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    Lift weights to fight overweight

    ARTICLE in CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING FEBRUARY 2014

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    Antonio Paoli

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    Tatiana Moro

    University of Padova

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    Antonino Bianco

    Universit degli Studi di Palermo

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    INVITED REVIEW

    Lift weights to fight overweightAntonio Paoli1, Tatiana Moro1 and Antonino Bianco2

    1Department of Biomedical Sciences, University of Padova, Padova, and 2Department of Sports and Exercise Science (DISMOT), University of Palermo, Palermo,Italy

    Summary

    CorrespondenceAntonio Paoli MD, Department of Biomedical Sci-

    ences, The physiological Laboratory, via Marzolo,

    3 35131 University of Padova, Padova, Italy.

    E-mail: [email protected]

    Accepted for publicationReceived 6 November 2013;

    accepted 23 January 2014

    Key wordsexcess postexercise oxygen consumption; exercise;

    metabolism; overweight; resistance training; weight

    control

    Although resistance training (RT) has long been accepted as a means for develop-ing and maintaining muscular strength, endurance, power and muscle mass, itsbeneficial relationship with health factors and chronic disease has only recentlybeen recognized in the scientific literature. Prior to 1990, resistance training wasnot a part of the recommended guidelines for exercise training and rehabilitationfor either the American Heart Association or the American College of Sports Med-

    icine (ACSM). In 1990, the ACSM recognized resistance training as a significantcomponent of a comprehensive fitness programme for healthy adults of all ages, aposition subsequently confirmed few years after. At present, even though interestin clinical applications of RT is increasing, there are still some concerns, amongphysicians, about the use of this exercise methodology in weight control pro-grammes. This review aims to explore the metabolic effects of RT and its efficacyand feasibility in overweight subjects.

    Introduction

    Health organizations report a worldwide increase in the preva-

    lence of overweight and obesity (Olshansky et al., 2005). Thisincrease is a great source of concern considering the fact thatobesity and in particular abdominal obesity is one of the prin-ciple risk factors for cardiovascular disease, and it is stronglyrelated to dyslipidaemia, hypertension, diabetes and metabolicsyndrome (Koh-Banerjee et al., 2004). Diet and exercise areconsidered the main tools to control body weight and bodyfat (Paoli et al., 2008), but nevertheless the exact dose andquality of diet (Paoli et al., 2013a,b) and exercise is still asubject of debate (Paoli et al., 2012a,b). The correct dose andquality of exercise, that is, the knowledge of how and howmuch should be suggested to patients is of importance for

    clinicians and medicine practitioners. The main question aboutthe effect of exercise on body weight regards the influence ithas on energy expenditure. Overall, daily energy expendituremay be briefly divided into three different components thatcan be categorized as (i) resting metabolism, (ii) thermiceffects of food and (iii) the energy expenditure of physicalactivity associated with exercise and non-exercise movement(Jequier, 2002). It has been demonstrated that in Westerncountries, the mean ratio of daily energy expenditure andresting energy expenditure (REE) is 166; in other words,only 40% of energy is expended on activity while the remaining

    60% is expended at rest (Black et al., 1996). Despite the rec-ommendations of national and international health organiza-tions for at least three 30-min sessions of vigorous exercise

    per week, it has been calculated, as a general example, thatthis would increase energy demands by only ffi1000 Kcal perweek (i.e. ffi5% of the average weekly expenditure about20 000 Kcal per week) (Black et al., 1996). Notwithstandingthese considerations, clinical practice and data from the litera-ture consistently point to the beneficial effect of exercise onfat loss (Jakicic & Gallagher, 2003). The only way to reconcilethis apparently contradictory evidence between experimentaland clinical data is to hypothesize the existence of other exer-cise-related factors involved in the fat loss effect other thanthe simple increase in energy expenditure during exercise.

    Mechanisms of physical activitys effects onbody weight control

    Three fundamental mechanisms have been taken into consid-eration to explain the effects of physical exercise on bodyweight control, and it may (i) reduce hunger, (ii) improvefitness levels and consequently might change behaviour relatedto non-exercise activity thermogenesis such as walking andstair climbing, (Jakicic & Gallagher, 2003) (iii) exert a posi-tive effect on resting metabolism. Regarding the latter, restingenergy expenditure (REE) is the largest component of the

