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The Acute Effects of Swimming on Appetite, Food Intake, and Plasma Acylated Ghrelin


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Swimming may stimulate appetite and food intake but empirical data are lacking. This study examined appetite, food intake, and plasma acylated ghrelin responses to swimming. Fourteen healthy males completed a swimming trial and a control trial in a random order. Sixty min after breakfast participants swam for 60 min and then rested for six hours. Participants rested throughout the control trial. During trials appetite was measured at 30 min intervals and acylated ghrelin was assessed periodically (0, 1, 2, 3, 4, 6, and 7.5 h. N = 10). Appetite was suppressed during exercise before increasing in the hours after. Acylated ghrelin was suppressed during exercise. Swimming did not alter energy or macronutrient intake assessed at buffet meals (total trial energy intake: control 9161 kJ, swimming 9749 kJ). These findings suggest that swimming stimulates appetite but indicate that acylated ghrelin and food intake are resistant to change in the hours afterwards.
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Hindawi Publishing Corporation
Journal of Obesity
Volume 2011, Article ID 351628, 8pages
Research Article
The Acute Effects of Swimming on Appetite, Food Intake, and
Plasma Acylated Ghrelin
James A. King, Lucy K. Wasse, and David J. Stensel
School of Sport, Exercise and Health Sciences, Loughborough University, Leicestershire LE11 3TU, UK
Correspondence should be addressed to David J. Stensel,
Received 30 April 2010; Revised 8 July 2010; Accepted 9 September 2010
Academic Editor: Eric Doucet
Copyright © 2011 James A. King et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Swimming may stimulate appetite and food intake but empirical data are lacking. This study examined appetite, food intake,
and plasma acylated ghrelin responses to swimming. Fourteen healthy males completed a swimming trial and a control trial in a
random order. Sixty min after breakfast participants swam for 60min and then rested for six hours. Participants rested throughout
the control trial. During trials appetite was measured at 30 min intervals and acylated ghrelin was assessed periodically (0, 1, 2, 3, 4,
6, and 7.5 h. N=10). Appetite was suppressed during exercise before increasing in the hours after. Acylated ghrelin was suppressed
during exercise. Swimming did not alter energy or macronutrient intake assessed at buet meals (total trial energy intake: control
9161 kJ, swimming 9749 kJ). These findings suggest that swimming stimulates appetite but indicate that acylated ghrelin and food
intake are resistant to change in the hours afterwards.
1. Introduction
Regular physical activity is important for the maintenance
of body weight and its composition within a healthy range
[1,2]. All forms of physical activity can contribute to success-
ful energy balance by increasing daily energy expenditure.
Swimming is an attractive mode of physical activity due to
the reduced musculoskeletal and thermoregulatory stresses
(i.e., elevation in body temperature) imposed in comparison
with other land-based activities such as running and cycling.
Swimming may therefore oer an appealing form of physical
activity for individuals seeking to prevent weight gain and/or
to maintain a reduced body weight after successful weight
Despite the attractiveness of swimming as a mode of
physical activity, the ability of swimming to favourably
influence body weight and body composition remains
contentious. In obese individuals research has shown that
swimming may not induce body weight and fat loss [3,4]
whereas walking and cycling interventions of similar inten-
sity and duration do [3]. Considering the heightened energy
output elicited by all forms of exertion the most logical
explanation for these findings is that swimming stimulates
a compensatory increase in energy intake [5]. This notion is
consistent with anecdotal reports of swimming stimulating
appetite. Specifically, it has been stated that individuals often
feel like “eating a horse” after an acute bout of swimming [6].
This suggestion is consistent with empirical research which
has described elevations in energy intake after cycling-based
exercise performed on a modified ergometer in cold water
[5,7]. Despite these findings, there remains a paucity of data
about the precise eects of swimming on appetite and food
The mechanisms by which exercise influences appetite
have recently begun to receive significant interest with
specific attention being given to peptides implicated in the
neuroendocrine regulation of feeding [8,9]. Ghrelin is an
acylated peptide secreted primarily from the stomach and
remains unique as the only circulating gut peptide that stim-
ulates appetite [10]. Defined roles of ghrelin in both short-
and long-term feeding regulation have been uncovered [11],
and more recently investigators have sought to determine
how exercise influences circulating levels of ghrelin [1214].
These studies suggest that intense exercise induces a transient
suppression in circulating acylated ghrelin concentrations.
Concomitant suppressions in hunger have been reported by
2Journal of Obesity
Broom and colleagues [12,14] raising the possibility that
acylated ghrelin may be important in determining changes
in appetite resulting from exercise.
The primary aim of this investigation was to examine
the influence of an acute bout of swimming on appetite and
energy intake in an eort to determine whether a stimulatory
increase in these variables may explain data suggesting a
relative inecacy of swimming for the purposes of weight
control. A subsidiary aim of this investigation was to explore
the potential role of acylated ghrelin as a mediator of appetite
and food intake, during and after exercise.
2. Methods
2.1. Participants. Following university ethical advisory com-
mittee approval 14 healthy male volunteers (age 22.0 ±
0.5 y, BMI 23.2 ±0.6 kg·m2, body fat 17.2 ±1.2%, mean
±SEM) gave their written informed consent to participate.
Participants were nonsmokers, had no known history of
cardiovascular/metabolic disease, were not dieting, did not
have any atypical dietary habits (assessed by the three-
factor eating questionnaire), were not taking medication,
and were not obese (BMI 29.9kg·m2)orhypertensive
(resting blood pressure <140/90 mmHg). Participants were
habitually active but were not trained athletes, with most
individuals typically participating in games activities such as
soccer, hockey, and rugby on a regular basis at a recreational
level. The nature of the study demanded that participants
were competent at swimming; however, it was ensured that
individuals taking part in swimming at a competitive level
were not recruited for the study.
2.2. Procedure. Prior to main trials participants visited the
laboratory to undergo screening and preliminary testing. On
arrival at the laboratory participants were provided with an
information sheet detailing the demands of the study. The
information sheet stated that the aims of the study were to
examine the eects of swimming on appetite, energy intake,
and acylated ghrelin but did not provide any indication of
the hypothesised direction of responses. After confirming
that participants understood the study demands written
informed consent was obtained. Thereafter, questionnaires
were completed to assess health status, physical activity
habits, and food preferences. Height was determined to
the nearest 0.1 cm using a stadiometer (Seca 214, Seca
Ltd, Germany), and body weight was measured to the
nearest 0.1 kg using a digital scale (Seca 770, Seca Ltd,
Germany). Body density was estimated via subcutaneous
fat measurements [15] made using skinfold callipers (Baty
International, West Sussex, UK), and body fat percentage was
then ascertained [16].
