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Journal of Obesity
Volume 2011, Article ID 482564, 9pages
doi:10.1155/2011/482564
Review Article
Evidence for Resistance Training as a Treatment
Therapy in Obesity
Barbara Strasser and Wolfgang Schobersberger
Institute for Sports Medicine, Alpine Medicine and Health Tourism, University for Health Sciences,
Medical Informatics and Technology, 6060 Hall in Tirol, Austria
Correspondence should be addressed to Barbara Strasser, barbara.strasser@umit.at
Received 14 May 2010; Accepted 16 June 2010
Academic Editor: Eric Doucet
Copyright © 2011 B. Strasser and W. Schobersberger. This is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.
Over the last decade, investigators have paid increasing attention to the effects of resistance training (RT) on several metabolic
syndrome variables. Evidence suggests that skeletal muscle is responsible for up to 40% of individuals’ total body weight and may
be influential in modifying metabolic risk factors via muscle mass development. Due to the metabolic consequences of reduced
muscle mass, it is understood that normal aging and/or decreased physical activity may lead to a higher prevalence of metabolic
disorders. The purpose of this review is to (1) evaluate the potential clinical effectiveness and biological mechanisms of RT in the
treatment of obesity and (2) provide up-to-date evidence relating to the impact of RT in reducing major cardiovascular disease risk
factors (including dyslipidaemia and type 2 diabetes). A further aim of this paper is to provide clinicians with recommendations
for facilitating the use of RT as therapy in obesity and obesity-related metabolic disorders.
1. Introduction
The inclusion of resistance training (RT) as an integral part
of an exercise therapy program has been endorsed by the
American Heart Association [1], the American College of
Sports Medicine [2], and the American Diabetes Association
[3]. While these recommendations are primarily based on the
effects of RT on muscle strength, cross-sectional studies have
shown that muscle mass is inversely associated with all-cause
mortality [4] and the prevalence of the metabolic syndrome
[5], independent of cardiorespiratory fitness levels.
Aging is associated with a loss of both muscle mass
and the metabolic quality of skeletal muscle. Sarcopenia,
the loss of muscle mass associated with aging, is a main
cause of muscle weakness in old age and leads consequently
to an increased risk for development of obesity-associated
insulin resistance and type 2 diabetes mellitus [6]. Research
supports the use of RT to prevent an age-related decline
in skeletal muscle mass (which is approximately 0.46 kg of
muscle per annum from the fifth decade on). Strong evidence
indicates that muscle maintains its plasticity and capacity
to hypertrophy, even into the 10th decade of life [7–9].
However, there is some evidence to suggest that muscle
strength and its effect on body composition and metabolic
risk factors may be more important than muscle mass [10].
Accordingly, the term of “dynapenia” to qualify the loss of
muscle strength with normal aging has been proposed [11].
A number of neural factors may be implicated in the age-
associated loss of muscle strength, but also alterations in
contractile properties are discussed.
Skeletal muscle is the primary metabolic target organ
for glucose and triglyceride disposal and is an important
determinant of resting metabolic rate. The potential con-
sequences of age-related reduction in skeletal muscle mass
are diverse, including reduced muscle strength and power,
reduced resting metabolic rate, reduced capacity for lipid
oxidation, and increased abdominal adiposity. With increas-
ing adiposity, the insulin-mediated glucose uptake in skeletal
muscle of elderly patients is reduced [12]. Evidence suggests
that the maintenance of a large muscle mass may reduce
metabolic risk factors—namely, obesity, dyslipidaemia, and
type 2 diabetes mellitus—associated with cardiovascular
2Journal of Obesity
disease [13–15]. Despite the fact that a high muscle mass
is associated with a favourable metabolic profile, one study
reported that a higher muscle mass can be associated with
metabolic disturbances in obese women [16]. The possible
mechanisms may include increased concentrations of free
androgens due to diminished levels of SHBG, a protein-
sparing effect due to increased lipid metabolism, and changes
in muscle capillarization and fiber composition due to
visceral adiposity.
