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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
1
, Abbie E Smith-Ryan
1*
and Layne E Norton
2
Abstract
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
Introduction
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: abbsmith@email.unc.edu
1
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 (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) 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
http://www.jissn.com/content/11/1/7
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
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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
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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
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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.
Limitations
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
viewpoint.
Conclusion
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
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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.
Abbreviations
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.
Authorscontributions
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
1
Department of Exercise and Sport Science, University of North Carolina at
Chapel Hill, 209 Fetzer Hall, CB# 8700, Chapel Hill, NC 27599-8700, USA.
2
BioLayne LLC, Tampa, FL, USA.
Received: 18 December 2013 Accepted: 20 February 2014
Published: 27 February 2014
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doi:10.1186/1550-2783-11-7
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
http://www.jissn.com/content/11/1/7
... Regardless of the length of the contest preparation phase, as energy availability decreases and body fat reduces, metabolic adaptations occur to restore baseline body mass [17]. These metabolic adaptations involve hormonal changes, particularly testosterone, estrogen, thyroid hormones (T3 and T4), ghrelin, insulin, and cortisol, along with a reduction of RMR [10,[17][18][19]. ...
... Regardless of the length of the contest preparation phase, as energy availability decreases and body fat reduces, metabolic adaptations occur to restore baseline body mass [17]. These metabolic adaptations involve hormonal changes, particularly testosterone, estrogen, thyroid hormones (T3 and T4), ghrelin, insulin, and cortisol, along with a reduction of RMR [10,[17][18][19]. These adaptations result in weight loss "plateaus," requiring further energy restrictions through dietary intake or exercise expenditure to continue the energy deficit for fat loss [17]. ...
... These metabolic adaptations involve hormonal changes, particularly testosterone, estrogen, thyroid hormones (T3 and T4), ghrelin, insulin, and cortisol, along with a reduction of RMR [10,[17][18][19]. These adaptations result in weight loss "plateaus," requiring further energy restrictions through dietary intake or exercise expenditure to continue the energy deficit for fat loss [17]. However, the consequences of extreme energy deficits can lead to low energy availability (LEA), where the body does not have enough energy to support optimal physiological function and metabolic systems are disrupted [20]. ...
Article
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Background: To date, there is limited consensus on post-contest recovery recommendations for natural physique athletes. The available literature emphasizes the negative consequences of extreme dieting associated with physique contests, yet offers only speculative suggestions to facilitate physiological recovery post-contest. This scoping review evaluates evidence-based recommendations for recovery in post-physique contests. Methods: The online search engines and databases Google Scholar, PubMed, and Scopus were searched systematically and 12 peer reviewed journal articles were included in the review. Results: Six key factors were identified that directly impacted on physiological recovery post-contest: (1) body composition, (2) recovery dietary intake, (3) resting metabolic rate (RMR) restoration, (4) endocrine measures recovery, (5) menstrual cycle recovery, and (6) psychological aspects of recovery. Conclusions: Three dietary strategies have been proposed to facilitate physiological recovery post-contest while bearing in mind body composition and future athlete outcomes; (1) a gradual increase in energy intake to maintenance requirements, (2) ad libitum eating, (3) an immediate return to maintenance energy requirements. Future research is required to determine the timeline in which full physiological recovery occurs post-contest and which strategies best support athlete health and performance during post-contest recovery.
... For the second meta-analysis, comparisons were made for changes in exercise performance in athletes with ≥ 2 markers of LEA at the end of the training block. Markers of LEA included a diagnosis of functional hypothalamic amenorrhea (FHA) as per clinical practice guidelines [20], an Table 1 Markers of low energy availability used for study inclusion RMR resting metabolic rate, FFM fat-free mass, BMD bone mineral density, DEXA dual-energy x-ray absorptiometry, T 3 triiodothyronine, IGF-1 insulin-like growth factor 1, EA energy availability Two of the following markers Functional hypothalamic amenorrhea as per clinical practice guidelines [20] EA < 30 kcal/kg FFM/day or evidence of an energy deficit from food and training records [21] Decreased BMD compared with prior DEXA scan or Z-score less than − 1.0 [22] Score ≥ 8 on the Low Energy Availability in Females Questionnaire [23] Decreased body mass, or fat mass measured by DEXA or sum of skin-folds [24] Suppressed RMR ratio [25] or decreased RMR relative to FFM [8,27] Decreased resting muscle glycogen content [30,31] Decreased levels of leptin [29,38,39], T 3 [28,40], testosterone (males only) [41], insulin [29,32,39], IGF-1 [42], osteocalcin [42], procollagen 1 N-terminal propeptide [33,42] Increased levels of hepcidin [34,35], cross-linked C-terminal telopeptide of type 1 collagen [28,42], growth hormone [32], β-hydroxybutyrate [32], and/or cortisol [32,36,37] Markers only needed to be measured to meet the inclusion criteria for review (independent of direction of change). All markers have been shown to be altered by low energy availability but it is uncertain how they may be affected by training stress alone energy availability < 30 kcal/kg FFM/day or evidence of an energy deficit from food and training records [21], decreased BMD compared with prior dual-energy X-ray absorptiometry (DEXA) scan or Z-score less than − 1.0 [22], score ≥ 8 on the Low Energy Availability in Females Questionnaire [23], decreased body mass or fat mass [24], a suppressed resting metabolic rate (RMR) ratio [25,26], decreased RMR relative to FFM [8,27], decreased resting muscle glycogen content [30,31], and changes in select biochemical markers that have been demonstrated to be altered in periods of LEA (see Table 1) [24,[28][29][30][32][33][34][35][36][37][38][39][40][41][42]. ...