Participants were then taken to the university swim-
ming pool to confirm swimming competence and to be
familiarised with procedures in anticipation of main trials.
For this, participants were asked to complete a 60min
intermittent swimming set which was to be performed
during the exercise trial. In this familiarisation session
participants were accustomed to wearing heart rate monitors
in the pool and taking recordings periodically. They were also
familiarised with the ratings of perceived exertion scale [17].
After an interval of at least one week participants then
completed two eight-hour trials (swimming and control) in
a randomized-crossover fashion. Each trial was separated
by at least one week. On the morning of main trials
participants arrived at the laboratory having fasted overnight
and not eaten breakfast. Main trials commenced at 09:00
with the consumption of a standard breakfast snack. This was
consumed within 5 min. On the exercise trial participants
rested within the laboratory for the first 40 min, after which
they were escorted to the university swimming pool via
motorised transport, in time for commencing swimming at
the beginning of the second trial hour. At this time, partici-
pants began a 60 min intermittent swimming set. The set was
composed of six 10 min blocks. In each block participants
swam continuously for seven min using their preferred stroke
and then rested for three min. The speed of swimming was
ultimately determined by the participant although they were
instructed to swim at a moderate intensity, defined as a rating
of perceived exertion between 12 and 14. During exercise
the distance completed was recorded. Heart rate was also
assessed using short range telemetry. Upon completion of
each swimming block participants rested on the pool side
with their legs immersed in the water. Ratings of perceived
exertion were then assessed. After completing the swimming
protocol participants were escorted back to the research
laboratory where they rested for a further six hours. Identical
procedures were completed in the control trial except that
no exercise was performed. Instead, during the equivalent
time period resting metabolic rate was assessed via indirect
calorimetry in order to permit the calculation of net energy
expenditure (gross energy expenditure minus resting energy
expenditure) during exercise.
2.3. Physical Activity and Dietary Standardization. Partic-
ipants completed a weighed food record of all items
consumed within the 24 h preceding their first main trial.
Alcohol and caeine were not permitted during this period.
This feeding pattern was replicated prior to the second main
trial. Participants refrained from strenuous physical activity
during this time.
2.4. Appetite and Environmental Conditions. At baseline, 0.5-
hour, 1-hour, and 30 min intervals thereafter appetite per-
ceptions (hunger, satisfaction, fullness, and prospective food
consumption) were assessed using 100 mm visual analogue
scales [18]. Environmental temperature and humidity were
also measured at these times using a handheld hygrometer
(Omega RH85, Manchester, UK). The temperature of the
swimming pool was monitored using a glass thermometer
(Fisher Scientific, UK).
2.5. Breakfast and Ad Libitum Buet Meals. During each
main trial all food was consumed within the research
laboratory and was quantified by the investigators. Main
trials commenced with breakfast consumption (09:00).
The breakfast provided was standardised to body weight
Journal of Obesity 3
and consisted of a commercial cereal bar (Kellogg’s Nutri-
grain). Participants received 1.06 g per kilogram of body
weight measured on the first trial visit. Identical amounts
were consumed across trials. For a 70kg individual this
provided 1092 kJ of energy, 6 g of fat, 4 g of protein, and 48 g
of carbohydrate.
At 3 h (12:00) and 7.5 h (16:30) into trials participants
were given access to a buet meal for a period of 30 min
from which they could consume food ad libitum.Thebuet
meal provided diversity in protein, fat, and carbohydrate
content in order to facilitate the detection of macronutrient
preferences (Table 3 ). Food was presented in excess of
expected consumption. Participants were told to eat until
satisfied and that additional food was available if desired.
Participants consumed meals in isolation so that social influ-
ence did not constrain food selection. Food consumption
was ascertained by examining the weighted dierence in
each food item remaining compared with the weight of that
initially presented. The energy and macronutrient content
of the items consumed was ascertained using manufacturer
2.6. Acylated Ghrelin. To explore the eects of swimming on
circulating concentrations of acylated ghrelin, blood samples
were collected from 10 of the 14 participants at baseline,
1 h (pre-exercise), 2 h (post-exercise), 3 h, 4 h, 6 h, and 7.5 h.
(We did not measure acylated ghrelin in four participants for
logistical reasons, i.e., the room we used for blood sampling
at the swimming pool was not always available). In both
the swimming and control trials baseline samples and the
equivalent pre- and postexercise blood samples were taken
via venepuncture of an antecubital vein. Thereafter, the
remaining samples were collected via a cannula (Venflon,
Becton Dickinson, Helsinborg, Sweden) positioned in an
antecubital vein. Details of sample preparation, collection,
and analysis have been described in depth previously [12,
14]. The within batch coecient of variation for the acylated
ghrelin ELISA assay was 6.4%.
2.7. Energy Expenditure Estimation. Energy expenditure dur-
ing swimming was estimated using equations based on mul-
tiples of resting metabolism (METs) [19]. Specifically, energy
expenditure was estimated by multiplying each participant’s
estimated resting energy expenditure (kJ·min1) in the
control trial by an appropriate MET value for the stroke used
during each seven- minute block of swimming: general breast
stroke (10 METs), general backstroke (7METs), slow crawl
(0.95 m·s1—8.0 METs), and fast crawl (>0.95 m·s1
11 METs).
2.8. Statistical Analysis. All data was analyzed using the
Statistical Package for the Social Sciences (SPSS) software
version 16.0 for Windows (SPSS Inc, Chicago, IL, US.). Area
under the concentration versus time curve calculations were
performed using the trapezoidal method. Student’s t-tests
for correlated data were used to assess dierences between
fasting and area under the curve values for appetite percep-
tions, acylated ghrelin, temperature, and humidity between
the control and swimming trials. Repeated measures, two-
factor ANOVA was used to examine dierences between
the swimming and control trials over time for appetite
perceptions, energy and macronutrient intake, and acylated
ghrelin. The Pearson product moment correlation coe-
cient was used to examine relationships between variables.