For the most part, recommendations to treat or prevent
overweight and obesity via physical activity have focused
on aerobic endurance training (AET). Data suggest that
RT may be an effective alternative for modifying metabolic
risk factors. From this backdrop, the purpose of this review
is to (1) evaluate the potential clinical effectiveness and
biological mechanisms of RT in the treatment of obesity
and (2) provide-up-to-date evidence on the impact of RT in
reducing cardiovascular disease (CVD) risk factors, namely,
dyslipidaemia and type 2 diabetes.
2. Metabolic Effects of Resistance Training
2.1. Weight Control. Both resting and activity-related energy
expenditure declines with age [17]; decreased energy expen-
diture can have a major adverse effect on weight maintenance
[18]. Studies on the usefulness of RT in the context of weight
loss have demonstrated mixed results. Although it is clear
that AET is associated with much greater energy expenditure
during the exercise session than RT, some studies have shown
that regular RT is effective in promoting weight loss in obese
persons [19,20]. A significant number of studies have shown
that RT is associated with a decrease in fat mass (FM) and a
concomitant increase in lean body mass (LBM) and thus has
little or no effectivechangeintotalbodyweight[21–27]. RT
increased muscle mass by a minimum of 1 to 2 kg in studies
of sufficient duration.
The implementation of RT within a dietary intake restric-
tion programme has been studied, along with a combined
dietary restriction and AET programme [28–32]. In terms of
relative effects, the addition of RT has been found to prevent
the loss of LBM, secondary to dietary restriction [33,34].
One study demonstrated that twice-weekly RT could prevent
age-associated loss of LBM, as well as associated resting
metabolic rate (RMR) which is closely correlated to losses in
LBM [35]. RT contributes to elevations of RMR as a result
of a greater muscle protein turnover [36]. Theoretically, a
gain of 1 kg in muscle mass should result in an RMR increase
of approximately 21 kcal/kg of new muscle. Thus, RT, when
sustained over years or decades, translates into clinically
important differences in daily energy expenditure and age-
associated fat gains. For example, a difference of 5 kg in LBM
translates to a difference in energy expenditure of 100 kcal
per day (equivalent to 4.7 kg FM per year) [37]. However, a
number of studies have shown that RT will increase RMR, at
least if the training is intense enough to induce an increase in
LBM [38–40].
In a randomized control trial [41], 35 overweight men
were randomized to either a control group, a diet-only
group, a diet group that performed AET, or a diet group
that performed both AET and RT. After 12 weeks, the
weight loss in the three intervention groups was similar and
significant, of which 69%, 78%, and 97%, respectively, were
accounted for by fat loss. This study highlights the potential
for RT to provide a unique stimulus to spare catabolism
of body protein, thus altering the relationship between the
LBM and FM. Exercise provided no additional stimulus for
greater weight loss compared with that obtained from dietary
restriction alone. The diet-only group also demonstrated a
significant reduction in LBM.
Another study randomly assigned 29 obese men to one of
three 16-week treatments, which consisted of a hypocaloric
diet alone or in combination with RT (at 80% of 1-RM)
or AET [19]. Whereas reduction in weight (−12.4 kg) and
total adipose tissue (−9.7 kg) were not significantly different
between the three groups, LBM was only preserved after the
exercise training (independent of the mode), compared with
the diet-only group (−2.5 kg). The principal finding of this
study was that dietary restriction combined with either AET
or RT increased the influence of diet alone on insulin levels
in obese men.
A further trial assessed whether increases in LBM and
decreases in FM from 15 weeks of twice weekly supervised
RT (at 80% of 1-RM) could be maintained over 6 months
of unsupervised exercise [25]. Over the total 39 weeks of RT,
the treatment group gained 0.89 kg more in LBM, lost 0.98 kg
more in FM, and lost 1.63% more in percent body fat when
compared to the control group. Findings demonstrated that
twice weekly RT did not result in any significant weight loss,
but potentially could prevent age-associated fat gains over
a period of years. Cited as feasible, was the likelihood that
the positive body composition changes associated with RT
could be maintained in an unsupervised exercise program
after completion of the supervised exercise regime.
