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Lift weights to fight overweight


ARTICLE in CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING FEBRUARY 2014
Impact Factor: 1.33 DOI: 10.1111/cpf.12136 Source: PubMed

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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
Antonio Paoli MD, Department of Biomedical Sciences, The physiological Laboratory, via Marzolo,
3 35131 University of Padova, Padova, Italy.
E-mail: antonio.paoli@unipd.it

Accepted for publication


Received 6 November 2013;
accepted 23 January 2014

Key words
excess postexercise oxygen consumption; exercise;
metabolism; overweight; resistance training; weight
control

Although resistance training (RT) has long been accepted as a means for developing and maintaining muscular strength, endurance, power and muscle mass, its
beneficial relationship with health factors and chronic disease has only recently
been recognized in the scientific literature. Prior to 1990, resistance training was
not a part of the recommended guidelines for exercise training and rehabilitation
for either the American Heart Association or the American College of Sports Medicine (ACSM). In 1990, the ACSM recognized resistance training as a significant
component of a comprehensive fitness programme for healthy adults of all ages, a
position subsequently confirmed few years after. At present, even though interest
in clinical applications of RT is increasing, there are still some concerns, among
physicians, about the use of this exercise methodology in weight control programmes. This review aims to explore the metabolic effects of RT and its efficacy
and feasibility in overweight subjects.

Introduction
Health organizations report a worldwide increase in the prevalence of overweight and obesity (Olshansky et al., 2005). This
increase is a great source of concern considering the fact that
obesity and in particular abdominal obesity is one of the principle risk factors for cardiovascular disease, and it is strongly
related to dyslipidaemia, hypertension, diabetes and metabolic
syndrome (Koh-Banerjee et al., 2004). Diet and exercise are
considered the main tools to control body weight and body
fat (Paoli et al., 2008), but nevertheless the exact dose and
quality of diet (Paoli et al., 2013a,b) and exercise is still a
subject of debate (Paoli et al., 2012a,b). The correct dose and
quality of exercise, that is, the knowledge of how and how
much should be suggested to patients is of importance for
clinicians and medicine practitioners. The main question about
the effect of exercise on body weight regards the influence it
has on energy expenditure. Overall, daily energy expenditure
may be briefly divided into three different components that
can be categorized as (i) resting metabolism, (ii) thermic
effects of food and (iii) the energy expenditure of physical
activity associated with exercise and non-exercise movement
(Jequier, 2002). It has been demonstrated that in Western
countries, the mean ratio of daily energy expenditure and
resting 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 recommendations of national and international health organizations for at least three 30-min sessions of vigorous exercise
per week, it has been calculated, as a general example, that
this would increase energy demands by only 1000 Kcal per
week (i.e. 5% of the average weekly expenditure about
20 000 Kcal per week) (Black et al., 1996). Notwithstanding
these considerations, clinical practice and data from the literature consistently point to the beneficial effect of exercise on
fat loss (Jakicic & Gallagher, 2003). The only way to reconcile
this apparently contradictory evidence between experimental
and clinical data is to hypothesize the existence of other exercise-related factors involved in the fat loss effect other than
the simple increase in energy expenditure during exercise.

Mechanisms of physical activitys effects on


body weight control
Three fundamental mechanisms have been taken into consideration to explain the effects of physical exercise on body
weight control, and it may (i) reduce hunger, (ii) improve
fitness levels and consequently might change behaviour related
to non-exercise activity thermogenesis such as walking and
stair climbing, (Jakicic & Gallagher, 2003) (iii) exert a positive effect on resting metabolism. Regarding the latter, resting
energy expenditure (REE) is the largest component of the