Correction of acylated ghrelin values for changes in plasma
volume did not alter the statistical significance of findings
therefore for simplicity the unadjusted values are presented.
Statistical significance was accepted at the 5% level. Results
are presented as mean ±SEM. A power calculation indicated
that 13 participants were needed to provide sucient power
(80%) to detect a 50% compensation in energy intake with
alpha set at 5%.
3. Results
3.1. Exercise Responses and Resting Oxygen Consumption.
During the 42 min of swimming (6 ×7 min intervals) the
mean distance completed was 1875 ±156 m. The mean
swimming speed performed was 0.74 ±0.1 m·s1, and this
elicited an estimated net energy expenditure (exercise minus
resting) of 1921 ±83 kJ. The corresponding mean heart rate
and rating of perceived exertion values during the sessions
were 155 ±5beats·min1and 14 ±0. To complete the
swimming session four participants swam breaststroke for
all of the intervals whilst three participants used only front
crawl and two participants used only backstroke. Three par-
ticipants used a combination of front crawl and breast stroke
whilst two participants alternated between breaststroke and
backstroke. Participants’ mean oxygen consumption at rest
during the second hour of the control trial (i.e., the time
when they were swimming during the exercise trial) was 0.32
±0.01 L·min1(6.5 ±0.3 kJ·min1).
3.2. Baseline Parameters. No between-trial dierences
existed at baseline for any of the ratings of appetite assessed
or in plasma concentrations of acylated ghrelin (student’s
t-test, P>.05 for each).
3.3. Appetite, Energy and Macronutrient Intake. Perceived
ratings of hunger and prospective food consumption were
suppressed during and immediately after swimming before
increasing above values exhibited during the control trial
in the hours after exercise (two-factor ANOVA, trial ×
time interaction; P<.05 for each). Conversely, perceived
ratings of fullness and satisfaction were increased transiently
during swimming before decreasing below control values
in the hours thereafter (two-factor ANOVA, trial ×time
interaction; P<.05 for each) (Figure 1). Analysis of the
appetite area under the curve (AUC) data confirmed these
results. After the morning meal the hunger AUC (3.5–8 h)
was significantly higher in the swimming trial as compared
with control (swimming 178 ±20, control 152 ±19;
student’s t-test, P=.028) whilst fullness tended to be
reduced (swimming 227 ±21, control 243 ±17; student’s
t-test, P=.052). Moreover, from baseline to consumption
of the morning buet meal the fullness AUC (0–3h) was
4Journal of Obesity
Tab le 1: Energy intake (kJ) in the control and swimming trials (n=
14). There were no significant dierences between the swimming
and control trials (P>.05).
Control Swimming
Morning meal 5517 ±434 5856 ±403
(3–3.5 h)
Afternoon meal 3644 ±459 3893 ±577
(7.5–8 h)
Total trial 9161 ±719 9749 ±809
Tab le 2: Macronutrient intake in the control and swimming trials.
Values are gram and (%) (n=14). There were no significant
dierences between the swimming and control trials (P>.05).
Control trial Fat Carbohydrate Protein
Morning meal
(3–3.5 h) 54 ±5 (34.1) 156 ±11
(49.1) 59 ±9 (16.8)
Afternoon meal
(7.5–8 h) 33 ±5 (33.8) 107 ±15
(49.9) 38 ±8 (16.3)
To t a l Tr i a l 8 7 ±8 (34.9) 263 ±21
(49.1) 97 ±9 (16.0)
Swimming trial Fat Carbohydrate Protein
Morning meal
(3–3.5 h) 55 ±5 (34.0) 164 ±12
(49.3) 60 ±8 (16.7)
Afternoon meal
(7.5–8 h) 35 ±5 (33.1) 117 ±20
(50.2) 38 ±7 (16.7)
To t a l Tr i a l 9 0 ±9 (34.2) 281 ±26
(49.4) 98 ±9 (16.4)
significantly higher in the swimming trial as compared with
control (swimming 74 ±12, control 54 ±8; student’s
t-test, P=.025) whilst prospective food consumption was
suppressed (swimming 221 ±12, control 231 ±11; P=
Energy intake was significantly higher at the morning
buet meals compared with the afternoon meals (two-
factor ANOVA, main eect of time; P=.003); however,
there were no between-trial dierences in energy intake
at either feeding opportunity (two-factor ANOVA, trial
and interaction main eects; P>.05 for each). Relative
energy intake (energy intake—net energy cost of exercise)
was therefore significantly lower on the swimming trial as
compared with control (swimming 7828 ±774 kJ, control
9163 ±720). Tab l e 1 presents the energy intake data for the
control and swimming trials.
Two-factor ANOVA showed no trial or interaction (trial
×time) main eects for macronutrient intake (absolute
amount or percentage intake) indicating that no significant
dierences existed between trials for the intake of fat,
carbohydrate or protein (Table 2 ).
3.4. Acylated Ghrelin. Data for ten participants showed that
plasma concentrations of acylated ghrelin were suppressed
during swimming and after consumption of the morning
buet meal (two-factor ANOVA, main eect of trial; P=
Tab le 3: Items presented at buet meals.
Rice Krispies—Cereal
Cereal Bar
White Bread
Brown Bread
Salted Crisps
Chocolate rolls
Chocolate muns
Plain muns
Chocolate bar (Mars fun size)
.038). On closer inspection of the data one participant was
a clear outlier exhibiting fasting values on both trials which
were approximately nine times (26 standard deviations)
higher than the mean fasting values of the other nine partici-
pants (949 pg·mL1for the outlier versus 108 ±10 pg·mL1
for the mean (±SEM) of the other nine participants). Upon
removal of this outlier the suppression of acylated ghrelin at
the end of the swimming bout and after the first meal on each
trial is displayed with greater clarity (two-factor ANOVA,
trial ×time interaction; P<.001) (Figure 2). Examination of
the acylated ghrelin AUC (outlier excluded, n=9) confirmed
suppressed concentrations of acylated ghrelin prior to the
first buet meal (0–3 h) on the swimming trial (swimming
473 ±232, control 505 ±217 pg·mL1·3 h) (student’s t-test,
To examine the relationship between acylated ghrelin and
energy intake, at both the morning and afternoon buet
meals correlations were performed between acylated ghrelin
values immediately prior to each meal and subsequent
energy intake. Moreover, correlations were also performed
using the acylated ghrelin AUC leading up to the morning
(0–3 h AUC) and afternoon (3–8 h AUC) buet meals. In
all instances no significant relationships were found between
acylated ghrelin and energy intake.