In a more recent study [42], an 8-week regime of RT
delivered 3 times weekly (at 60% of 1-RM) significantly
changed participants’ body mass (+0.58%), percentage of
body fat (−13.05%), LBM (+5.05%), and FM (−12.11%)
when compared to the control group. This study supported
a relationship between RT and body mass index (BMI),
demonstrated by an increase in BMI. Therefore, the use of
BMI in ascribing CVD risk should be used with caution
in those individuals with an increased LBM (as would be
expected following RT).
More recently, the effects of a 6-month RT program (at
50% to 80% of 1-RM) were analysed in relation to exercise-
induced oxidative stress and homocysteine and cholesterol in
normal-weight and overweight older adults [43]. Oxidative
stress is suggested to be a potential contributor in the
early and advanced stages of CVD [44]. In the study,
49 older adults were stratified by BMI and randomly
assigned to either a control nonexercise group or an RT
group. Findings demonstrated that lipid hydroperoxides
(PEROXs) and homocysteine levels were lower in both the
overweight and normal weight RT groups compared with
control groups. Change in muscle strength was associated
with homocysteine at 6 months, whereas the change in
PEROXs was associated with the change in body fat. This
Journal of Obesity 3
study showed that RT reduces exercise-induced oxidative
stress and homocysteine, regardless of adiposity. Such a
result indicates that this protection can be afforded in
an older, overweight/obese population as effectively as in
healthy older adults, which might indicate protection against
oxidative insults (i.e., ischemia). A potential mechanism
for RT-induced reduction of oxidative stress could include
contraction-induced antioxidant enzyme up-regulation [45].
2.2. Visceral Adipose Tissue. Adipose tissue is a major
endocrine organ, secreting substances such as adiponectin,
leptin, resistin, tumor necrosis factor α, interleukin 6, and
plasminogen activator inhibitor-1 that may play a critical
role in the pathogenesis of the metabolic syndrome [46].
Excessive central obesity and especially visceral adipose tissue
have been linked with the development of dyslipidaemia,
hypertension, insulin resistance, type 2 diabetes, and CVD
[8,12]. A relative increase in body fat is linked with a decline
in insulin sensitivity in both obese and elderly individuals
[47,48].
Several studies have demonstrated decreases in visceral
adipose tissue after RT programs [24,26–28,49,50]. Treuth
et al. observed significant decreases in visceral fat in older
men and women after 16 weeks of RT [26,27]. In two
studies, Ross et al. measured regional fat losses after 16
weeks of exercise combined with dietary interventions in
middle-aged obese men [28,49]. In their first study [49],
testsofbothdietplusAETanddietplusRT(at70%
to 80% of 1-RM) elicited similar losses of visceral fat,
which were greater than losses of whole-body subcutaneous
fat. In a follow-up study [28], they isolated the effects of
AET and RT (at 70% to 80% of 1-RM) by comparing
the responses to diet alone. All 3 groups lost significant
amounts of total body fat, and all 3 groups experienced a
significantly greater visceral fat loss compared with whole-
body subcutaneous fat loss. The changes amounted to a
40% reduction in visceral fat in the diet plus RT group,
39% in the diet plus AET group, and a 32% reduction
in the diet-only group. One study raised the possibility of
gender specificity in visceral fat reduction response to RT
[24]. Hunter et al. studied older women and men after 25
weeks of RT (at 65% to 80% of 1-RM). Results demonstrated
that both genders significantly increased muscle mass and
decreased whole-body fat mass. However, women also lost
a significant amount of subcutaneous and visceral adipose
tissue (−6% and −11%, resp.), whereas the men did
not.
Although more research is needed to clarify these
possible gender-specific responses, the overall available body
of literature supports the use of RT, with or without AET,
and with or without diet modification, as an effective
intervention in the reduction of abdominal obesity. It seems
that RT has the potential to reduce visceral fat deposits
through both immediate effects (e.g., during weight loss
or weight maintenance) and delayed effects (during weight
regain). The results of the two Ross et al. studies [28,49]
suggest a potential for low volume, high-intensity RT to
achieve reductions in total and regional adipose tissue when
used in conjunction with a calorie-restriction diet. However,
this observation requires confirmation by additional studies.