... Markers of LEA included a diagnosis of functional hypothalamic amenorrhea (FHA) as per clinical practice guidelines [20], an Table 1 Markers of low energy availability used for study inclusion RMR resting metabolic rate, FFM fat-free mass, BMD bone mineral density, DEXA dual-energy x-ray absorptiometry, T 3 triiodothyronine, IGF-1 insulin-like growth factor 1, EA energy availability Two of the following markers Functional hypothalamic amenorrhea as per clinical practice guidelines [20] EA < 30 kcal/kg FFM/day or evidence of an energy deficit from food and training records [21] Decreased BMD compared with prior DEXA scan or Z-score less than − 1.0 [22] Score ≥ 8 on the Low Energy Availability in Females Questionnaire [23] Decreased body mass, or fat mass measured by DEXA or sum of skin-folds [24] Suppressed RMR ratio [25] or decreased RMR relative to FFM [8,27] Decreased resting muscle glycogen content [30,31] Decreased levels of leptin [29,38,39], T 3 [28,40], testosterone (males only) [41], insulin [29,32,39], IGF-1 [42], osteocalcin [42], procollagen 1 N-terminal propeptide [33,42] Increased levels of hepcidin [34,35], cross-linked C-terminal telopeptide of type 1 collagen [28,42], growth hormone [32], β-hydroxybutyrate [32], and/or cortisol [32,36,37] Markers only needed to be measured to meet the inclusion criteria for review (independent of direction of change). All markers have been shown to be altered by low energy availability but it is uncertain how they may be affected by training stress alone energy availability < 30 kcal/kg FFM/day or evidence of an energy deficit from food and training records [21], decreased BMD compared with prior dual-energy X-ray absorptiometry (DEXA) scan or Z-score less than − 1.0 [22], score ≥ 8 on the Low Energy Availability in Females Questionnaire [23], decreased body mass or fat mass [24], a suppressed resting metabolic rate (RMR) ratio [25,26], decreased RMR relative to FFM [8,27], decreased resting muscle glycogen content [30,31], and changes in select biochemical markers that have been demonstrated to be altered in periods of LEA (see Table 1) [24,[28][29][30][32][33][34][35][36][37][38][39][40][41][42]. Given that FFM is the greatest contributor to RMR [43], we assessed RMR relative to FFM rather than absolute RMR. ...
... Finally, the power section was modified such that a study was given 1 point if it provided a power calculation and 0 points if it did not. The highest possible score was 28, with studies categorized as excellent (26)(27)(28), good (20)(21)(22)(23)(24)(25), fair (15)(16)(17)(18)(19), and poor (≤ 14). For studies where selection bias did not apply, the 6 points from this section were removed so that the highest possible score was 22. Corresponding levels were excellent (20)(21)(22), good , fair , and poor (≤ 8). ...