3.5. Body Mass, Fluid Intake, and Environmental Conditions.
There were no significant dierences between the control and
swimming trials (all P>.05) in body weight (control 76.7 ±
2.1, swimming 76.5 ±2.2 kg), water intake (control 1402 ±
219, swimming 1302 ±226 mL) laboratory atmospheric
Journal of Obesity 5
Hunger (0-100)
PFC (0-100) Satisfaction (0-100)
Time (hours)
Time (hours)
Fullness (0-100)
Figure 1: Ratings of hunger (a), fullness (b), satisfaction (c), and prospective food consumption (d) in the swimming () and control ()
trials. Values are mean ±SEM (n=14). Black rectangle indicates breakfast snack, hatched rectangle indicates swimming, and diagonal
rectangles indicate buet meals. Two-factor ANOVA revealed a trial ×time interaction eect for each (P<.05).
temperature (control 21.6 ±0.3, swimming 21.4 ±0.3C),
and relative humidity (control 37.8 ±4.1, swimming 37.8 ±
4.1%). The atmospheric temperature and relative humidity
at the swimming pool were 26.4 ±0.8C and 50.9 ±1.7%,
respectively. The temperature of the swimming pool water
was 28.1 ±0.1C.
4. Discussion
The main findings arising from this investigation are three-
fold. Firstly, moderate intensity swimming exhibited a bipha-
sic influence on appetite with an inhibition existent during
exercise and a later stimulation in the hours thereafter.
Secondly, swimming did not influence ad libitum energy
or macronutrient intake. Finally, our exploratory analyses
showed that swimming transiently suppressed circulating
concentrations of the orexigenic peptide, acylated ghrelin;
however, no eects were apparent after exercise. This out-
come indicates that acylated ghrelin does not mediate the
reported stimulation of appetite after swimming.
The suppression of appetite (decreased hunger and
prospective food consumption/elevated satisfaction and full-
ness) observed during swimming is a novel finding yet is
consistent with previous research showing a transient inhibi-
tion of appetite resulting from land-based exercise modalities
such as running and cycling [20,21]. This phenomenon has
been termed exercise-induced anorexia [22] and has been
consistently observed during land-based activities performed
at moderate intensities or higher (>60% VO2max). Broom
et al. [12] reported suppressed hunger and plasma acylated
ghrelin during treadmill running and suggested a potential
role of acylated ghrelin in determining suppressed appetite
during exercise. The findings from the present study con-
firm that acylated ghrelin and appetite are concomitantly
suppressed during swimming; however, the absence of any
significant correlations between acylated ghrelin and any of
the appetite markers assessed, during exercise or immediately
after, suggests that there may not be a strong association
between these variables. Given the diversity of the role
of ghrelin in human physiology [23] it is possible that
6Journal of Obesity
Time (hours)
Acylated ghrelin (pg·mL1)
Figure 2: Plasma concentrations of acylated ghrelin in the swim-
ming () and control () trials. Values are mean ±SEM (n=
9). Black rectangle indicates breakfast snack, hatched rectangle
indicates swimming, diagonal rectangles indicate buet meals. Two-
factor ANOVA revealed a significant trial ×time interaction eect
the transient suppression of circulating acylated ghrelin
observed during exercise is entirely unrelated to appetite
regulation. At present though, the physiological relevance of
In the hours after consumption of the morning buet
meal, ratings of hunger and prospective food consumption
were higher in the swimming trial than the control trial
whilst ratings of fullness were reduced. These findings
indicate that swimming stimulated a delayed increase in
appetite. This response is contrary to research which has
examined appetite responses to land-based activities which
have typically shown no acute compensation in appetite
after performing exercise, even when significant amounts
of energy are expended [2022,24]. The mechanism
responsible for these discrepant findings is not immediately
clear. It has been suggested that changes in body temperature
may be important [5,6]; however, this is unlikely in the
present study as appetite was not stimulated until more than
two hours after swimming. By this time core temperature
would almost certainly have normalised. White et al. [5]
speculate that the cooling and then subsequent reheating
of the body may be associated with the release of “certain
hormones” which stimulate the appetite. In the present study
we measured circulating concentrations of acylated ghrelin, a
peptide responsible for stimulating appetite and food intake
[25,26]. The present findings suggest that acylated ghrelin
is not responsible for the augmented appetite response after
swimming as circulating concentrations were not dierent
from control after the morning buet meal. It remains
possible that compensatory changes in fasting or meal-
related acylated ghrelin profiles may occur over a longer
duration; however, further work is needed to examine this. It
must also be considered that appetite is regulated on an acute
basis by many circulating peptides in addition to acylated
ghrelin, including peptide YY, pancreatic polypeptide, and
glucagon-like peptide-1 [10]. It is therefore feasible that
changes in these peptides may have influenced the acylated
ghrelin and appetite responses observed.
Research indicates that swimming may be less eective
than land-based activities for inducing weight loss or
reductions in body fat [3,4]. Consistent with this, it has
been observed that levels of adiposity are typically higher in
swimmers than equal calibre runners [27,28]. It has been
suggested that an unparalleled stimulation of appetite and
energy intake after swimming may explain these findings [6].
Despite the changes in appetite observed, the present inves-
tigation did not find any significant dierences in energy
or macronutrient intake between the swimming and control
trials, either during the morning or afternoon meals. These
findings are dicult to reconcile. It is known that food intake
is influenced by a host of physiological, environmental,
psychological, and social factors, some of which are learned
over time and are resistant to change [29]. In this study it
seems that the factors influencing appetite were insucient
to overcome other competing forces governing food intake.
Nonetheless, as a consequence of the lack of change in energy
intake, participants therefore failed to compensate for the
energy expended during exercise and relative energy intake
(energy intake—net energy cost of exercise) was subse-
quently lower on the swimming trial as compared with con-
trol (swimming 7828 ±774 kJ, control 9163 ±720 kJ; stu-
dent’s t-test, P=.008). This outcome contradicts the sugges-
tion that energy intake is augmented by swimming and there-
fore does not support the notion that swimming is an inef-
fective exercise modality for successful body weight control.