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

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

daily energy budget and, consequently, any increase in REE in


response to exercise could potentially have a great impact on
health promotion and weight control. Even though there is
considerable individual variation in REE, it is well established
that fat-free mass (lean body mass) is the main factor that
influences REE, accounting for 5070% of the individual variation (Westerterp et al., 1992; Zhang et al., 2002). There is a
linear relationship between lean body mass and resting energy
metabolism but with broad interindividual variance (Wang
et al., 2000; Muller et al., 2002). It is evident that muscle mass
represents the majority (88%) of metabolically active fat-free
mass (FFM) with the metabolically active organs representing
only 12% of FFM, but while the former provides an energy
expenditure of approximately only 15 Kcal kg1 per day, the
energy 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 human
studies with long-term exercise protocols, separating the
effects of training and nutrition, have demonstrated that the
positive effect of training on REE is mainly mediated by
the increase in free fat mass (i.e. muscle) (Byrne & Wilmore,
2001). Interestingly, these studies also found that the combination of endurance and resistance training leads to an overall
decrease in REE (Westerterp et al., 1992; Byrne & Wilmore,
2001), but that this exercise-related decrease was evident with
endurance training, while a net increase in REE was found after
RT (Hunter et al., 2008). These results explain why in recent
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
training (RT) has only been incorporated recently as an
important component of exercise protocols for weight control
in some guidelines (Kraemer & Ratamess, 2005; Donnelly
et al., 2009).

Resistance training and metabolism


Resistance training acts in a substantially different way compared with endurance training (ET), and it increases muscle
mass in the long term (Paoli et al., 2010, 2013a,b) but also
increases excess postexercise oxygen consumption (EPOC)
immediately after the training session (Schuenke et al., 2002).
In 1984, Gaesser and Brooks defined the recovery period in
which an increase in oxygen uptake is observed as excess
postexercise oxygen consumption (EPOC). EPOC can be
divided into two phases: short term (due to the so-called oxygen debt or fast component of excess postexercise oxygen
consumption) and long term (slow component of excess postexercise oxygen consumption due to various mechanisms not
yet completely understood but most likely linked to the restoration of homeostasis). As a matter of fact, after intense or
prolonged exercise, oxygen consumption remains increased
for several hours and is referred to as the slow component of
excess postexercise oxygen consumption (EPOC). This elevated
postexercise metabolism plays a part in the energy cost of
exercise and in the overall effect of exercise in body weight

control. Even though the beneficial effect on health and


weight control of a 24-h increase in metabolism is evident
(Hunter et al., 2000), the optimal amount and type of exercise
routine remains to be established. We recently discussed that
resistance training should be investigated more thoroughly
and rigorously by taking into account the variables involved
including (i) muscle action used, (ii) type of resistance used,
(iii) volume (total number of sets and repetitions), (iv) exercises selected and workout structure (e.g. the number of muscle 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 Knuttgen
asserted, if EPOC increased exponentially as a function of
exercise intensity, whereas it increased linearly as a function
of exercise duration (Knuttgen, 2007), a high-intensity resistance training programme could affect positively resting
metabolism. 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 are
several reports that weight training may require more recovery
energy and a longer duration EPOC (Haddock & Wilkin,
2006) compared with endurance training. Despite this, there
are surprisingly few studies published on the specific influence
of high-intensity resistance training on metabolism.

Effects of exercise intensity on weight control


Some studies reported that higher-intensity resistance exercise
generates greater EPOC than lower-intensity resistance exercise
(Haltom et al., 1999; Thornton & Potteiger, 2002), and the
reason for this greater EPOC could be attributed to a greater
perturbation of energy homeostasis (Melanson et al., 2002,
2005; Schuenke et al., 2002). In this regard, we recently demonstrated that a high-intensity resistance training programme
can induce a greater EPOC in the 24 h after the training session (Paoli et al., 2012a,b) (Fig.1) and that this kind of RT,
mixed with a high-intensity endurance interval training, can
improve body composition and blood lipids (Paoli et al.,
2013a,b). It is clear that the intensity of exercise is a keystone
of postexercise energy expenditure not only in endurance
exercise such as cycling (Little et al., 2010) but also in resistance training. The mechanisms underlying these effects are
not still clear, but we can raise some hypotheses:
1) the greater increase in blood lactate (which is evidence of a
major metabolic stress derived from high-intensity resistance
training and may reflect the utilization of lactate as fuel in the
aerobic pathway) imposes an increase in postexercise energy
expenditure (Binzen et al., 2001). Lactate removal, though,
may only be part of the process, in fact, if lactate is infused
during the postexercise period, it does not elicit a further
increase in EPOC (Barnard & Foss, 1969). However, lactate
may explain, together with an increase in body temperature
(Gaesser & Brooks, 1984), only the short-term component of
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.,