Overall, strong evidence supports the notion that regular
RT can effectively alter body composition in obese men and
women, independently from dietary restriction. It has been
shown that RT increases LBM, muscular strength, and resting
metabolic rate, and mobilizes the visceral and subcutaneous
adipose tissue in the abdominal region. Further, RT lowers
exercise-induced oxidative stress and homocysteine levels in
overweight and obese older adults, associated with CVD.
Considering the benefits of RT on body composition in
obese men and women, the question is are there any studies
that have investigated the effects of RT in obese adolescents?
The majority of RT research with children to date has
focused on preadolescents and the safety and efficacy of this
type of training rather than the potential metabolic health
benefits. There is only a small amount of evidence that
children and adolescents may derive metabolic health-related
adaptations from supervised RT. However, methodological
limitations within the body of this literature make it difficult
to determine the optimal RT prescription for metabolic
fitness in children and adolescents, and the extent and
duration of such benefits. More robustly designed single
modality randomized controlled trials utilizing standardized
reporting and precise outcome assessments are required to
determine the extent of health outcomes attributable solely
to RT and to enable the development of evidence-based
obesity prevention and treatment strategies in this cohort.
Furthermore, further studies with postintervention follow-
ups of at least six months are required in order to assess
whether RT prescriptions can be maintained as part of a
regular lifestyle, and whether improved body composition
can be maintained over longer periods.
2.3. Metabolic Risk Reduction. Epidemiologic studies show
a strong association for obesity with CVD [51]andtype2
diabetes (T2D) [52]. Obesity-induced risk factors such as
plasma cholesterol, elevated plasma glucose, and elevated
blood pressure increase the risk for CVD and have thus
been called the “metabolic complications” of obesity [53].
Published evidence indicates that the risk for CVD associated
with the metabolic syndrome is greater than the sum of
its individual risk factors [54]. Apparent is that improved
glycemic control, decreased fat mass, improved blood lipid
profiles, and decreased blood pressure are important factors
in reducing coronary heart disease (CHD) in people with
metabolic risk.
2.3.1. Dyslipidaemia. At present, a small amount of conflict-
ing data exists on the effects of RT on blood lipid levels in
healthy elderly people, and in patients with dyslipidaemia.
In a recent trial, 131 subjects were randomly assigned to
an RT group, an AET group, a combined RT and AET
group, or a nonexercising control group [55]. Findings
demonstrated that exercise mode did not impact upon
blood lipids. In contrast, total cholesterol (TC), low-density
lipoprotein cholesterol (LDL), and plasma triglyceride (TG)
were significantly lower in all groups. These data are
4Journal of Obesity
comparable with another study that investigated the effects
of RT and AET on metabolic parameters in 60 obese women
[56]. After 20 weeks of training without diet, significant
decreases in TG and TC levels were noted in each of the study
groups. Fahlman et al. demonstrated that both AET and
RT groups experienced increased high-density lipoprotein
cholesterol (HDL-C) and decreased TG at the end of a 10-
week training period in 45 healthy elderly women [57]. The
RT group (at 80% of 1-RM) also had significantly lower LDL-
C and TC compared with controls. These favourable changes
occurred without concurrent changes in weight or diet.
None of the above studies included patients with abnor-
mal lipid profiles. Unfortunately, no information is available
on the effects of RT on subjects with dyslipidaemia. Several
earlier studies examined the relationship between RT and
plasma lipoprotein levels, with mixed results. In one study,
premenopausal women were randomly assigned to an RT
program or a control group for 5 months [58]. The RT
group showed a significant decrease in TC and LDL-C, while
no significant changes were noted in serum HDL-C or TG
levels in either group. Changes in body composition showed
no significant correlations with changes in TC or LDL-C.
Another study determined the effects of 20 weeks of RT
on lipid profiles in sixteen untrained males with abnormal
lipoprotein-lipid levels and at least two other risk factors for
CHD [59]. The training program resulted in no significant
changes in plasma concentrations of TG, TC, and HDL-C.