When comparing the present findings to previous data
water temperature emerges as an important variable influ-
encing food intake responses to exercise performed in water.
White et al. [5] examined energy intake responses in healthy
participants who performed cycling exercise while immersed
in either cold water (20C) or neutral water (33C) and
compared these responses to control responses (i.e., while
resting in a dry environment). Energy intake was significantly
higher after exercise in cold water (3653kJ) as compared
with the neutral water (2544 kJ) and the resting trials
(2586 kJ). These results indicate that exercise in cold water
stimulates energy intake. In similar fashion, Dressendorfer
[7] submitted six trained males to 30 min of modified
cycling in cold water (22C), warm water (34C), cycling
on land, and a resting control trial. Participants consumed
significantly more energy in the cold water trial than all
other trials at a buet meal provided immediately after
exercise. Furthermore, energy intake in the warm water trial
was significantly less than all other trials. Collectively, these
findings suggest that water temperature and possibly sub-
sequent core body temperature are important determinants
of feeding responses after exercise in water. Despite these
established findings, no study has previously examined the
specific eects of swimming (rather than modified cycling)
on appetite and food intake. Our findings appear to support
the notion that exercise only in cold water stimulates food
intake because in the present study the water temperature
was moderate (28–28.5C) and no change in energy intake
was observed. The idea that exercise only in cold water
Journal of Obesity 7
stimulates food intake is also supported by the finding
that metabolic rate (and hence energy expenditure) is not
increased by immersion in water at a temperature of 32C
(not that dissimilar from the temperature of the water in
the present study) whereas metabolic rate is increased by
C) [30]and
by cold air, possibly due to activation of brown adipose
tissue [31]. It might be anticipated that immersion in
water will only increase appetite and food intake if the
water temperature lowers core temperature, eliciting an
increase in metabolic rate either by shivering or nonshivering
thermogenesis although this is speculation. Unfortunately
core temperature was not assessed in the present study,
therefore the exact relationship between this variable and
energy intake cannot be explored. Further work is needed to
examine this issue.
This investigation has some notable limitations. Firstly,
an immersed, resting control trial was not included therefore
making it dicult to determine whether the reported
increase in appetite was due to immersion in water or
the physical work completed. Despite this, the majority
of previous investigations which have examined appetite
responses to exercise have not observed increases in appetite
afterwards [9], thus we believe that our findings still oer
novel, interesting data. Secondly, although we have examined
energy/macronutrient intake responses over an extended
period, it remains possible that changes may occur over
a longer duration of time, for example, on the day after
exercise. An even longer period of observation would be
necessary in future studies to test this hypothesis. Thirdly,
this study did not directly compare the eects of swimming
with those of other modes of exercise and this limits the
extent to which conclusions can be drawn in this regard.
Finally, participants were young, healthy males and we
do not know if these findings would generalise to other
populations such as females, the elderly or overweight and
obese individuals. Additional work is required to examine
these issues, particularly in overweight individuals as it is
within this population that findings hold the most clinical
In conclusion, this investigation has shown that an acute
bout of moderate intensity swimming suppresses appetite
during exercise before leading to an increase later on in
the day. Despite this, energy intake and macronutrient
selection appear resistant to change over the duration of time
examined. Circulating concentrations of acylated ghrelin
were suppressed during swimming and this may possibly
have contributed to the reduction in appetite observed.
Nonetheless, acylated ghrelin does not appear to mediate
the reported increase in appetite in the hours after exercise.
These findings provide novel information regarding the
influence of swimming on the acute regulation of energy
The authors would like to thank all of the participants for
dedicating their time to take part in this study. They would
like to thank Mr. James Carson and Mr. Michael Sawrey
for their assistance with participant recruitment and data
collection. They would also like to thank Miss Karen Shilton
for organising access to the university swimming pool.
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... Acute exercise suppresses acylated ghrelin and increases GLP-1 and PYY, which could be associated with satiety control (145). The temporary suppression of appetite occurs around 60% of the VO 2 peak (146-150) and has been shown in different types of exercise, such as running (146, 147, 149), cycling (148,151,152), swimming (153), high-intensity interval exercise (154,155) and resistance training (156) (see Table 2). However, peptide signaling may vary according to the exercise intensity and volume, diet, temperature, trainability, and the period of the day the exercise is performed (18,154,(174)(175)(176)(177). ...
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Obesity is one of the major pandemics of the 21st century. Due to its multifactorial etiology, its treatment requires several actions, including dietary intervention and physical exercise. Excessive fat accumulation leads to several health problems involving alteration in the gut-microbiota-brain axis. This axis is characterized by multiple biological systems generating a network that allows bidirectional communication between intestinal bacteria and brain. This mutual communication maintains the homeostasis of the gastrointestinal, central nervous and microbial systems of animals. Moreover, this axis involves inflammatory, neural, and endocrine mechanisms, contributes to obesity pathogenesis. The axis also acts in appetite and satiety control and synthesizing hormones that participate in gastrointestinal functions. Exercise is a nonpharmacologic agent commonly used to prevent and treat obesity and other chronic degenerative diseases. Besides increasing energy expenditure, exercise induces the synthesis and liberation of several muscle-derived myokines and neuroendocrine peptides such as neuropeptide Y, peptide YY, ghrelin, and leptin, which act directly on the gut-microbiota-brain axis. Thus, exercise may serve as a rebalancing agent of the gut-microbiota-brain axis under the stimulus of chronic low-grade inflammation induced by obesity. So far, there is little evidence of modification of the gut-brain axis as a whole, and this narrative review aims to address the molecular pathways through which exercise may act in the context of disorders of the gut-brain axis due to obesity.
... Markers such as lymphocytes and prolactin are affected by pool swimming training (Mihailescu et al. 2021). The effect of swimming as a part of weight loss program may not affect appetite-related control hormones while competitive training does (King et al. 2011;Fico et al. 2020). To analyze these parameters was not the aim of our study. ...
