceral fat changes in obese women. Int J ova E, Crampes F, Thalamas C, Harant I, training on blood pressure and lipoproteins
Obes (2011); 35: 700–713. Marques MA, Lafontan M, Berlan M. Exer- in middle-aged overweight men. Lipids Health
Jakicic JM, Gallagher KI. Exercise consider- cise-induced lipid mobilization in subcuta- Dis (2013a); 12: 131.
ations for the sedentary, overweight adult. neous adipose tissue is mainly related to Paoli A, Rubini A, Volek JS, Grimaldi KA.
Exerc Sport Sci Rev (2003); 31: 91–95. natriuretic peptides in overweight men. Am Beyond weight loss: a review of the thera-
Jequier E. Pathways to obesity. Int J Obes J Physiol Endocrinol Metab (2008); 295: E505– peutic uses of very-low-carbohydrate (keto-
(2002); 26(Suppl 2): S12–S17. E513. genic) diets. Eur J Clin Nutr (2013b); 67:
Knuttgen HG. Strength training and aerobic Muller MJ, Bosy-Westphal A, Kutzner D, Hel- 789–796.
exercise: comparison and contrast. J Strength ler M. Metabolically active components of Pedersen BK. Muscles and their myokines.
Cond Res (2007); 21: 973–978. fat-free mass and resting energy expenditure J Exp Biol (2011); 214: 337–346.
Koh-Banerjee P, Wang Y, Hu FB, Spiegelman in humans: recent lessons from imaging Poehlman ET, Melby C. Resistance training
D, Willett WC, Rimm EB. Changes in body technologies. Obes Rev (2002); 3: 113–122. and energy balance. Int J Sport Nutr (1998);
weight and body fat distribution as risk fac- Olshansky SJ, Passaro DJ, Hershow RC, Lay- 8: 143–159.
tors for clinical diabetes in US men. Am J den J, Carnes BA, Brody J, Hayflick L, Butler Schuenke MD, Mikat RP, McBride JM. Effect
Epidemiol (2004); 159: 1150–1159. RN, Allison DB, Ludwig DS. A potential of an acute period of resistance exercise on
Kraemer WJ, Ratamess NA. Progression and decline in life expectancy in the United excess post-exercise oxygen consumption:
resistance training. Pres Counc Phys Fit Sports States in the 21st century. N Engl J Med implications for body mass management.
(2005); 6: 1–8. (2005); 352: 1138–1145. Eur J Appl Physiol (2002); 86: 411–417.
Kreider RB, Rasmussen C, Kerksick CM, Wil- Ormsbee MJ, Choi MD, Medlin JK, Geyer Sothern MS, Loftin JM, Udall JN, Suskind
born C, Taylor Lt, Campbell B, Magrans- GH, Trantham LH, Dubis GS, Hickner RC. RM, Ewing TL, Tang SC, Blecker U. Safety,
Courtney T, Fogt D, Ferreira M, Li R, Regulation of fat metabolism during resis- feasibility, and efficacy of a resistance train-
Galbreath M, Iosia M, Cooke M, Serra M, tance exercise in sedentary lean and obese ing program in preadolescent obese chil-
Gutierrez J, Byrd M, Kresta JY, Simbo S, men. J Appl Physiol (2009); 106: 1529– dren. Am J Med Sci (2000); 319: 370–375.
Oliver J, Greenwood M. A carbohydrate- 1537. Souza SC, Chau MD, Yang Q, Gauthier MS,
restricted diet during resistance training Paoli A. Resistance training: the multifaceted Clairmont KB, Wu Z, Gromada J, Dole WP.
promotes more favorable changes in body side of exercise. Am J Physiol Endocrinol Metab Atrial natriuretic peptide regulates lipid
composition and markers of health in obese (2012); 302: E387. mobilization and oxygen consumption in
women with and without insulin resistance. Paoli A, Bianco A. Not all exercises are cre- human adipocytes by activating AMPK.
Phys Sportsmed (2011); 39: 27–40. ated equal. Am J Cardiol (2012); 109: 305. Biochem Biophys Res Commun (2011); 410:
LaForgia J, Withers RT, Gore CJ. Effects of Paoli A, Bianco A, Neri M, Palma A. What is 398–403.