These results are in agreement with those that determined
the effects of 12 weeks of RT (at 60% to 70% of 1-RM)
on lipoprotein-lipid levels in sixteen sedentary obese women
[60]. In contrast, another study examined the effects of 16
weeks of high-intensity RT on risk factors for CHD in eleven
healthy, untrained males [13]. The RT program resulted in
a 13% increase in HDL-C, a 5% reduction in LDL-C, and
an 8% decrease in the TC/HDL-C ratio, despite not showing
changes in body weight or percent body fat.
These findings indicate that RT has the potential to lower
risk factors for CHD, independent of changes in body weight
or body composition. The results of a prospective study
that focused on lipid and lipoprotein levels in previously
sedentary men and women undergoing 16 weeks of RT
were similar [61]. Women participants demonstrated a 9.5%
reduction of TC, a 17.9% decrease in LDL-C, and a 28.3%
lowering of TG. Among the men, LDL-C was reduced by
16.2%, while the ratios of TC and LDL-C versus HDL-C
were lowered by 21.6% and 28.9%, respectively. Thus, RT
may result in favourable changes in lipid and lipoprotein
levels in previously sedentary men and women. However,
limitations exist; only one of the above-mentioned studies
was conducted with subjects with dyslipidaemia, and no
information is available about the effect of RT on patients
with dyslipidaemia alone.
2.3.2. Type 2 Diabetes. Most available studies relate to AET in
the treatment of insulin resistance (IR) and type 2 diabetes
(T2D). Several systematic reviews focused on the relation-
ship between exercise and/or physical activity and glycemic
control in patients with T2D [62–64]. Results indicated that
physical training significantly improves glycemic control and
reduces visceral adipose tissue and plasma TG in people with
T2D, even without weight loss.
RT has been shown to improve insulin-stimulated glu-
cose uptake in patients with impaired glucose tolerance or
manifest T2D [48]. RT, and subsequent increases in muscle
mass, may improve glucose and insulin responses to a glucose
load in healthy individuals [65,66] and in diabetic men
and women [67,68] and improves insulin sensitivity in
diabetic or insulin-resistant middle-aged and older men and
women [68–71]. In addition, high-intensity RT has been
found to decrease glycosylated haemoglobin (HbA1c) levels
in diabetic men and women, regardless of age [21,22,72–
76].
A recent meta-analysis of 27 randomized controlled trials
examined the effects of different modes of exercise on glucose
control, and risk factors for complications in patients with
T2D [77]. Results demonstrated that differences among the
effects of AET, RT, and combined training on HbA1c were
minor. For training lasting ≥12 weeks, the overall effect was
a small beneficial reduction (HbA1c 0.8% ±0.3%). Aerobic
and combined exercise had small or moderate effects on
blood pressure (BP). All three modes of exercise produced
trivial or unclear effects on blood lipids. The effects of
RT on glycemic control and risk factors associated with
CVD in T2D were small (HbA1c), unclear (BP), or trivial
(blood lipids). Findings supported the notion that combined
training was generally superior to RT alone.
The clinical significance of a 0.5% decrease in HbA1c
can be gauged by examining large prospective intervention
studies investigating morbidity and mortality outcomes in
people with T2D [78]. Data suggests that a 1% rise in HbA1c
represents a 21% increase in risk for any diabetes-related
death, a 14% increased risk for myocardial infarction, and
a 37% increased risk for microvascular complications. The
impact of a decrease of 0.5% HbA1c equates to a 50%
improvement towards a target value of 7% HbA1c, and a
25% improvement towards a normal value of 6% HbA1c, for
a person diagnosed with 8% HbA1c.
It is unclear whether an improvement in glycemic control
can be maintained in the longer term. For example, in the
6-month postintervention follow-up period reported by one
author [79], participants continuing with supervised RT
(at 70% to 80% of 1-RM) maintained the improvement in
glycemic control, whilst in a 6-month home-based follow-up
group, the improvements were lost [80]. The hypothesized
reason for this difference is the difficulty of motivating people
with T2D to maintain RT prescriptions as part of a regular
lifestyle.