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    daily energy budget and, consequently, any increase in REE inresponse to exercise could potentially have a great impact onhealth promotion and weight control. Even though there isconsiderable individual variation in REE, it is well establishedthat fat-free mass (lean body mass) is the main factor thatinfluences REE, accounting for 5070% of the individual vari-ation (Westerterp et al., 1992; Zhang et al., 2002). There is a

    linear relationship between lean body mass and resting energymetabolism but with broad interindividual variance (Wanget al., 2000; Muller et al., 2002). It is evident that muscle massrepresents the majority (88%) of metabolically active fat-freemass (FFM) with the metabolically active organs representingonly 12% of FFM, but while the former provides an energyexpenditure of approximately only 15 Kcal kg1 per day, theenergy expenditure of the latter is 468 Kcal kg1 per day.Thus, muscle accounts for only a minor part (less than 20%)of total daily energy expenditure. Nevertheless, many humanstudies with long-term exercise protocols, separating theeffects of training and nutrition, have demonstrated that the

    positive effect of training on REE is mainly mediated bythe increase in free fat mass (i.e. muscle) (Byrne & Wilmore,2001). Interestingly, these studies also found that the combi-nation of endurance and resistance training leads to an overalldecrease in REE (Westerterp et al., 1992; Byrne & Wilmore,2001), but that this exercise-related decrease was evident withendurance training, while a net increase in REE was found afterRT (Hunter et al., 2008). These results explain why in recentyears there has been a lot of interest in the specific effects ofRT on weight control, and it is also the case that resistancetraining (RT) has only been incorporated recently as animportant component of exercise protocols for weight controlin some guidelines (Kraemer & Ratamess, 2005; Donnellyet al., 2009).

    Resistance training and metabolism

    Resistance training acts in a substantially different way com-pared with endurance training (ET), and it increases musclemass in the long term (Paoli et al., 2010, 2013a,b) but alsoincreases excess postexercise oxygen consumption (EPOC)immediately after the training session (Schuenke et al., 2002).In 1984, Gaesser and Brooks defined the recovery period inwhich an increase in oxygen uptake is observed as excesspostexercise oxygen consumption (EPOC). EPOC can be

    divided into two phases: short term (due to the so-called oxy-gen debt or fast component of excess postexercise oxygenconsumption) and long term (slow component of excess post-exercise oxygen consumption due to various mechanisms notyet completely understood but most likely linked to the resto-ration of homeostasis). As a matter of fact, after intense orprolonged exercise, oxygen consumption remains increasedfor several hours and is referred to as the slow component ofexcess postexercise oxygen consumption (EPOC). This elevatedpostexercise metabolism plays a part in the energy cost ofexercise and in the overall effect of exercise in body weight

    control. Even though the beneficial effect on health andweight control of a 24-h increase in metabolism is evident(Hunteret al., 2000), the optimal amount and type of exerciseroutine remains to be established. We recently discussed thatresistance training should be investigated more thoroughlyand rigorously by taking into account the variables involvedincluding (i) muscle action used, (ii) type of resistance used,

    (iii) volume (total number of sets and repetitions), (iv) exer-cises selected and workout structure (e.g. the number of mus-cle groups trained), (v) the sequence of exercise performance,(vi) rest intervals between sets, (vii) repetition velocity and(viii) training frequency (Paoli, 2012; Paoli & Bianco, 2012;Paoli et al., 2012a,b). It can be argued that, as Knuttgenasserted, if EPOC increased exponentially as a function ofexercise intensity, whereas it increased linearly as a functionof exercise duration (Knuttgen, 2007), a high-intensity resis-tance training programme could affect positively restingmetabolism. Thus, RT could act through two different ways:increase in lean body mass (chronic/long-term effect) and

    transient increase in metabolism (EPOC). In fact, there areseveral reports that weight training may require more recoveryenergy and a longer duration EPOC (Haddock & Wilkin,2006) compared with endurance training. Despite this, thereare surprisingly few studies published on the specific influenceof high-intensity resistance training on metabolism.

    Effects of exercise intensity on weight control

    Some studies reported that higher-intensity resistance exercisegenerates greater EPOC than lower-intensity resistance exercise(Haltom et al., 1999; Thornton & Potteiger, 2002), and thereason for this greater EPOC could be attributed to a greaterperturbation 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 programmecan induce a greater EPOC in the 24 h after the training ses-sion (Paoli et al., 2012a,b) (Fig.1) and that this kind of RT,mixed with a high-intensity endurance interval training, canimprove body composition and blood lipids (Paoli et al.,2013a,b). It is clear that the intensity of exercise is a keystoneof postexercise energy expenditure not only in enduranceexercise such as cycling (Little et al., 2010) but also in resis-tance training. The mechanisms underlying these effects arenot still clear, but we can raise some hypotheses:

    1)the greater increase in blood lactate (which is evidence of amajor metabolic stress derived from high-intensity resistancetraining and may reflect the utilization of lactate as fuel in theaerobic pathway) imposes an increase in postexercise energyexpenditure (Binzen et al., 2001). Lactate removal, though,may only be part of the process, in fact, if lactate is infusedduring the postexercise period, it does not elicit a furtherincrease in EPOC (Barnard & Foss, 1969). However, lactatemay explain, together with an increase in body temperature(Gaesser & Brooks, 1984), only the short-term component ofEPOC;

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

    Resistance training and overweight, A. Paoli et al.2

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    2) an increase in b-adrenergic system activity (Hunter et al.,2006);