Article
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Background: Overreaching is the transient reduction in performance that occurs following training overload and is driven by an imbalance between stress and recovery. Low energy availability (LEA) may drive underperformance by compounding training stress; however, this has yet to be investigated systematically. Objective: The aim of this study was to quantify changes in markers of LEA in athletes who demonstrated underperformance, and exercise performance in athletes with markers of LEA. Methods: Studies using a ≥ 2-week training block with maintained or increased training loads that measured exercise performance and markers of LEA were identified using a systematic search following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Changes from pre- to post-training were analyzed for (1) markers of LEA in underperforming athletes and (2) performance in athletes with ≥ 2 markers of LEA. Results: From 56 identified studies, 14 separate groups of athletes demonstrated underperformance, with 50% also displaying ≥ 2 markers of LEA post-training. Eleven groups demonstrated ≥ 2 markers of LEA independent of underperformance and 37 had no performance reduction or ≥ 2 markers of LEA. In underperforming athletes, fat mass (d = - 0.29, 95% confidence interval [CI] - 0.54 to - 0.04; p = 0.02), resting metabolic rate (d = - 0.63, 95% CI - 1.22 to - 0.05; p = 0.03), and leptin (d = - 0.72, 95% CI - 1.08 to - 0.35; p < 0.0001) were decreased, whereas body mass (d = - 0.04, 95% CI - 0.21 to 0.14; p = 0.70), cortisol (d = - 0.06, 95% CI - 0.35 to 0.23; p = 0.68), insulin (d = - 0.12, 95% CI - 0.43 to 0.19; p = 0.46), and testosterone (d = - 0.31, 95% CI - 0.69 to 0.08; p = 0.12) were unaltered. In athletes with ≥ 2 LEA markers, performance was unaffected (d = 0.09, 95% CI - 0.30 to 0.49; p = 0.6), and the high heterogeneity in performance outcomes (I2 = 84.86%) could not be explained by the performance tests used or the length of the training block. Conclusion: Underperforming athletes may present with markers of LEA, but overreaching is also observed in the absence of LEA. The lack of a specific effect and high variability of outcomes with LEA on performance suggests that LEA is not obligatory for underperformance.
... The maintenance of a healthy body mass, or the loss of body mass during dieting, is generally framed in terms of the balance between energy intake and energy expenditure. On the expenditure side, RMR is the largest contributor, and the least modifiable component [44], while exercise associated thermogenesis (EAT), non-exercise associated thermogenesis (NEAT), and the thermic effect of food (TEF) are more modifiable. Since NEAT is the largest of those three components, a major aspect of our experimental design was to reduce the confounding effect of changes in NEAT by monitoring physical activity and encouraging the participants to maintain their normal levels of NEAT and EAT. ...
... Since NEAT is the largest of those three components, a major aspect of our experimental design was to reduce the confounding effect of changes in NEAT by monitoring physical activity and encouraging the participants to maintain their normal levels of NEAT and EAT. That intervention was especially important because metabolic compensation following weight-loss can result in a decrease in NEAT and a decrease in the motivation to exercise, which will lead to a decrease in EAT [44]. At the same time, our experimental design ensured that energy intake was constant at each participant's habitual daily energy consumption. ...
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Background: The ketogenic diet (KD) has been shown to result in body mass loss in people with disease as well as healthy people, yet the effect of the KD on thyroid function and metabolism are unknown. Objective: We aimed to determine the effects of a KD, compared with an isocaloric high-carbohydrate low-fat (HCLF) diet, on resting metabolic rate and thyroid function in healthy individuals. Design: Eleven healthy, normal-weight participants (mean(SD) age: 30(9) years) completed this randomized crossover-controlled study. For a minimum of three weeks on each, participants followed two isocaloric diets: a HCLF diet (55%carbohydrate, 20%fat, 25%protein) and a KD (15%carbohydrate, 60%fat, 25% protein), with a one-week washout period in-between. Importantly, while on the KD, the participants were required to remain in a state of nutritional ketosis for three consecutive weeks. Crossover analyses and linear mixed models were used to assess effect of diet on body mass, thyroid function and resting metabolic rate. Results: Both dietary interventions resulted in significant body mass loss (p<0.05) however three weeks of sustained ketosis (KD) resulted in a greater loss of body mass (mean (95%CI): -2.9 (-3.5, -2.4) kg) than did three weeks on the HCLF diet (-0.4 (-1.0, 0.1) kg, p < 0.0001). Compared to pre-diet levels, the change in plasma T3 concentration was significantly different between the two diets (p = 0.003), such that plasma T3 concentration was significantly lower following the KD diet (4.1 (3.8, 4.4) pmol/L, p<0.0001) but not different following the HCLF diet (4.8 (4.5, 5.2) pmol/L, p = 0.171. There was a significant increase in T4 concentration from pre-diet levels following the KD diet (19.3 (17.8, 20.9) pmol/L, p < 0.0001), but not following the HCLF diet (17.3 (15.7, 18.8) pmol.L, p = 0.28). The magnitude of change in plasma T4 concentration was not different between the two diets (p = 0.4). There was no effect of diet on plasma thyroid stimulating hormone concentration (p = 0.27). There was a significantly greater T3:T4 ratio following the HCLF diet (0.41 (0.27, 0.55), p < 0.0001) compared to pre-diet levels but not following the KD diet (0.25 (0.12, 0.39), p = 0.80). Conclusions: Although the diets were isocaloric and physical activity and resting metabolic rate remained constant, the participants lost more mass after the KD than after the HCLF diet. The observed significant changes in triiodothyronine concentration suggest that unknown metabolic changes occur in nutritional ketosis, changes that warrant further investigation. Trial registration: Pan African Clinical Trial Registry: PACTR201707002406306 URL: https://pactr.samrc.ac.za/.
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