2006);
3) hormonal variations: in response to exercise-induced
trauma, an increase in metabolic hormonal concentration is
seen (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 in
resting metabolism) (MacDougall et al., 1995) and could contribute to greater EPOC after high-intensity resistance training
(Binzen et al., 2001; Gasier et al., 2012);
Moreover, an important effect of high-intensity exercise is
the improvement in utilization of fatty acids instead of glucose
that could lead to a getter utilization of fat stores. This effect
can be highlighted by a decrease in respiratory exchange ratio
(RER). The respiratory exchange ratio (i.e. the ratio between
CO2 expired and O2 consumed) is a good way to identify the
origin of energy substrates: when RER is close to 07, it
means that the major energy source is lipids, while when the
ratio is near 1, carbohydrates are the main source of energy.
It is clear that an improvement in fat oxidation can help
weight control. Fasting or very low carbohydrate diet can lead
to a decrease in RER (Paoli et al., 2012a,b, 2013a,b), but also
training can have the same result (Paoli et al., 2011, 2012a,b).
The increase in the rate of fatty acid oxidation (i.e. the reduction in RER) indicates that triacylglycerol/fatty acid cycling is
an important supporter of the energy cost in the prolonged

component of EPOC as it is an index that the organism is


using fatty acids rather than glycogen to satisfy the energy
cost of exercise (Bahr et al., 1990) and seems to be a compensatory sparing of glycogen after any kind of resistance training
(Poehlman & Melby, 1998).
Several causes could explain the RER lowering after resistance training (see Fig. 2):
1) glucose metabolic pathways are directed to replenish glycogen stores first instead of being used for energy supply. This
means that glucose and all gluconeogenic precursors will be
spared from further oxidation and will be converted to glucose and glycogen, so lipids become the preferred oxidation
substrate (Borsheim & Bahr, 2003);
2) the AMP kinases/acetyl CoA carboxylase (AMPK/ACC)
pathway. It has been demonstrated that intense exercise
increases AMPK (Gibala, 2009); thus, AMPK can phosphorylate ACC, decreasing its activity; the decreased ACC activity
leads to a decrease in the rate of the synthesis of malonyl
CoA, and consequently, there is a release of inhibition of
carnitine palmitoyltransferase I (CPT1) activity leading to an
increase in lipid oxidation (Winder, 2001);
3) an increase in atrial natriuretic peptide (ANP) stimulated by
exercise could play a role in the increased rate of lipid oxidation; production of ANP is related to the intensity of exercise
(Moro et al., 2008; de Almeida et al., 2012), it has been demonstrated that ANP increases lipolysis (Souza et al., 2011), and
this pathway appears to be more suitable than the increase in

Figure 1 Changes in resting energy expenditure (REE) and respiratory exchange ratio
(RER) at basal condition and 22 h after a session 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 training 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


to be related to lipolysis after RT (Ormsbee et al., 2009);
4) growth hormone increase also could explain a part of the
increase in lipid oxidation; it was demonstrated by Bottaro
et al. et al. (Bottaro et al., 2009) that intense exercise with
incomplete recovery might stimulate GH production in a
significant manner;
5) there is some new evidence that suggests how some cytokines and other peptides (myokines) that are produced and
released by muscle fibres can exert autocrine, paracrine or
endocrine effects that might influence the metabolic effect of
exercise (Pedersen, 2011). A recent paper describes a new
polypeptide hormone, irisin, which is regulated by PGC1-a; it
is secreted from muscle into the bloodstream and may activate
thermogenic mechanisms in adipose tissue this might also
play a role in short time reported to lower RER (Bostrom
et al., 2012).
Some concerns could be raised about the feasibility of RT
and in particular high-intensity RT in unfit overweight subjects (LaForgia et al., 2006), but there is experimental evidence 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). More
recently, our group has demonstrated the safety and feasibility, after a familiarization period, of high-intensity resistance
training in sedentary and overweight subjects (Paoli et al.,
2010, 2013a,b)

Conclusions
Taken together, these recent findings suggest that resistance
training could positively affect body composition and that it
could usefully be included in lifestyle weight control programmes. In our opinion, the general medicine practitioner
should become familiar with this kind of training and its metabolic effects in order to recommend it to patients with
weight problems.

Acknowledgments
The authors thank Keith Grimaldi for improving English
language of this article. The authors have no disclosures and
no conflict of interests.

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