exercise intensity and duration on the Fitness: definition, history and health bene- Thornton MK, Potteiger JA. Effects of resis-
excess post-exercise oxygen consumption. fits. A review. Rivista della Facolta di Scienze tance exercise bouts of different intensities
J Sports Sci (2006); 24: 1247–1264. Motorie dell’Universita degli studi di Palermo (J Sport but equal work on EPOC. Med Sci Sports Exerc
Little JP, Safdar A, Wilkin GP, Tarnopolsky Sci and Sport Law) (2008); I: 143–166. (2002); 34: 715–722.
MA, Gibala MJ. A practical model of low- Paoli A, Pacelli F, Bargossi AM, Marcolin G, Thornton MK, Rossi SJ, McMillan JL. Compar-
volume high-intensity interval training Guzzinati S, Neri M, Bianco A, Palma A. ison of two different resistance training
induces mitochondrial biogenesis in human Effects of three distinct protocols of fitness intensities on excess post-exercise oxygen
skeletal muscle: potential mechanisms. training on body composition, strength and consumption in African American women
J Physiol (2010); 588: 1011–1022. blood lactate. J Sports Med Phys Fitness (2010); who are overweight. J Strength Cond Res
MacDougall JD, Gibala MJ, Tarnopolsky MA, 50: 43–51. (2011); 25: 489–496.
MacDonald JR, Interisano SA, Yarasheski Paoli A, Marcolin G, Zonin F, Neri M, Sivieri Wang Z, Heshka S, Gallagher D, Boozer CN,
KE. The time course for elevated muscle A, Pacelli QF. Exercising fasting or fed to Kotler DP, Heymsfield SB. Resting energy
protein synthesis following heavy resistance enhance fat loss? Influence of food intake expenditure-fat-free mass relationship: new
exercise. Can J Appl Physiol (1995); 20: 480– on respiratory ratio and excess postexercise insights provided by body composition
486. oxygen consumption after a bout of endur- modeling. Am J Physiol Endocrinol Metab
McGuigan MR, Tatasciore M, Newton RU, ance training. Int J Sport Nutr Exerc Metab (2000); 279: E539–E545.
Pettigrew S. Eight weeks of resistance train- (2011); 21: 48–54. Westerterp KR, Meijer GA, Janssen EM, Saris
ing can significantly alter body composition Paoli A, Grimaldi K, Bianco A, Lodi A, Cenci WH, Ten Hoor F. Long-term effect of phys-
in children who are overweight or obese. L, Parmagnani A. Medium term effects of a ical activity on energy balance and body
J Strength Cond Res (2009); 23: 80–85. ketogenic diet and a Mediterranean diet on composition. Br J Nutr (1992); 68: 21–30.
Melanson EL, Sharp TA, Seagle HM, Donahoo resting energy expenditure and respiratory Willis LH, Slentz CA, Bateman LA, Shields
WT, Grunwald GK, Peters JC, Hamilton JT, ratio. BMC Proc (2012a); 6: P37. AT, Piner LW, Bales CW, Houmard JA,
Hill JO. Resistance and aerobic exercise Paoli A, Moro T, Marcolin G, Neri M, Bianco Kraus WE. Effects of aerobic and/or resis-
have similar effects on 24-h nutrient A, Palma A, Grimaldi K. High-Intensity tance training on body mass and fat mass in

© 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd
6 Resistance training and overweight, A. Paoli et al.

overweight or obese adults. J Appl Physiol muscle. J Appl Physiol (2001); 91: 1017– metabolic rate in relation to body mass
(2012); 113: 1831–1837. 1028. index and body composition. Int J Obes Relat
Winder WW. Energy-sensing and signaling Zhang K, Sun M, Werner P, Kovera AJ, Albu Metab Disord (2002); 26: 376–383.
by AMP-activated protein kinase in skeletal J, Pi-Sunyer FX, Boozer CN. Sleeping

© 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd