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Optimized body composition provides a competitive advantage in a variety of sports. Weight reduction is common among athletes aiming to improve their strength-to-mass ratio, locomotive efficiency, or aesthetic appearance. Energy restriction is accompanied by changes in circulating hormones, mitochondrial efficiency, and energy expenditure that serve to minimize the energy deficit, attenuate weight loss, and promote weight regain. The current article reviews the metabolic adaptations observed with weight reduction and provides recommendations for successful weight reduction and long term reduced-weight maintenance in athletes.
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R E V I E W Open Access
Metabolic adaptation to weight loss: implications
for the athlete
Eric T Trexler
, Abbie E Smith-Ryan
and Layne E Norton
Optimized body composition provides a competitive advantage in a variety of sports. Weight reduction is common
among athletes aiming to improve their strength-to-mass ratio, locomotive efficiency, or aesthetic appearance.
Energy restriction is accompanied by changes in circulating hormones, mitochondrial efficiency, and energy
expenditure that serve to minimize the energy deficit, attenuate weight loss, and promote weight regain. The
current article reviews the metabolic adaptations observed with weight reduction and provides recommendations
for successful weight reduction and long term reduced-weight maintenance in athletes.
Keywords: Weight loss, Energy restriction, Body composition, Energy expenditure, Metabolic rate, Energy deficit,
Weight maintenance, Uncoupling proteins, Mitochondrial efficiency
In a variety of competitive sports, it is considered advan-
tageous to achieve low levels of body fat while retaining
lean body mass. The metabolic effects of this process
have been given little context within athletics, such as
physique sports (i.e. bodybuilding, figure), combat sports
(i.e. judo, wrestling), aesthetic sports (i.e. gymnastics,
figure skating), and endurance sports. Previous literature
has documented cases of male bodybuilders reducing
body fat to less than 5% of total body mass [1,2], and
studies documenting physiological profiles of male wres-
tlers [3] and judo athletes [4] present body fat ranges
that extend below 5%. A study on elite female gymnasts
and runners reported an average body fat percentage
(BF%) of 13.72% for the entire sample, with subgroups
of middle-distance runners and artistic gymnasts aver-
aging 12.18% and 12.36%, respectively [5]. Elite female
runners have also reported percent body fat levels below
10% [6]. Energy deficits and extremely low levels of body
fat present the body with a significant physiological chal-
lenge. It has been well documented that weight loss and
energy restriction result in a number of homeostatic
metabolic adaptations aimed at decreasing energy ex-
penditure, improving metabolic efficiency, and increasing
cues for energy intake [7-9]. While the unfavorable endo-
crine effects of contest preparation have been documented
in male bodybuilders [1,2,10], anecdotal reports from phys-
ique athletes also describe a state in which metabolic rate
has slowed to an extent that exceeds the predicted magni-
tude, making weight loss increasingly difficult despite low
caloric intakes and high training volumes. Although such
reports could potentially be related to inaccurate dietary
reporting [11,12], these claims may be substantiated by a
number of metabolic adaptations to weight loss, including
adaptive thermogenesis [13-15], increased mitochondrial
efficiency [16-19], and hormonal alterations that favor
decreased energy expenditure, decreased satiety, and in-
creased hunger [1,2,10]. As a dieting phase progresses,
such adaptations may threaten dietary adherence, make
further weight loss increasingly difficult, and predispose
the individual to rapid weight regain following the cessa-
tion of the diet. Although data documenting the attain-
ment and recovery from extreme changes in body
composition is limited, the present article aims to investi-
gate the condition of metabolic adaptation described by
competitors and identify potential mechanisms to explain
such a phenomenon.
The endocrine response to an energy deficit
A number of hormones play prominent roles in the
regulation of body composition, energy intake, and en-
ergy expenditure. The hormones of the thyroid gland,
* Correspondence:
Department of Exercise and Sport Science, University of North Carolina at
Chapel Hill, 209 Fetzer Hall, CB# 8700, Chapel Hill, NC 27599-8700, USA
Full list of author information is available at the end of the article
© 2014 Trexler et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (, which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain
Dedication waiver ( applies to the data made available in this article,
unless otherwise stated.
Trexler et al. Journal of the International Society of Sports Nutrition 2014, 11:7
particularly triiodothyronine (T3), are known to play an
important and direct role in regulating metabolic rate.
Increases in circulating thyroid hormones are associated
with an increase in the metabolic rate, whereas lowered
thyroid levels result in decreased thermogenesis and
overall metabolic rate [20]. Leptin, synthesized primarily
in adipocytes, functions as an indicator of both short
and long-term energy availability; short-term energy
restriction and lower body fat levels are associated with
decreases in circulating leptin. Additionally, higher con-
centrations of leptin are associated with increased satiety
and energy expenditure [21]. Insulin, which plays a cru-
cial role in inhibiting muscle protein breakdown [22]
and regulating macronutrient metabolism, is considered
another adiposity signal[23]. Similar to leptin, high
levels of insulin convey a message of energy availability
and are associated with an anorexigenic effect. Con-
versely, the orexigenic hormone ghrelin functions to
stimulate appetite and food intake, and has been shown
to increase with fasting, and decrease after feeding [24].
Testosterone, known primarily for its role in increasing
muscle protein synthesis and muscle mass [22], may also
play a role in regulating adiposity [25]. Changes in fat
mass have been inversely correlated with testosterone
levels, and it has been suggested that testosterone may
repress adipogenesis [25]. More research is needed to
delineate the exact mechanism (s) by which testosterone
affects adiposity. Cortisol, a glucocorticoid that influ-
ences macronutrient metabolism, has been shown to
induce muscle protein breakdown [22], and increased
plasma cortisol within the physiologic range has in-
creased proteolysis in healthy subjects [26]. Evidence
also suggests that glucocorticoids may inhibit the action
of leptin [27].
Results from a number of studies indicate a general
endocrine response to hypocaloric diets that promotes
increased hunger, reduces metabolic rate, and threatens
the maintenance of lean mass. Studies involving energy
restriction, or very low adiposity, report decreases in
leptin [1,10,28], insulin [1,2], testosterone [1,2,28], and thy-
roid hormones [1,29]. Subsequently, increases in ghrelin
[1,10] and cortisol [1,30,31] have been reported with en-
ergy restriction. Further, there is evidence to suggest that
unfavorable changes in circulating hormone levels persist
as subjects attempt to maintain a reduced body weight,
even after the cessation of active weight loss [32,33].
Low energy intake and minimal body fat are perceived
as indicators of energy unavailability, resulting in a
homeostatic endocrine response aimed at conserving en-
ergy and promoting energy intake. It should be noted
that despite alterations in plasma levels of anabolic and
catabolic hormones, losses of lean body mass (LBM)
often fail to reach statistical significance in studies on
bodybuilding preparation [1,2]. Although the lack of
significance may relate to insufficient statistical power,
these findings may indicate that unfavorable, hormone-
mediated changes in LBM can potentially be attenuated
by sound training and nutritional practices. Previous re-
search has indicated that structured resistance training
[34] and sufficient protein intake [35-37], both com-
monly employed in bodybuilding contest preparation,
preserve LBM during energy restriction. Further, Maestu
et al. speculate that losses in LBM are dependent on the
magnitude of weight loss and degree of adiposity, as the
subjects who lost the greatest amount of weight and
achieved the lowest final body fat percentage in the study
saw the greatest losses of LBM [2]. The hormonal envir-
onment created by low adiposity and energy restriction
appears to promote weight regain and threaten lean mass
retention, but more research is needed to determine the
chronic impact of these observed alterations in circulat-
ing anabolic and catabolic hormones.
Weight loss and metabolic rate
An individuals total daily energy expenditure (TDEE)
is comprised of a number of distinct components
(Figure 1). The largest component, resting energy ex-
penditure (REE), refers to the basal metabolic rate
(BMR) [8]. The other component, known as non-resting
energy expenditure (NREE), can be further divided into
exercise activity thermogenesis (EAT), non-exercise ac-
tivity thermogenesis (NEAT), and the thermic effect of
food (TEF) [8].
Figure 1 Components of total daily energy expenditure (TDEE).
BMR = basal metabolic rate; NEAT = non-exercise activity thermogenesis;
TEF = thermic effect of food; EAT = exercise activity thermogenesis;
REE = resting energy expenditure; NREE = non-resting energy
expenditure. Adapted from Maclean et al., 2011.
Trexler et al. Journal of the International Society of Sports Nutrition 2014, 11:7 Page 2 of 7
Metabolic rate is dynamic in nature, and previous lit-
erature has shown that energy restriction and weight
loss affect numerous components of energy expenditure.
In weight loss, TDEE has been consistently shown to de-
crease [38,39]. Weight loss results in a loss of metabolic-
ally active tissue, and therefore decreases BMR [38,39].
Interestingly, the decline in TDEE often exceeds the
magnitude predicted by the loss of body mass. Previous
literature refers to this excessive drop in TDEE as adap-
tive thermogenesis, and suggests that it functions to pro-
mote the restoration of baseline body weight [13-15].
Adaptive thermogenesis may help to partially explain the
increasing difficulty experienced when weight loss plat-
eaus despite low caloric intake, and the common pro-
pensity to regain weight after weight loss.
Exercise activity thermogenesis also drops in response
to weight loss [40-42]. In activity that involves locomo-
tion, it is clear that reduced body mass will reduce the
energy needed to complete a given amount of activity.
Interestingly, when external weight is added to match
the subjects baseline weight, energy expenditure to
complete a given workload remains below baseline [41].
It has been speculated that this increase in skeletal
muscle efficiency may be related to the persistent
hypothyroidism and hypoleptinemia that accompany
weight loss, resulting in a lower respiratory quotient and
greater reliance on lipid metabolism [43].
The TEF encompasses the energy expended in the
process of ingesting, absorbing, metabolizing, and stor-
ing nutrients from food [8]. Roughly 10% of TDEE is at-
tributed to TEF [44,45], with values varying based on the
macronutrient composition of the diet. While the rela-
tive magnitude of TEF does not appear to change with
energy restriction [46], such dietary restriction involves
the consumption of fewer total calories, and therefore
decreases the absolute magnitude of TEF [41,46]. NEAT,
or energy expended during non-exercisemovement
such as fidgeting or normal daily activities, also de-
creases with an energy deficit [47]. There is evidence to
suggest that spontaneous physical activity, a component
of NEAT, is decreased in energy restricted subjects, and
may remain suppressed for some time after subjects re-
turn to ad libitum feeding [29]. Persistent suppression
of NEAT may contribute to weight regain in the post-
diet period.
In order to manipulate an individuals body mass, en-
ergy intake must be adjusted based on the individuals
energy expenditure. In the context of weight loss or
maintaining a reduced body weight, this process is com-
plicated by the dynamic nature of energy expenditure. In
response to weight loss, reductions in TDEE, BMR, EAT,
NEAT, and TEF are observed. Due to adaptive thermo-
genesis, TDEE is lowered to an extent that exceeds the
magnitude predicted by losses in body mass. Further,
research indicates that adaptive thermogenesis and de-
creased energy expenditure persist after the active weight
loss period, even in subjects who have maintained a re-
duced body weight for over a year [14,48]. These changes
serve to minimize the energy deficit, attenuate further loss
of body mass, and promote weight regain in weight-
reduced subjects.
Adaptations in mitochondrial efficiency
A series of chemical reactions must take place to derive
ATP from stored and ingested energy substrates. In aer-
obic metabolism, this process involves the movement
of protons across the inner mitochondrial membrane.
When protons are transported by ATP synthase, ATP is
produced. Protons may also leak across the inner mem-
brane by way of uncoupling proteins (UCPs) [49]. In this
uncoupled respiration, energy substrate oxidation and
oxygen consumption occur, but the process does not
yield ATP. Proton leak is a significant contributor to
energy expenditure, accounting for roughly 20-30% of
BMR in rats [50-52].
In the condition of calorie restriction, proton leak is
reduced [16-19]. Uncoupling protein-1 and UCP-3, the
primary UCPs of brown adipose tissue (BAT) and skel-
etal muscle [53], are of particular interest due to their
potentially significant roles in energy expenditure and
uncoupled thermogenesis. Skeletal muscles large contri-
bution to energy expenditure [54] has directed attention
toward literature reporting decreases in UCP-3 expres-
sion in response to energy restriction [55,56]. Decreased
UCP-3 expression could potentially play a role in de-
creasing energy expenditure, and UCP-3 expression has
been negatively correlated with body mass index and
positively correlated with metabolic rate during sleep
[57]. Despite these correlations, more research is needed
to determine the function and physiological relevance of
UCP-3 [58], as contradictory findings regarding UCP-3
and weight loss have been reported [18].
Uncoupling Protein-1 appears to play a pivotal role in
the uncoupled thermogenic activity of BAT [59]. Energy
restriction has been shown to decrease BAT activation
[60] and UCP-1 expression [61], indicating an increase
in metabolic efficiency. Along with UCP-1 expression,
thyroid hormone and leptin affect the magnitude of
uncoupled respiration in BAT. Thyroid hormone (TH)
and leptin are associated with increased BAT activation,
whereas glucocorticoids oppose the BAT-activating func-
tion of leptin [59]. Evidence indicates that TH plays a
prominent role in modulating the magnitude of proton
leak [53], with low TH levels associated with decreased
proton leak [62]. The endocrine response to energy re-
striction, including increased cortisol and decreased TH
and leptin [1,10,28-31], could potentially play a regula-
tory role in uncoupled respiration in BAT. It is not clear
Trexler et al. Journal of the International Society of Sports Nutrition 2014, 11:7 Page 3 of 7
if decreases in proton leak and UCP expression persist
until weight reverts to baseline, but there is evidence to
suggest a persistent adaptation [19,55,56], which mirrors
the persistent downregulation of TH and leptin [32,33].
Changes observed in proton leak, UCP expression, and
circulating hormones appear to influence metabolic effi-
ciency and energy expenditure. In the context of energy
restriction, the observed changes are likely to make
weight loss increasingly challenging and promote weight
regain. It has been reported that females have more BAT
than males [63], and that energy-restricted female rats
see greater decreases in BAT mass and UCP-1 than
males [64], indicating a potential sex-related difference
in uncoupled respiration during weight loss. Subjects
identified as diet-resistantshow decreased proton leak
and UCP-3 expression compared to diet-responsive
subjects during maintenance of a reduced bodyweight
[65]. More research is needed to determine if these dif-
ferential responses to hypocaloric diets make sustained
weight loss more difficult for females and certain predis-
posed diet-resistantindividuals. While future research
may improve our understanding of the magnitude and
relative importance of mitochondrial adaptations to en-
ergy restriction, current evidence suggests that increased
mitochondrial efficiency, and a decline in uncoupled res-
piration, might serve to decrease the energy deficit in
hypocaloric conditions, making weight maintenance and
further weight reduction more challenging.
Practical applications for weight loss in athletes
Hypocaloric diets induce a number of adaptations that
serve to prevent further weight loss and conserve energy.
It is likely that the magnitude of these adaptations are
proportional to the size of the energy deficit, so it is rec-
ommended to utilize the smallest possible deficit that
yields appreciable weight loss. This may decrease the
rate of weight loss, but attenuate unfavorable adapta-
tions that challenge successful reduction of fat mass.
Weight reduction should be viewed as a stepwise
process in this context; as weight loss begins to plateau,
energy intake or expenditure should be adjusted to
re-opentheenergydeficit.Large caloric deficits are
also likely to induce greater losses of LBM [66,67] and
compromise athletic performance and recovery [68,69],
which are of critical importance to athletes. Participation
in a structured resistance training program [34] and suffi-
cient protein intake [35-37] are also likely to attenuate
losses in LBM. Additionally, high protein diets (25%
PRO) are associated with increased satiety and thermo-
genesis, making them a better option for the calorie-
restricted athlete [70].
In the world of physique sports, periodic refeeding
has become common in periods of extended dieting. A
refeed consists of a brief overfeeding period in which
caloric intake is raised slightly above maintenance levels,
and the increase in caloric intake is predominantly
achieved by increasing carbohydrate consumption. While
studies have utilized refeeding protocols that last three
days [71,72], physique athletes such as bodybuilders and
figure competitors often incorporate 24-hour refeeds,
once or twice per week. The proposed goal of periodic
refeeding is to temporarily increase circulating leptin and
stimulate the metabolic rate. There is evidence indicating
that leptin is acutely responsive to short-term overfeed-
ing [72], is highly correlated with carbohydrate intake
[71,73], and that pharmacological administration of lep-
tin reverses many unfavorable adaptations to energy re-
striction [33]. While interventions have shown acute
increases in leptin from short-term carbohydrate over-
feeding, the reported effect on metabolic rate has been
modest [71]. Dirlewanger et al. reported a 7% increase in
TDEE; this increase amounts to approximately 138 kilo-
calories of additional energy expenditure, of which 36
kilocalories can be attributed to the thermic effect of
carbohydrate intake [71]. More research is needed to de-
termine if acute bouts of refeeding are an efficacious
strategy for improving weight loss success during pro-
longed hypocaloric states. A theoretical model of meta-
bolic adaptation and potential strategies to attenuate
adaptations is presented in Figure 2.
In the period shortly after cessation of a restrictive
diet, body mass often reverts toward pre-diet values
[29,74,75]. This body mass is preferentially gained as fat
mass, in a phenomenon known as post-starvation obes-
ity [29]. While many of the metabolic adaptations to
weight loss persist, a dramatic increase in energy intake
results in rapid accumulation of fat mass. It is common
for individuals to overshoottheir baseline level of body
fat, and leaner individuals (including many athletes) may
be more susceptible to overshooting than obese individ-
uals [74,75]. In such a situation, the individual may
increase body fat beyond baseline levels, yet retain a
metabolic rate that has yet to fully recover. There is evi-
dence to suggest that adipocyte hyperplasia may occur
early in the weight-regain process [76], and that repeated
cycles of weight loss and regain by athletes in sports
with weight classes are associated with long-term weight
gain [77]. Therefore, athletes who aggressively diet for a
competitive season and rapidly regain weight may find it
more challenging to achieve optimal body composition
in subsequent seasons.
To avoid rapid fat gain following the cessation of a
diet, reverse dietinghas also become popular among
physique athletes. Such a process involves slowly in-
creasing caloric intake in a stepwise fashion. In theory,
providing a small caloric surplus might help to restore
circulating hormone levels and energy expenditure
toward pre-diet values, while closely matching energy
Trexler et al. Journal of the International Society of Sports Nutrition 2014, 11:7 Page 4 of 7
intake to the recovering metabolic rate in an effort to re-
duce fat accretion. Ideally, such a process would eventu-
ally restore circulating hormones and metabolic rate to
baseline levels while avoiding rapid fat gain. While anec-
dotal reports of successful reverse dieting have led to an
increase in its popularity, research is needed to evaluate
its efficacy.
Although there is a substantial body of research on
metabolic adaptations to weight loss, the majority of the
research has utilized animal models or subjects that
are sedentary and overweight/obese. Accordingly, the
current article is limited by the need to apply this data
to an athletic population. If the adaptations described in
obese populations serve to conserve energy and attenu-
ate weight loss as a survival mechanism, one might
speculate that the adaptations may be further augmented
in a leaner, more highly active population. Another limi-
tation is the lack of research on the efficacy of periodic
refeeding or reverse dieting in prolonged weight reduc-
tion, or in the maintenance of a reduced bodyweight.
Until such research is available, these anecdotal methods
can only be evaluated from a mechanistic and theoretical
Weight loss is a common practice in a number of sports.
Whether the goal is a higher strength-to-mass ratio,
improved aesthetic presentation, or more efficient loco-
motion, optimizing body composition is advantageous to
a wide variety of athletes. As these athletes create an en-
ergy deficit and achieve lower body fat levels, their
weight loss efforts will be counteracted by a number
of metabolic adaptations thatmaypersistthroughout
weight maintenance. Changes in energy expenditure,
Figure 2 A theoretical model of metabolic adaptation and potential strategies to attenuate adaptations. A/A/T hormones = Anabolic,
Anorexigenic, and Thermogenic hormones; O/C hormones =Orexigenic and Catabolic hormones. Dotted lines represent inhibition.
Trexler et al. Journal of the International Society of Sports Nutrition 2014, 11:7 Page 5 of 7
mitochondrial efficiency, and circulating hormone con-
centrations work in concert to attenuate further weight
loss and promote the restoration of baseline body mass.
Athletes must aim to minimize the magnitude of these
adaptations, preserve LBM, and adequately fuel perform-
ance and recovery during weight reduction. To accom-
plish these goals, it is recommended to approach weight
loss in a stepwise, incremental fashion, utilizing small en-
ergy deficits to ensure a slow rate of weight loss. Partici-
pation in a structured resistance training program and
adequate protein intake are also imperative. More re-
search is needed to verify the efficacy of periodic refeed-
ing and reverse dieting in supporting prolonged weight
reduction and attenuating post-diet fat accretion.
BAT: Brown adipose tissue; BF%: Body fat percentage; BMR: Basal metabolic
rate; EAT: Exercise activity the rmoge nesis; LBM: Le an body mass;
NEAT: Non-exercise activity thermogenesis; NREE: Non-resting energy
expenditure; REE: Resting energy expenditure; TDEE: Total daily energy
expenditure; TEF: Thermic effect of food; TH: Thyroid Hormone;
T3: Triiodothyronine; UCP: Uncoupling protein.
Competing interests
The authors declare that they have no competing interests.
ETT conceived of the review topic and drafted the manuscript. AES
conceived, drafted and revised the manuscript. LEN helped to draft and
revise the manuscript. All authors read and approved the final manuscript.
Author details
Department of Exercise and Sport Science, University of North Carolina at
Chapel Hill, 209 Fetzer Hall, CB# 8700, Chapel Hill, NC 27599-8700, USA.
BioLayne LLC, Tampa, FL, USA.
Received: 18 December 2013 Accepted: 20 February 2014
Published: 27 February 2014
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Cite this article as: Trexler et al.:Metabolic adaptation to weight loss:
implications for the athlete. Journal of the International Society of Sports
Nutrition 2014 11:7.
Trexler et al. Journal of the International Society of Sports Nutrition 2014, 11:7 Page 7 of 7
... 151 Accordingly, it is well established that problematic LEA can result in energy conservation reflected in reduced RMR. 152 While some studies have reported lower RMR in athletes with apparent LEA compared with healthy counterparts, 62 153 154 others have failed to demonstrate this. 81 130 155 156 Challenges relating to the precise measurement of RMR include poor global availability of the method, high variability with poor measurement validity and reliability, lack of athlete-specific and sport-specific prediction equations and lack of consensus on which thresholds of RMR (absolute or ratio) constitute increased risk. ...
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Relative Energy Deficiency in Sport (REDs) has various different risk factors, numerous signs and symptoms and is heavily influenced by one’s environment. Accordingly, there is no singular validated diagnostic test. This 2023 International Olympic Committee’s REDs Clinical Assessment Tool—V.2 (IOC REDs CAT2) implements a three-step process of: (1) initial screening; (2) severity/risk stratification based on any identified REDs signs/symptoms (primary and secondary indicators) and (3) a physician-led final diagnosis and treatment plan developed with the athlete, coach and their entire health and performance team. The CAT2 also introduces a more clinically nuanced four-level traffic-light (green, yellow, orange and red) severity/risk stratification with associated sport participation guidelines. Various REDs primary and secondary indicators have been identified and ‘weighted’ in terms of scientific support, clinical severity/risk and methodological validity and usability, allowing for objective scoring of athletes based on the presence or absence of each indicator. Early draft versions of the CAT2 were developed with associated athlete-testing, feedback and refinement, followed by REDs expert validation via voting statements (ie, online questionnaire to assess agreement on each indicator). Physician and practitioner validity and usability assessments were also implemented. The aim of the IOC REDs CAT2 is to assist qualified clinical professionals in the early and accurate diagnosis of REDs, with an appropriate clinical severity and risk assessment, in order to protect athlete health and prevent prolonged and irreversible outcomes of REDs.
... restriction may be marked by new short-term obstacles affecting the commitment to the process. The obstacles can include a significant increase in hunger and metabolic adaptations(CUMMINGS et al., 2002; MACLEAN et al., 2011; SUMITHRAN et al., 2015; DHURANDHAR et al., 2016;MELANSON et al., 2013), increase in stress levels and hormonal imbalance(ROSSOW et al., 2013;TREXLER et al., 2017TREXLER et al., , 2014, worsening sleep quality(PARDUE et al., 2017), and menstrual irregularities in female athletes(HALLIDAY et al., 2016; HULMI et al., 2017).The significant metabolic adaptations that occur through successive adjustments aiming to maintain the caloric deficit over time create a "low energy availability" situation, a scientific concept that describes the low energy amount available for essential metabolic functions(LOGUE et al., 2020;LOUCKS et al., 2011;NATTIV et al., 2007). Possible alternatives to overcome this through nutritional adjustments generating greater satiety(ELLO-MARTIN et al., 2005;HALTON and HU, 2004; HANSEN et al., 2019; HOWARTH et al., 2001) and training adjustments, including caloric maintenance periods (intermittent diet) and rest(BYRNE et al., 2018;PEOS et al., 2019;ROBERTS et al., 2020) is a possibility. ...
Conference Paper
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There are diverse reasons for weight loss, from aesthetic issues to medical needs. The world is experiencing an obesity epidemic, evidenced by a global increase in trending cases, so must be treated as a public health problem. Although the requirement for weight loss is consuming consistently fewer calories than you burn over time, there are confusion and conflicting information on how to go about doing this. It occurs in a dynamic and changeable environment, involving behavioral, psychological, and motivational aspects. Obstacles appear along the way, making adherence difficult. There is no structured and systematic way in the literature to approach this process scientifically. The objective of this article is to propose a systematic model for weight loss management, applying the improvement kata approach. As for the research methods, was made a qualitative research, with bibliographic search consulting databases MEDLINE(Pubmed), SCOPUS, Artigo Completo 2 Emerald, and books, guiding the model's construction. Using information technology, 9 experts with experience in different areas received an explanatory text for the model evaluation. The analysis' consolidation shows 100% consensus regarding the model's consistency, with 44% claiming using something similar in their practice. Therefore, this study evidences a structured and systematic approach for weight loss management.
... Conversely, previous work has proposed that fat-free mass is the largest contributor to RMR [8,9]. The varying degrees of influence on RMR from body composition parameters may have important implications for weight loss interventions [10], body composition goals [11], and the selection of appropriate RMR-prediction equations [1]. ...
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The purpose of this study was to examine sex differences in resting metabolic rate (RMR) and associations between measured RMR and body composition parameters in athletes. One-hundred and ninety collegiate men (n = 98; age: 20.1 ± 1.6 yr.; body mass: 92.7 ± 17.5 kg; height: 181.6 ± 6.2 cm, body mass index: 28.0 ± 4.7 kg/m2) and women (n = 92; age: 19.4 ± 1.1 yr.; body mass: 65.2 ± 11.0 kg; height: 168.0 ± 6.6 cm, body mass index: 23.0 ± 3.6 kg/m2) athletes volunteered to participate in this study. Athletes completed a body composition assessment using air displacement plethysmography and RMR using indirect calorimetry. Assessments were completed in a fasted state and after refraining from intense physical activity > 24 h prior to testing. Data were collected during the 2016–2019 seasons. Men had a higher RMR compared to women (2595 ± 433 vs. 1709 ± 308 kcals; p < 0.001); however, when adjusted for body mass (p = 0.064) and fat-free mass (p = 0.084), the observed differences were not significant. Height, body mass, body mass index, fat-free mass, and fat mass were positively associated with RMR in both men and women athletes (r = 0.4–0.8; p < 0.001). Body mass (men: β = 0.784; women: β = 0.832)) was the strongest predictor of RMR. Men athletes have a higher absolute RMR compared to their women counterparts, which is influenced by greater body mass and fat-free mass. Body mass is the strongest predictor of RMR in both men and women athletes.
... The placebo group results contrast other studies, where RMR had significantly decreased after weight loss attempts [64,65]. This difference can be attributed to the small energy deficit of the prescribed diets in the present study, combined with the study's short intervention period [66]. In overweight premenopausal women, metabolic adaptation (i.e., a decrease in RMR at the end of the diet) has been shown to delay the time needed to achieve weight loss goals [67]. ...
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Evidence of the effectiveness of zinc (Zn) and selenium (Se) on resting metabolic rate (RMR) and physical function parameters in people with overweight and obesity is scarce, while the effects of zinc and selenium on thyroid function and body composition are still a topic of debate and controversy. The aim of this randomized, double-blind, and placebo-controlled trial was to examine the effects of a hypocaloric diet and Se-Zn co-supplementation on RMR, thyroid function, body composition, physical fitness, and functional capacity in overweight or obese individuals. Twenty-eight overweight-obese participants (mean BMI: 29.4 ± 4.7) were randomly allocated (1:1) to the supplementation group (n = 14, 31.1 ± 5.5 yrs, 9 females) and the placebo group (n = 14, 32.1 ± 4.8 yrs, 6 females). The participants received Zn (25 mg of zinc gluconate/day) and Se (200 mcg of L-selenomethionine/day) or placebo tablets containing starch for eight weeks. The participants of both groups followed a hypocaloric diet during the intervention. RMR, thyroid function, body composition, cardiorespiratory fitness (VO2max), and functional capacity (sit-to-stand tests, timed up-and-go test, and handgrip strength) were assessed before and after the intervention. A significant interaction was found between supplementation and time on RMR (p = 0.045), with the intervention group's RMR increasing from 1923 ± 440 to 2364 ± 410 kcal/day. On the other hand, no interaction between supplementation and time on the thyroid function was found (p > 0.05). Regarding the effects of Zn/Se co-administration on Se levels, a significant interaction between supplementation and time on Se levels was detected (p = 0.004). Specifically, the intervention group's Se serum levels were increased from 83.04 ± 13.59 to 119.40 ± 23.93 μg/L. However, Zn serum levels did not change over time (90.61 ± 23.23 to 89.58 ± 10.61 umol/L). Even though all body composition outcomes improved in the intervention group more than placebo at the second measurement, no supplement × time interaction was detected on body composition (p > 0.05). Cardiorespiratory fitness did not change over the intervention. Yet, a main effect of time was found for some functional capacity tests, with both groups improving similarly over the eight-week intervention period (p < 0.05). In contrast, a supplement x group interaction was found in the performance of the timed up-and-go test (TUG) (p = 0.010), with the supplementation group improving more. In conclusion, an eight-week intervention with Zn/Se co-supplementation combined with a hypocaloric diet increased the RMR, TUG performance, and Se levels in overweight and obese people. However, thyroid function, Zn levels, body composition, and the remaining outcomes of exercise performance remained unchanged.
... Emerging evidence, however, suggests that when it comes to diet, relying solely on a calorie deficit may not be sufficient for long-term weight control [3]. Maintaining a calorie deficit is often challenging and can result in a reduction in metabolic rate, which may lead to weight regain [4,5]. Moreover, it is now recognized that the types and timing of food intake may have different metabolic effects on the body and influence the effectiveness of weight loss efforts [6][7][8]. ...
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This scoping review assessed the knowledge, attitudes, and practices of general practitioners (GPs) regarding dietary advice for weight management. A systematic search of PubMed, EMBASE, CINAHL, and MEDLINE was conducted for any qualitative, quantitative, and mixed-methods studies published in the past five years that informed GPs’ dietary advice for weight control. Thirteen studies were included in the analysis after screening 881 papers. These studies tended to focus mostly on GPs’ practices rather than their knowledge and attitudes. The most frequently mentioned dietary advice was to reduce calorie intake; however, 32 different types of dietary advice were identified in the literature, including approaches such as intermittent fasting and a ketogenic diet that are not recommended in current guidelines. GPs showed varying levels of knowledge and attitudes regarding the best dietary advice for patients. Further research is needed to better understand GP perspectives, with efforts to assist GPs in providing tailored advice based on the latest evidence to improve patient outcomes required.
Multi-ingredient thermogenic supplements can acutely increase resting energy expenditure (REE) and subjective energy. However, less is understood about the effects of chronic consumption on body composition, metabolism, and subjective variables such as mood, sleep quality, and eating behaviors. Fifty-two healthy, exercise-trained participants (50% female; mean ± SD age: 23.5 ± 3.0 years; body fat percentage: 27.3 ± 8.0%) were randomized 2:2:1 to take a whey protein supplement alone (PRO; n = 20), in combination with a thermogenic supplement (PRO + FB; n = 19), or no supplement at all (CON; n = 13) for four weeks. Body composition, anthropometric, metabolic, hemodynamic, and subjective outcomes were collected before and after the intervention. Greater changes in REE occurred in PRO + FB as compared to CON (111.2 kcal/d, 95% CI 2.4 to 219.9 kcal/d, p = 0.04), without significant differences between PRO and CON (42.7 kcal/d, 95% CI −65.0 to 150.3 kcal/d, p = 0.61) or between PRO + FB and PRO (68.5 kcal/d, 95% CI −28.3, 165.3, p = 0.21). No changes in hemodynamic outcomes (blood pressure and heart rate) were observed. In exercising adults, four weeks of supplementation with protein and a multi-ingredient thermogenic product maintained fasted REE as compared to no supplementation, for which a decrease in REE was observed, without differential effects on body composition, anthropometrics, or subjective variables.
El entrenamiento deportivo es fundamental a través de la preparación de los deportistas y más aún cuando se trabaja a determinadas alturas sobre el nivel del mar, de esta manera en la presente investigación se fundamentó en realizar un trabajo de adaptación en altitud con deportistas de atletismo paralímpicos y caracterizar esta población deportiva, ya que son escasos los estudios en la literatura, desarrollando inicialmente un protocolo de laboratorio sobre un ergómetro estera sin fin, con análisis de gases directo para conocer sus características fisiológicas, participaron 6 sujetos con discapacidad visual de la Liga de atletismo de Cundinamarca, donde 4 fueron de género masculino y 2 femenino, a partir de este momento dio inicio a un plan de entrenamiento en altura, el cual se continua trabajando, ya que la investigación está en curso y una duración de 6 meses, con sesiones específicas con hipoxia ante el esfuerzo físico y adaptaciones con el fin de optimizar el rendimiento de los atletas, encontrando resultados tomados en el laboratorio de fisiología del ejercicio de la Unidad Ciencias del Deporte de Bogotá (UCAD), se han determinado valores medios del Volumen Máximo de Oxígeno consumido durante el esfuerzo (VO2 máx.) de 52,5 ± 7,71, una frecuencia cardiaca máxima de 174,5 ± 3,94 ppm y una velocidad de desplazamiento de 14,25 ± 1,90 km/h, de esta manera se ha logrado caracterizar a los deportistas, encontrando variables muy altas y favorables para esta modalidad deportiva, teniendo en cuenta su condición de discapacidad.
Yeme bozuklukları; düzensiz yeme davranışlarıyla başlayabilen, çeşitli sebeplerle ortaya çıkabilen, ciddi komplikasyonlara yol açabilen ve yüksek mortalite oranına sahip psikiyatrik bozukluklardır. Adölesan dönemde görülen beden-benlik ilişkisi, fiziksel ve sosyal olarak kabul görme/beğenilme arzusu yeme bozukluğunu artıran risk faktörlerindendir. Sporculuktaki mükemmeliyetçilik ve rekabetçilik durumu adölesan dönemle birleştiğinde bu oran çok daha fazla artmaktadır. Özellikle adölesan sporcularda; bedensel imaj kaygıları, takım arkadaşlarıyla kıyas, kaslı olma, zayıf görünme, başarı beklentisi, aile/çevre/antrenör baskısı gibi çok çeşitli endişeler sebebiyle sporcu olmayanlara göre yeme bozukluğu prevalansı çok daha yüksektir. Dönemin getirdiği parametreler de incelenerek adölesan sporcuları değerlendirmek tanı kriterleri açısından elzemdir. Spor hekimi, spor diyetisyeni, psikiyatrist, psikolog ve antrenörler iş birliği ile çalışmalı; tanı ve tedavi için multidisipliner yol izlenmelidir. Bu aşamada sporcuya özgü kullanılan tarama araçları, takip değerlendirmeleri kullanılmalıdır. Tanı, tedavi ve tüm yeme bozukluklarını önleme yaklaşımlarında; sporcunun, ailenin, antrenörün ve tüm spor çalışanlarının eğitimi oldukça önemlidir. Sporcu ve sporcuyla çalışan ekipte her bireyin bilinçli olması çeşitli yeme bozukluklarını önleyebilecek, olası durumlarda erken müdaheleyle hızlı iyileşmeyi sağlayacaktır. Bu çalışma; sporcular üzerinde düzensiz yeme ve yeme bozukluğunda tanı ve tedavi yöntemlerini değerlendirmek amacıyla güncel literatür taranarak yapılmıştır.
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Objective: To investigate the endocrine profile, body composition, and state of mood in male Olympic athletes participating in sports that do or do not emphasize leanness. Design: Cross-sectional study. Setting: Research unit at a university hospital. Participants: Forty-four Swedish male Olympic athletes participating in 26 different sport disciplines. Main outcome measures: Body composition was determined by dual-energy x-ray absorptiometry, and blood levels of steroid hormones and biomarkers of nutritional status were analyzed. In addition, states of mood were assessed employing the profile of mood states (POMS) test. The athletes were divided into 2 groups on the basis of whether their sporting discipline emphasized leanness or not. Results: In all subjects, body composition, hormone levels, and POMS scores were within normal ranges. However, the leanness athletes (n = 18) displayed significantly lower proportion of body fat (P < 0.01), higher spinal bone mineral density (P < 0.05), lower serum levels of free testosterone and leptin (P < 0.05), and higher serum levels of insulin-like growth factor binding protein 1 (P < 0.05) than nonleanness athletes (n = 26). Leanness athletes also had higher POMS scores for depression and anger, and a higher global POMS score (P < 0.05), the latter being positively correlated to the frequency of illness (r = 0.42, P < 0.01) before the Olympic Games. Conclusion: Although there were no indications of energy deficiency or endocrine disturbance in the leanness athletes, their higher POMS scores and frequency of illness may indicate the potential harmfulness of their pursuit of outstanding athletic performance.
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Dieting makes you fat - the title of a book published in 1983 - embodies the notion that dieting to control body weight predisposes the individual to acquire even more body fat. While this notion is controversial, its debate underscores the large gap that exists in our understanding of basic physiological laws that govern the regulation of human body composition. A striking example is the key role attributed to adipokines as feedback signals between adipose tissue depletion and compensatory increases in food intake. Yet, the relative importance of fat depletion per se as a determinant of post-dieting hyperphagia is unknown. On the other hand, the question of whether the depletion of lean tissues can provide feedback signals on the hunger-appetite drive is rarely invoked, despite evidence that food intake during growth is dominated by the impetus for lean tissue deposition, amidst proposals for the existence of protein-static mechanisms for the regulation of growth and maintenance of lean body mass. In fact, a feedback loop between fat depletion and food intake cannot explain why human subjects recovering from starvation continue to overeat well after body fat has been restored to pre-starvation values, thereby contributing to 'fat overshooting'. In addressing the plausibility and mechanistic basis by which dieting may predispose to increased fatness, this paper integrates the results derived from re-analysis of classic longitudinal studies of human starvation and refeeding. These suggest that feedback signals from both fat and lean tissues contribute to recovering body weight through effects on energy intake and thermogenesis, and that a faster rate of fat recovery relative to lean tissue recovery is a central outcome of body composition autoregulation that drives fat overshooting. A main implication of these findings is that the risk of becoming fatter in response to dieting is greater in lean than in obese individuals.
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After weight loss, changes in the circulating levels of several peripheral hormones involved in the homeostatic regulation of body weight occur. Whether these changes are transient or persist over time may be important for an understanding of the reasons behind the high rate of weight regain after diet-induced weight loss. We enrolled 50 overweight or obese patients without diabetes in a 10-week weight-loss program for which a very-low-energy diet was prescribed. At baseline (before weight loss), at 10 weeks (after program completion), and at 62 weeks, we examined circulating levels of leptin, ghrelin, peptide YY, gastric inhibitory polypeptide, glucagon-like peptide 1, amylin, pancreatic polypeptide, cholecystokinin, and insulin and subjective ratings of appetite. Weight loss (mean [±SE], 13.5±0.5 kg) led to significant reductions in levels of leptin, peptide YY, cholecystokinin, insulin (P<0.001 for all comparisons), and amylin (P=0.002) and to increases in levels of ghrelin (P<0.001), gastric inhibitory polypeptide (P=0.004), and pancreatic polypeptide (P=0.008). There was also a significant increase in subjective appetite (P<0.001). One year after the initial weight loss, there were still significant differences from baseline in the mean levels of leptin (P<0.001), peptide YY (P<0.001), cholecystokinin (P=0.04), insulin (P=0.01), ghrelin (P<0.001), gastric inhibitory polypeptide (P<0.001), and pancreatic polypeptide (P=0.002), as well as hunger (P<0.001). One year after initial weight reduction, levels of the circulating mediators of appetite that encourage weight regain after diet-induced weight loss do not revert to the levels recorded before weight loss. Long-term strategies to counteract this change may be needed to prevent obesity relapse. (Funded by the National Health and Medical Research Council and others; number, NCT00870259.).
Although brown adipose tissue in infants and young children is important for regulation of energy expenditure, there has been considerable debate on whether brown adipose tissue normally exists in adult humans and has physiologic relevance in this population. In the last decade, radiologic studies in adults have identified areas of adipose tissue with high 18F-fluorodeoxyglucose (18F-FDG) uptake, putatively identified as brown fat. This radiologic study assessed the presence of physiologically significant brown adipose tissue among 1972 adult patients who had 3640 consecutive 18F-FDG positron-emission tomographic and computed tomographic whole-body scans between 2003 and 2006. Brown adipose tissue was defined as areas of tissue that were more than 4 mm in diameter, had the CT density of adipose tissue, and had maximal standardized uptake values of 18F-FDG of at least 2.0 gm per mL. A sample of 204 date-matched patients without brown adipose tissue served as the control group. Using these criteria, positron-emission tomographic and computed tomographic scans identified brown adipose tissue in 106 of the 1972 patients (5.4%). The most common location for substantial amounts of brown adipose tissue was the region extending from the anterior neck to supraclavicular region. Immunohistochemical staining for uncoupling protein 1 in this region confirmed the identity of immunopositive, multilocular adipocytes as brown adipose tissue. More brown adipose tissue was detected in women (7.5% [76/1013]) than in men (3.1% [30/959]); the female:male ratio was 2.4:1.0 (P 64) (P 64 years) (P for trend = 0.007). These findings show that functional brown adipose tissue is prevalent in adult humans, and significantly more frequently in women. The inverse correlation of body mass index with the amount of brown adipose tissue, especially in older patients, suggests to the investigators a possible role of brown adipose tissue in protecting against obesity.
Unlabelled: Bodybuilding is a sport in which competitors are judged on muscular appearance. This case study tracked a drug-free male bodybuilder (age 26-27 y) for the 6 mo before and after a competition. Purpose: The aim of this study was to provide the most comprehensive physiological profile of bodybuilding competition preparation and recovery ever compiled. Methods: Cardiovascular parameters, body composition, strength, aerobic capacity, critical power, mood state, resting energy expenditure, and hormonal and other blood parameters were evaluated. Results: Heart rate decreased from 53 to 27 beats/min during preparation and increased to 46 beats/min within 1 mo after competition. Brachial blood pressure dropped from 132/69 to 104/56 mmHg during preparation and returned to 116/64 mmHg at 6 mo after competition. Percent body fat declined from 14.8% to 4.5% during preparation and returned to 14.6% during recovery. Strength decreased during preparation and did not fully recover during 6 months of recovery. Testosterone declined from 9.22 to 2.27 ng/mL during preparation and returned back to the baseline level, 9.91 ng/mL, after competition. Total mood disturbance increased from 6 to 43 units during preparation and recovered to 4 units 6 mo after competition. Conclusions: This case study provides a thorough documentation of the physiological changes that occurred during natural bodybuilding competition and recovery.
Numerous laboratory studies involving both animal and human models indicate that weight loss induces changes in leptin, ghrelin and insulin sensitivity, which work to promote weight regain. It is unclear, however, whether these biological changes serve as a biomarker for predicting weight regain in free-living humans in which biological, behavioral and environmental factors are likely at play. We identified 12 studies published between January 1995 and December 2011 that reported changes in leptin, ghrelin or insulin during intentional weight loss with a follow-up period to assess regain. Two of the nine studies examining leptin suggested that larger decreases were associated with great regain, three studies found the opposite (smaller decreases were associated with regain) while four studies found no significant relationship; none of the studies supported the hypothesis that increases in ghrelin during weight loss were associated with regain. One study suggested that improvements in insulin resistance were associated with weight gain, but five subsequent studies reported no association. Changes in leptin, ghrelin or insulin sensitivity, taken alone, are not sufficient to predict weight regain following weight loss in free-living humans. In future studies, it is important to include a combination of physiological, behavioral and environmental variables in order to identify subgroups at greatest risk of weight regain.International Journal of Obesity accepted article preview online, 26 June 2013; doi:10.1038/ijo.2013.118.
Understanding the metabolic factors that contribute to obesity development and weight loss success are critical in combating obesity and obesity related disorders. This review provides an overview of energy metabolism with a particular focus on mitochondrial function in health and in obesity. Mitochondrial proton leak contributes significantly to whole body energy expenditure and the potential role of energy uncoupling in weight loss success is discussed. We provide evidence to support the hypothesis that differences in energy efficiency are important regulators of body weight and weight loss success. This article is protected by copyright. All rights reserved.
An increase in the sensation of hunger and overeating after a period of chronic energy deprivation can be part of an autoregulatory phenomenon attempting to restore body weight. To gain insights into the role of fat and lean tissue depletion as determinants of such a hyperphagic response in hu- mans, we reanalyzed the individual data on food intake and body composition available for the 12 starved and refed men in the classical Minnesota Experiment after a shift from a 12-wk period of restricted refeeding to an ad libitum refeeding period of 8 wk. For each individual, the following were determined: 1) the total hyperphagic response during the ad libitum refeeding period, cal- culated as the energy intake in excess of that during the prestar- vation (control) period: 2) the degree of fat recovery and that of fat-free-mass (FFM) recovery before ad libitum refeeding, calcu- lated as the deviation in fat and FFM from their respective pre- starvation values (ie, the amount of fat or FFM before ad libitum refeeding as a percentage of fat or FFM during the control period); and 3) the deficit in energy intake before ad libitum refeeding, calculated as the difference between the energy intake during the period of restricted refeeding and that during the control period. The results indicate that 1) the total hyperphagic response is inversely correlated with the degree of fat recovery (r = -0.6) as well as with that of FFM recovery (r = -0.5), 2) the correlation between hyperphagia and FFM recovery persists after adjustment for fat recovery, and 3) the correlations between hyperphagia and fat recovery or FFM recovery persist after adjustment for the variance in the energy deficit during the preceding period of restricted refeeding. Taken together, these results in humans sug- gest that poststarvation hyperphagia is determined to a large extent by autoregulatory feedback mechanisms from both fat and lean tissues. These findings, which have implications for both the treatment of obesity and for nutritional rehabilitation after malnu- trition and cachexia, have been integrated into a compartmental model of autoregulation of body composition, and can be used to explain the phenomenon of poststarvation overshoot in body fat. Am J C/in Nutr 1997:65:717-23.
An excessive food supply has resulted in an increasing prevalence of overweight and obesity, conditions accompanied by serious health problems. Several studies have confirmed the significant inverse correlation between testosterone and obesity. Indeed after decades of intense controversy, a consensus has emerged that androgens are important regulators of fat mass and distribution in mammals and that androgen status affects cellularity in vivo. The high correlation of testosterone levels with body composition and its contribution to the balance of lipid metabolism are also suggested by the fact that testosterone lowering is associated with important clinical disorders such as dyslipidemia, atherosclerosis, cardiovascular diseases, metabolic syndrome and diabetes. In contrast, testosterone supplementation therapy in hypogonadic men has been shown to improve the lipid profile by lowering cholesterol, blood sugar and insulin resistance. Leptin, ghrelin and adiponectin are some of the substances related to feeding as well as androgen regulation. Thus, complex and delicate mechanisms appear to link androgens with various tissues (liver, adipose tissue, muscles, coronary arteries and heart) and the subtle alteration of some of these interactions might be the cause of correlated diseases. This review underlines some aspects regarding the high correlations between testosterone physiology and body fat composition.