During ageing, anabolic status is essential to prevent the decrease in quantity and quality of skeletal muscle mass (SMM). Exercise modulates endocrine markers of muscle status. We studied the differences of endocrine markers for muscle status in 62 non-sarcopenic Mexican swimmer adults aged 30-70 y/o, allocated into two groups: the systematic training (ST) group including master athletes with a physical activity level (PAL) >1.6, and the non-systematic training group (NST) composed by subjects with a PAL <1.5. Body composition, diet, biochemical and endocrine markers were analyzed. The ST group showed lower myostatin (MSTN) and irisin (IRI) levels, two strong regulators of SMM. The insulin growth factor-1 (IGF-1) was higher in the ST. This is consistent with most of the evidence in young athletes and resistance training programs, where IGF-1 and IRI seem to play a crucial role in maintaining anabolic status in master athletes.
... Higher EI in weight reduced obese or sleep deprived subjects (one night of sleep deprivation reduced core temperature and increased heat loss due to a cold stimulus [52]), could also be related to reduced body temperature. In line with this idea, evidence suggests that swimming compared to other types of exercise may increase appetite and EI [53,54]. An orexigenic effect of swimming was identified that may not be explained solely by the EE of muscles [55], but may also be due to increased heat loss with immersion in cool water. ...
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Coupling energy intake (EI) to increases in energy expenditure (EE) may be adaptively, compensatorily, or maladaptively leading to weight gain. This narrative review examines if functioning of the homeostatic responses depends on the type of physiological perturbations in EE (e.g., due to exercise, sleep, temperature, or growth), or if it is influenced by protein intake, or the extent, duration, timing, and frequency of EE. As different measures to increase EE could convey discrepant neuronal or humoral signals that help to control food intake, the coupling of EI to EE could be tight or loose, which implies that some ways to increase EE may have advantages for body weight regulation. Exercise, physical activity, heat exposure, and a high protein intake favor weight loss, whereas an increase in EE due to cold exposure or sleep loss likely contributes to an overcompensation of EI, especially in vulnerable thrifty phenotypes, as well as under obesogenic environmental conditions, such as energy dense high fat—high carbohydrate diets. Irrespective of the type of EE, transient elevations in the metabolic rate seem to be general risk factors for weight gain, because a subsequent decrease in energy requirement is not compensated by an adequate adaptation of appetite and EI.
... These effects should, in theory, result in reduced appetite and energy intake at the subsequent meal according to ghrelin's orexigenic [37] and PYY's anorexigenic characteristics [38]. Whilst reductions in subjective appetite are commonly reported during or immediately after exercise [39,40], these reductions are usually corrected shortly after exercise has ceased and before eating, but endocrine alterations can persist [41]. Whilst aerobic exercise does, on the whole, produce weight loss, the typical weight loss observed is far from what would be predicted on the basis of the energy deficit created by acute studies [42][43][44]. ...
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Purpose: We previously observed increased energy intake (EI) at the meal before planned afternoon exercise, but the proximity of the meal to exercise might have reduced the scale of the pre-exercise anticipatory eating. Therefore, this study examined EI in the 24 h before fasted morning exercise. Methods: Fourteen males, experienced with gym-based aerobic exercise (age 25 ± 5 years, BMI 23.8 ± 2.5 kg/m 2), completed counterbalanced exercise (EX) and resting (REST) trials. On day 1, subjects were told the following morning's activity (EX/ REST), before eating ad-libitum laboratory-based breakfast and lunch meals and a home-based afternoon/evening food pack. The following morning, subjects completed 30-min cycling and 30-min running (EX; 3274 ± 278 kJ) or 60-min supine rest (REST; 311 ± 34 kJ) fasted. Appetite was measured periodically, and EI quantified. Results: Afternoon/evening EI (EX 7371 ± 2176 kJ; REST 6437 ± 2070 kJ; P = 0.017) and total 24-h EI (EX 14,055 ± 3672 kJ; REST 12,718 ± 3379 kJ; P = 0.011) were greater during EX, with no difference between trials at breakfast (P = 0.761) or lunch (P = 0.071). Relative EI (EI minus energy expended through EX/REST) was lower in EX (EX 10,781 ± 3539 kJ; REST 12,407 ± 3385 kJ; P = 0.004). Conclusion: This study suggests planned fasted aerobic exercise increases EI during the preceding afternoon/evening, precipitating a ~ 10% increase in EI in the preceding 24-h. However, this increase did not fully compensate for energy expended during exercise; meaning exercise induced an acute negative energy balance.
... However, we would not be able to tease out chronic effects from the acute effects of exercise. In this context, an acute bout of swimming had no influence on food intake or ghrelin concentrations (11). ...
Swimming is a favorable and ideal modality of exercise for individuals with obesity and arthritis as it encompasses a minimal weight-bearing stress and a reduced heat load. However, the available evidence indicates that regular swimming may not be effective in reducing body weight and body fatness. A current hypothesis is that exercise in cold water stimulates appetite. We determined the effect of swimming training on appetite-related hormones. Thirty-nine adults with obesity and osteoarthritis were randomly assigned to 12 weeks of supervised swimming or cycling training. In the initial few weeks, participants exercised for 20-30 minutes/day, 3 days/week, at an exercise intensity of 40-50% of heart rate reserve (HRR). Subsequently, the intensity and duration of exercise were progressively increased to 40-45 minutes/day, 3 days/week, at an intensity of 60-70% of HRR. Fasting plasma concentrations of ghrelin, insulin, leptin, and peptide YY did not change with the swimming or cycling exercise training (p>0.05). Swimming exercise did not negatively influence appetite-related hormones in adults with obesity and osteoarthritis to impair weight loss.