In another study [22], the combination of RT (at
70% to 80% of 1-RM) and moderate dietary restriction
was associated with a threefold greater decrease in HbA1c
levels after 6 months compared with moderate weight loss
without RT. This result was not mediated by concomitant
reductions in body weight, waist circumference, and FM.
It is apparent that an increase in LBM after RT may be
an important mediator in improved glycemic control. One
study specifically discussed the effects of an increase in the
number of GLUT4 transporters [48], because the transporter
Journal of Obesity 5
protein GLUT4 expression at the plasma membrane is related
to fibre volume in human skeletal muscle fibres [81]. A
further study found that the improvement in LBM after a 10-
week moderate RT-program had a greater impact on HbA1c
levels than the reduction in FM, suggesting that increases in
muscle mass improved glycemic control [72]. Furthermore,
RT-induced changes in HbA1c have been inversely correlated
with changes in the quadriceps cross-sectional area [71]. It
has been proposed that hyperglycemia has a direct adverse
effect on muscle contractile function and force generation
[82].
A recent meta-analysis sought to investigate the existence
of a dose-response relationship between intensity, duration,
and frequency of RT and the metabolic clustering in patients
with T2D [83]. Findings demonstrated that RT significantly
reduced glycated hemoglobin by 0.48% HbA1c (95% CI: 0.76
to −0.21, P=.0005), fat mass by 2.33 kg (95% CI: −4.71
to 0.04, P=.05), and systolic BP by 6.19 mmHg (95% CI:
1.00 to 11.38, P=.02). There was no statistically significant
effect of RT on TC, HDL-C, LDL-C, TG, and diastolic BP.
It appears that RT regimes of longer duration are most
beneficial, whilst higher intensity more likely has a harmful
effect on glycemic control. The meta-analysis confirmed the
notion that RT does not increase BP (as was once thought),
and that RT may even benefit resting BP. The BP-lowering
effect of RT seems to be independent of weight loss and is
believed to be mediated via reduced sympathetically induced
vasoconstriction in the trained state [84,85]. It should be
noted that a decrease of approximately 6.2mmHg for resting
systolic BP is significant, since a reduction of as little as
3 mmHg in systolic BP has been estimated to reduce CHD
by 5–9%, stroke by 8–14%, and all-cause mortality by 4%
[86]. Progressively higher volumes of RT may reduce resting
systolic BP, and more significantly, diastolic BP. Interpretive
caution is warranted, due to the fact that the above analyses
were based on a limited number of study groups.
3. Prescription of Resistance Training
It is well understood that when performed regularly and
with sufficient intensity, RT stimulates skeletal muscle to
synthesize new muscle proteins (hypertrophy). However,
the effective amount of RT to promote muscle growth in
relatively sedentary diseased or aged individuals is an area in
need of further investigation. It is believed that 1 to 2 sets
of 8 to 12 repetitions per set with an intensity greater that
60% of 1-repetition maximum (1RM—the maximum load
that can be lifted once only throughout a complete range of
motion), with 8 to 10 exercises per session and 2 to 3 sessions
per week, are likely to be beneficial for maximising the health
effects of increased skeletal muscle mass [87]. A recent study
examining the effects of systematic RT in the elderly (76.2±
3.2 years) demonstrated that RT consisting of two training
sessions per week was at least as efficient as RT involving
three trainings sessions per week, provided that the number
of sets performed was equal [88]. These findings contradict
results of a previous study reporting that RT three days per
week elicits superior strength gains when compared with RT
two days per week [89]. However, the latter study was low
volume: higher frequency produced better results. A more
recent review demonstrated that there was no difference in
mean rates of increase in the whole muscle cross-sectional
area between two and three RT sessions per week for longer
periods of training [90]. But, caution is urged on the fact
that the methods (machines, dynamometer) of measuring
muscle strength and expressing it (absolute, relative to body
weight or muscle mass) are not standardized. Thus, the true
increases in muscle strength are difficult to determine in
research protocols. Therefore, to compare results of different
studies, muscle strength should be determined in kilo pound
(kp) or Newton (N; SI unit).