    3)hormonal variations: in response to exercise-inducedtrauma, an increase in metabolic hormonal concentration isseen (e.g. cortisol, catecholamines and thyroid hormone),which could increase metabolism (Schuenke et al., 2002);4)the increased protein resynthesis due to postexercise muscle

    damage is energy expensive (approximately 20% increase inresting metabolism) (MacDougall et al., 1995) and could con-tribute to greater EPOC after high-intensity resistance training(Binzenet al., 2001; Gasier et al., 2012);

    Moreover, an important effect of high-intensity exercise isthe improvement in utilization of fatty acids instead of glucosethat could lead to a getter utilization of fat stores. This effectcan be highlighted by a decrease in respiratory exchange ratio(RER). The respiratory exchange ratio (i.e. the ratio betweenCO2 expired and O2 consumed) is a good way to identify theorigin of energy substrates: when RER is close to 07, itmeans that the major energy source is lipids, while when theratio is near 1, carbohydrates are the main source of energy.It is clear that an improvement in fat oxidation can helpweight control. Fasting or very low carbohydrate diet can leadto a decrease in RER (Paoli et al., 2012a,b, 2013a,b), but alsotraining can have the same result (Paoli et al., 2011, 2012a,b).The increase in the rate of fatty acid oxidation (i.e. the reduc-tion in RER) indicates that triacylglycerol/fatty acid cycling isan important supporter of the energy cost in the prolonged

    component of EPOC as it is an index that the organism isusing fatty acids rather than glycogen to satisfy the energycost of exercise (Bahr et al., 1990) and seems to be a compen-satory sparing of glycogen after any kind of resistance training(Poehlman & Melby, 1998).

    Several causes could explain the RER lowering after resis-tance training (see Fig. 2):

    1)glucose metabolic pathways are directed to replenish glyco-gen stores first instead of being used for energy supply. Thismeans that glucose and all gluconeogenic precursors will bespared from further oxidation and will be converted to glu-cose and glycogen, so lipids become the preferred oxidationsubstrate (Borsheim & Bahr, 2003);2)the AMP kinases/acetyl CoA carboxylase (AMPK/ACC)pathway. It has been demonstrated that intense exerciseincreases AMPK (Gibala, 2009); thus, AMPK can phosphory-late ACC, decreasing its activity; the decreased ACC activityleads to a decrease in the rate of the synthesis of malonylCoA, and consequently, there is a release of inhibition of

    carnitine palmitoyltransferase I (CPT1) activity leading to anincrease in lipid oxidation (Winder, 2001);

    3)an increase in atrial natriuretic peptide (ANP) stimulated byexercise could play a role in the increased rate of lipid oxida-tion; production of ANP is related to the intensity of exercise(Moro et al., 2008; de Almeida et al., 2012), it has been dem-onstrated that ANP increases lipolysis (Souza et al., 2011), andthis pathway appears to be more suitable than the increase in

    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 orhigh-intensity interval resistance training.** P

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    catecholamines that have a very short half-life and appears notto be related to lipolysis after RT (Ormsbee et al., 2009);4)growth hormone increase also could explain a part of theincrease in lipid oxidation; it was demonstrated by Bottaroet al. et al. (Bottaro et al., 2009) that intense exercise withincomplete recovery might stimulate GH production in asignificant manner;

    5) there is some new evidence that suggests how some cyto-kines and other peptides (myokines) that are produced andreleased by muscle fibres can exert autocrine, paracrine orendocrine effects that might influence the metabolic effect ofexercise (Pedersen, 2011). A recent paper describes a newpolypeptide hormone, irisin, which is regulated by PGC1-a; itis secreted from muscle into the bloodstream and may activatethermogenic mechanisms in adipose tissue this might alsoplay a role in short time reported to lower RER (Bostromet al., 2012).

    Some concerns could be raised about the feasibility of RTand in particular high-intensity RT in unfit overweight sub-jects (LaForgia et al., 2006), but there is experimental evi-dence supporting the suitability of RT in such individuals(Sothern et al., 2000; Bouchard et al., 2009; McGuigan et al.,

    2009; Ibanez et al., 2010; Idoate et al., 2011; Kreider et al.,2011; Thornton et al., 2011; Willis et al., 2012). Morerecently, our group has demonstrated the safety and feasibil-ity, after a familiarization period, of high-intensity resistancetraining in sedentary and overweight subjects (Paoli et al.,2010, 2013a,b)

    Conclusions

    Taken together, these recent findings suggest that resistancetraining could positively affect body composition and that itcould usefully be included in lifestyle weight control pro-grammes. In our opinion, the general medicine practitionershould become familiar with this kind of training and its met-abolic effects in order to recommend it to patients withweight problems.

    Acknowledgments

    The authors thank Keith Grimaldi for improving Englishlanguage of this article. The authors have no disclosures andno conflict of interests.

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