Single bouts of land-based exercise suppress appetite and do not typically alter energy intake in the short-term, whereas it has been suggested that water-based exercise may evoke orexigenic effects. The primary aim was to systematically review the available literature investigating the influence of water-based exercise on energy intake in adults (PROSPERO ID number CRD42022314349). PubMed, Medline, Sport-Discus, Academic Search Complete, CINAHL and Public Health Database were searched for peer-reviewed articles published in English from 1900 to May 2022. Included studies implemented a water-based exercise intervention versus a control or comparator. Risk of bias was assessed using the revised Cochrane ‘Risk of bias tool for randomised trials’ (RoB 2.0). We identified eight acute (same day) exercise studies which met the inclusion criteria. Meta-analysis was performed using a fixed effects generic inverse variance method on energy intake (8 studies (water versus control), 5 studies (water versus land) and 2 studies (water at two different temperatures)). Appetite and appetite-related hormones are also examined but high heterogeneity did not allow a meta-analysis of these outcome measures. We identified one chronic exercise training study which met the inclusion criteria with findings discussed narratively. Meta-analysis revealed that a single bout of exercise in water increased ad-libitum energy intake compared to a non-exercise control (mean difference [95% CI]: 330 [118, 542] kJ, P = 0.002). No difference in ad libitum energy intake was identified between water and land-based exercise (78 [-176, 334] kJ, P = 0.55). Exercising in cold water (18–20 °C) increased energy intake to a greater extent than neutral water (27–33 °C) temperature (719 [222, 1215] kJ; P < 0.005). The one eligible 12-week study did not assess whether water-based exercise influenced energy intake but did find that cycling and swimming did not alter fasting plasma concentrations of total ghrelin, insulin, leptin or total PYY but contributed to body mass loss 87.3 (5.2) to 85.9 (5.0) kg and 88.9 (4.9) to 86.4 (4.5) kg (P < 0.05) respectively. To conclude, if body mass management is a person's primary focus, they should be mindful of the tendency to eat more in the hours after a water-based exercise session, particularly when the water temperature is cold (18–20 °C).
Despite the irrefutable benefits of achieving the UK Chief Medical Officers physical activity guidelines, including the prevention and treatment of non-communicable diseases for people with obesity, misrepresentation of physical activity and exercise in mainstream media has become a public health problem. This poor representation of physical activity and exercise is damaging and could contribute to uncertainty regarding the role of energy expenditure in weight management. When healthcare professionals fail to promote physical activity and exercise in the populations that need it, the impact of this misinformation can be very damaging. This chapter addresses physical activity, exercise, and weight management issues for people with obesity. By firstly challenging misconceptions that exercise makes you hungrier and eat more at the next meal and thereafter presenting evidence that physical activity can contribute to weight loss but more importantly weight loss maintenance and the prevention of weight regain. Finally, examples of key considerations when trying to increase physical activity and exercise in people with obesity are provided.KeywordsPhysical activityExerciseEnergy expenditureObesity
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Background Ghrelin is a peptide hormone predominantly produced by the stomach. It exerts a wide range of functions including stimulating growth hormone release and regulating appetite, food intake, and glucose and lipid metabolism. Since physical exercise affects all these aspects, a particular interest is accorded to the relationship between ghrelin and exercise. This systematic review aimed to summarize the current available data on the topic for a better understanding of the relationship. Methods An extensive computerized search was performed in the PubMed and SPORTDiscus databases for retrieving relevant articles. The search contained the following keywords: ghrelin, appetite-related peptides, gastrointestinal peptides, gastrointestinal hormones, exercise, acute exercise, chronic exercise, training, and physical activity. Studies investigating the effects of acute/chronic exercise on circulating forms of ghrelin were included. Results The initial search identified 840 articles. After screening, 80 articles were included. Despite a heterogeneity of studies and a variability of the findings, the review suggests that acute exercise suppresses acyl ghrelin production regardless of the participants and the exercise characteristics. Long- and very long-term exercise training programs mostly resulted in increased total and des-acyl ghrelin production. The increase is more noticeable in overweight/obese individuals, and is most likely due to weight loss resulting from the training program. Conclusion The review suggests that exercise may impact ghrelin production. While the precise mechanisms are unclear, the effects are likely due to blood flow redistribution and weight loss for acute and chronic exercise, respectively. These changes are expected to be metabolically beneficial. Further research is needed for a better understanding of the relationship between ghrelin and exercise.
We tested the effect of different intensities of acute exercise on hunger, and post-exercise energy intake, and neurophysiological measures of attention towards food- and non-food stimuli in women. In a within-subjects crossover design, forty-two women completed no exercise, moderate-intensity exercise, and vigorous-intensity exercise sessions separated by one week, in a counterbalanced fashion. At each session, participants completed a passive viewing task of food (high- and low-calorie) and non-food pictures while electroencephalogram (EEG) data were recorded. The early posterior negativity (EPN), P3, and late positive potential (LPP) components of the event-related potential (ERP) measured neurophysiological responses. Subjective ratings of hunger were measured before and immediately after each condition using a visual analog scale (VAS) and food intake was measured using an ad libitum snack buffet offered at the end of each condition. Results indicated that hunger levels increased as time passed for all sessions. EPN amplitude was larger to non-food compared to food images; P3 amplitude was larger to food than non-food stimuli. LPP amplitude did not differ by high-calorie, low-calorie, or non-food images. Notably, there were no significant main effects or interactions of any ERP component amplitude as a function of exercise intensity. Food intake also did not differ by rest or moderate or vigorous exercise, although subjective arousal ratings to the images were higher after moderate and vigorous exercise compared to rest. Food images also had higher arousal and valence ratings than non-food images overall. Findings indicate that, in this sample, acute moderate and vigorous exercise compared to rest did not disproportionately affect neurophysiological measures of attention to food or non-food stimuli, caloric intake, or hunger.
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Overweight and obesity affects more than 66% of the adult population and is associated with a variety of chronic diseases. Weight reduction reduces health risks associated with chronic diseases and is therefore encouraged by major health agencies. Guidelines of the National Heart, Lung, and Blood Institute (NHLBI) encourage a 10% reduction in weight, although considerable literature indicates reduction in health risk with 3% to 5% reduction in weight. Physical activity (PA) is recommended as a component of weight management for prevention of weight gain, for weight loss, and for prevention of weight regain after weight loss. In 2001, the American College of Sports Medicine (ACSM) published a Position Stand that recommended a minimum of 150 min wk(-1) of moderate-intensity PA for overweight and obese adults to improve health; however, 200-300 min wk(-1) was recommended for long-term weight loss. More recent evidence has supported this recommendation and has indicated more PA may be necessary to prevent weight regain after weight loss. To this end, we have reexamined the evidence from 1999 to determine whether there is a level at which PA is effective for prevention of weight gain, for weight loss, and prevention of weight regain. Evidence supports moderate-intensity PA between 150 and 250 min wk(-1) to be effective to prevent weight gain. Moderate-intensity PA between 150 and 250 min wk(-1) will provide only modest weight loss. Greater amounts of PA (>250 min wk(-1)) have been associated with clinically significant weight loss. Moderate-intensity PA between 150 and 250 min wk(-1) will improve weight loss in studies that use moderate diet restriction but not severe diet restriction. Cross-sectional and prospective studies indicate that after weight loss, weight maintenance is improved with PA >250 min wk(-1). However, no evidence from well-designed randomized controlled trials exists to judge the effectiveness of PA for prevention of weight regain after weight loss. Resistance training does not enhance weight loss but may increase fat-free mass and increase loss of fat mass and is associated with reductions in health risk. Existing evidence indicates that endurance PA or resistance training without weight loss improves health risk. There is inadequate evidence to determine whether PA prevents or attenuates detrimental changes in chronic disease risk during weight gain.