Systematic reviews comparing RT frequencies in patients
with metabolic or cardiovascular risk revealed no apparent
association between RT frequencies and changes in risk
factors for CVD [91,92]. However, it should be noted
that only a few studies were conducted with subjects with
metabolic risk, and most of the included RT studies had
a training frequency of three days per week. Regression-
based analyses from recently performed meta-analysis by
Strasser et al. suggest there is no apparent association
between RT frequency and glycemic control, but indicate a
trend to a negative correlation for some outcomes of lipid
profile in patients with abnormal glucose regulation [83].
The effect of RT on resting systolic BP and diastolic BP
seems to be dose-dependent, since decreases in resting BP
were more pronounced when the RT program was of high
volume. Apparent was that relatively modest increases in
RT frequency had hypotensive effects, since resting BP was
reduced to a greater extent when exercising three times per
week compared to twice a week [83].
On the basis of a combination of literature findings and
in-house laboratory results [21,79,88,93–95], some basic
recommendations for the design of programmes for elderly
adults with metabolic risk based are provided.
(i) During the first two weeks of exercise, the weights
should be kept to a minimal level so that patients
learn the exercise techniques. A minimal weight
allows muscles to adapt to the training and prevents
muscle soreness.
(ii) From the third week, the objective of the training
is hypertrophy. Participants should start with three
sets per muscle group per week, on 3 nonconsecutive
days of the week. One set should consist of 10–
15 repetitions, without interruption, until severe
fatigue occurs and completion of further repetitions
is impossible.
(iii) The training load should be systematically increased
to keep the maximum possible repetitions between
10 to 15 per set. A repetition maximum of 10 to 15
repetitions corresponds with 60–70% 1-RM [15].
(iv) The number of sets for each muscle per week should
be increased progressively every four weeks by one set
to a maximum of 10 sets per week on (Table 1).
6Journal of Obesity
Tab le 1: Systematic adjustment of the weekly RT volume in sets per
muscle group per week (S/MG/W) for improvement in maximum
strength in rehabilitation, health, and leisure sports.
Stage S/MG/W Frequency
11 1-2
22 2
33 2
44 2
56 2-3
68 2-3
710 2-3
BG: Blood glucose
HbA1c: Glycated hemoglobin
TC: Total cholesterol
HDL-C: High-density lipoprotein cholesterol
LDL-C: Low-density lipoprotein cholesterol
TG: Plasma triglyceride
−40
−30
−20
−10
0
10
20 BG HbA1C TC HDL-C TGLDL-C
−28
−15
0.4
−4.6
−11.3
−11
.6
10.5
2.4
−11.9
−5.4
−34.5
−0.4
Figure 1: Percent change in metabolic parameters after 4 months
RT (black) or AET (white) in patients with T2D. Whiskers represent
standard deviation [18].
(v) The RT program should consist of exercises for all
major muscle groups. Exercises to strengthen the
upper body could include bench press (pectoralis),
chest cross (horizontal flexion of the shoulder joint),
shoulder press (trapezius), pull downs (latissimus
dorsi), bicep curls, tricep extensions, and exercises for
abdominal muscles (sit-ups). Lower body exercises
could include leg press (quadriceps femoris).
4. Conclusions
Based on this review of the literature, there is a strong
support for the notion that RT is at least as effective as AET
in reducing some major cardiovascular disease risk factors
(Figure 1). Findings demonstrate that RT may be an effective
alternative to improve body composition and maintain
reduced FM in obese patients after exercise training or energy
intake restriction. Furthermore, it has been shown that
RT preferentially mobilizes the visceral and subcutaneous
adipose tissue in the abdominal region. There is now sub-
stantial support for RT decreasing glycosylated hemoglobin
levels in people with an abnormal glucose metabolism and
improves tendency lipoprotein-lipid profiles. Decreased fat
mass, improved glycemic control and blood lipid profiles
are important for reducing microvascular and macrovascular
complications in people with metabolic risk. On this basis,
RT is considered a potential adjunct in the treatment of
metabolic disorders by decreasing known major risk factors
for metabolic syndromes. As such, RT is recommended in the
management of obesity and metabolic disorders.
Conflict of Interests
The authors have no conflict of interests that are directly
relevant to the content of this original research paper.
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