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In this review, we discuss the effects of acute and chronic exercise on appetite and food intake regulation, the potential mechanisms involved and its relationship with hormonal and metabolic changes that affect energy balance. The mechanisms of post exercise short-term appetite modification remain unclear and although the role of orexigenic and anorexigenic peptides is possible hypotheses, it still remains unproven. Motivation to eat and food intake in response to acute exercise seem to be modulated by gender, body weight and eating behavior. In general, acute exercise has no effect on subsequent El in men, whereas in women an increase in El is usually observed, either decreasing or abolishing the effects of exercise on EB. Normal weight women, unlike men, report an increased palatability of foods with exercise and do not experience the transient suppression of hunger observed immediately after exercise. The evidence to date emphasizes the need to increase physical exercise levels, particularly because of the high prevalence of obesity. More research is needed to explain the mechanisms behind the post exercise adjustments in short-term appetite control, and their long-term consequences.
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The beneficial effects of regular exercise are primarily based on data using land-based exercise. Currently, no data exist that demonstrate the efficacy of swimming exercise for the treatment of obesity and cardiovascular risk factors, despite the fact that swimming is a widely recommended exercise mode. Eighteen previously sedentary obese individuals were divided into a swim-training group and a non-exercising control group. The training group swam at 60% of maximal heart rate reserve for 45 min per day for 3 days per week for 10 weeks, whereas the control group remained sedentary. The swim-training programme produced significant cardiovascular training effects, as evidenced by reductions (P < 0.05) in resting and submaximal heart rate values in the training group. Significant reductions (P < 0.05) were also observed in the rating of perceived exertion and blood lactate concentrations during fixed submaximal exercise on an arm cycle ergometer. Caloric and macronutrient intake estimated from the dietary records stayed constant before and after training. Body mass, body fat percentage (36 +/- 2% vs. 35 +/- 2%) and body mass index, as well as regional adiposity, showed no statistically significant changes. Neither the training nor the control groups experienced significant changes in fasting serum glucose and insulin concentrations and glucose-insulin ratio during the study. Total, high-density lipoprotein (HDL)- and low-density lipoprotein (LDL)-cholesterol did not change significantly in either group. It was concluded that swim training of the duration, frequency and intensity used in the present study failed to elicit favourable modifications in these traditional cardiovascular risk factors.
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Using positron-emission tomography (PET), we found that cold-induced glucose uptake was increased by a factor of 15 in paracervical and supraclavicular adipose tissue in five healthy subjects. We obtained biopsy specimens of this tissue from the first three consecutive subjects and documented messenger RNA (mRNA) and protein levels of the brown-adipocyte marker, uncoupling protein 1 (UCP1). Together with morphologic assessment, which showed numerous multilocular, intracellular lipid droplets, and with the results of biochemical analysis, these findings document the presence of substantial amounts of metabolically active brown adipose tissue in healthy adult humans.
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Resistance (muscle strengthening) exercise is a key component of exercise recommendations for weight control, yet very little is known about the effects of resistance exercise on appetite. We investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 +/- 0.3 yr, body mass index 23.1 +/- 0.4 kg/m(2), maximum oxygen uptake 62.1 +/- 1.8 (means +/- SE) undertook three, 8-h trials, 1) resistance exercise: a 90-min free weight lifting session followed by a 6.5-h rest period, 2) aerobic exercise: a 60-min run followed by a 7-h rest period, 3) control: an 8-h rest, in a randomized crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way ANOVA revealed significant (P < 0.05) interaction effects for hunger, acylated ghrelin, and PYY, indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and increased PYY during aerobic exercise. A significant trial effect was observed for PYY, indicating higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve: control 1,411 +/- 110, resistance 1,381 +/- 97, aerobic 1,750 +/- 170 pg/ml 8 h). These findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrelin and PYY influence subsequent food intake.
Food choices and diet composition have been studied less often than energy intake in subjects with varying levels of physical activity. The reported effects of exercise on food choices are not fully consistent, especially on the short term. Type of exercise, intensity, duration can affect the results as well as subjects' characteristics (gender, age, previous training and fitness). A crucial role could also be played by psychological (chronic dieting, attitudes toward health and food, long-established food habits and preferences) and social (traditions, food availability, appropriate times and places) factors. In short-term intervention studies, where a meal is ingested a few minutes following a bout of exercise of varying duration and intensity, an increase in CHO intake is most often reported, while increased protein intake is an occasional observation. In long-term (several weeks) training interventions, intake is assessed from dietary records. Again CHO intake is augmented in exercised subjects as compared to controls, while that of saturated fats and cholesterol may also be affected. Epidemiological studies (without dietary or exercise intervention) often report that habitually active persons eat more and ingest more fruits and vegetables than less active peers. It is not known to what extent such food choices are driven by biological needs (e.g. replacement of glycogen) or elicited by social and psychological factors.
It is the position of the American Dietetic Association that successful weight management to improve overall health for adults requires a lifelong commitment to healthful lifestyle behaviors emphasizing sustainable and enjoyable eating practices and daily physical activity. Given the increasing incidence of overweight and obesity along with the escalating health care costs associated with weight-related illnesses, health care providers must discover how to effectively treat this complex condition. Food and nutrition professionals should stay current and skilled in weight management to assist clients in preventing weight gain, optimizing individual weight loss interventions, and achieving long-term weight loss maintenance. Using the American Dietetic Association's Evidence Analysis Process and Evidence Analysis Library, this position paper presents the current data and recommendations for weight management. The evidence supporting the value of portion control, eating frequency, meal replacements, and very-low-energy diets are discussed as well as physical activity, behavior therapy, pharmacotherapy, and surgery. Public policy changes to create environments that can assist all populations to achieve and sustain healthful lifestyle behaviors are also reviewed.