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This is the author’s version of a work that was submitted/accepted for pub-lication in the following source:
Martins, Catia, Stensvold, Dorthe, Finlayson, Graham, Holst, Jens, Wisloff,Ulrik, Kulseng, Bard, Morgan, Linda, & King, Neil A.(2015)Effect of moderate- and high-intensity acute exercise on appetite in obeseindividuals.Medicine & Science in Sports & Exercise, 47 (1), pp. 40-48.
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https://doi.org/10.1249/MSS.0000000000000372
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Title: Effect of moderate and high intensity acute exercise on appetite in obese individuals
Catia Martins1,2; Dorthe Stensvold3; Graham Finlayson4; Jens Holst5; Ulrik Wisloff3; Bård
Kulseng1,2; Linda Morgan6 and Neil A. King7
1 Obesity Research Group, Department of Cancer Research and Molecular Medicine, Faculty
of Medicine, Norwegian University of Science and Technology, Trondheim, Norway; 2 Center for Obesity, Department of Surgery, St. Olav Hospital – Trondheim University
Hospital, Trondheim, Norway 3 K.G. Jebsen Center for Exercise in Medicine at Department of Circulation and Medical
Imaging, Trondheim, Norway. 4 BioPsychology Group, Institute of Psychological Sciences, University of Leeds, Leeds,
United Kingdom
5 Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark
6 Department of Nutrition and Metabolism, University of Surrey, Guildford, UK 7 Institute of Health and Biomedical Innovation, Queensland University of Technology,
Brisbane, Australia
Corresponding author: Catia Martins
Institutt for Kreftforskning og molekylær medisin
Medisinsk teknisk forskningssenter
Olav Kyrres gt. 9, N-7489 Trondheim - Norway
email: [email protected]
Running title: Acute exercise and appetite in the obese
Word count: 3970 words
Funding: Liaison Committee between the Central Norway Regional Health Authority (RHA)
and the Norwegian University of Science and Technology (NTNU).
Conflict of interest: The authors declare that there is no conflict of interest that would
prejudice the impartiality of this scientific work.
2
Abstract:
Purpose: The impact of acute exercise, and exercise intensity, on appetite control in obese
requires further study. The aim of this study was to compare the effects of acute isocaloric
bouts (250kcal) of high-intensity intermittent cycling (HIIC) and moderate-intensity
continuous cycling (MICC), or short-duration HIIC (S-HIIC) (125kcal), and a resting control
condition, on the appetite hormones responses, subjective feelings of appetite, energy intake
(EI) and food reward in overweight/obese individuals.
Methods: Randomized cross-over study in twelve overweight/obese volunteers. Participants
were assigned to the control, MICC, HIIC and S-HIIC conditions, 1 week apart, in a counter-
balanced order. Exercise was performed 1 hour after a standard breakfast. An ad libitum test
lunch was served 3h after breakfast. Fasting/postprandial plasma samples of insulin, acylated
ghrelin (AG), polypeptide YY3-36 (PYY3-36) and glucagon-like peptide 1 (GLP-1) and
subjective feelings of appetite were measured every 30 minutes for 3h. Nutrient and taste
preferences were measured at the beginning and end of each condition using the Leeds Food
Preference Questionnaire
Results: Insulin levels were significantly reduced and GLP-1 levels significantly increased
during all exercise bouts, compared with rest. AG plasma levels were lower in the MICC and
HIIC, but not S-HIIC, compared with control. There were no significant differences for PYY3-
36 plasma levels, hunger or fullness ratings, EI or food reward.
Conclusion: Our findings suggest that, in overweight/obese individuals, isocaloric bouts of
moderate or high-intensity exercise lead to a similar appetite response. This strengthens
previous findings in normal-weight individuals that acute exercise, even at high intensity does
not induce any known physiological adaptation that would lead to increased EI.
Keywords: ghrelin, polypeptide YY, glucagon-like peptide 1, food reward
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Introduction:
1. Obesity has become a global epidemic worldwide (33). This picture is undeniably linked to a
decrease in physical activity (PA) levels over the past few decades, driven by dramatic
changes in lifestyle (31). Although the role of PA in preventing weight gain is widely
accepted (12), its impact on weight loss, in the absence of energy restriction, seems to be only
modest (25). The ability of exercise to create a negative energy balance (EB) relies directly on
its ability to increase energy expenditure (EE), but also indirectly on its potential to modulate
energy intake (EI) and appetite (16, 18). It has already been shown that the lower than
expected weight loss experienced by some in response to an exercise intervention can be
explained, at least partially, by a compensatory increase on EI (15).
2. Appetite is controlled by a series of complex processes in the brain and multiple hormones
released peripherally (for a review see Blundell, 2006 (3)). Determining how acute exercise
impacts on appetite will provide a better understanding of its role on food intake and body
weight homeostasis. Moreover EI responses to acute exercise may also be influenced by
changes in the hedonic system, with changes for example in food preferences (2).
3. The majority of the studies, in normal-weight individuals, indicates that acute exercise does
not increase hunger or EI, even at high intensities, and that exercise is, therefore, able to
induce a short-term negative EB (18). Acute exercise does not seem to influence total ghrelin
(TG) (an orexigenic hormone) concentrations (18), and several studies have shown a
significant suppression in the active component of the hormone, acylated ghrelin (AG), in
response to high-intensity exercise (5, 13, 20), but not brisk walking (14). Moreover, exercise
has been shown to increases the release of satiety hormones such as polypeptide YY (PYY)
and glucagon-like peptide 1(GLP-1) in normal-weight individuals (19). Overall, the available
evidence suggests that acute exercise does not induce physiological adaptations leading to
increased EI in the short-term (18).
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4. However, few studies have been performed in the obese. Ueda and colleagues (2009) reported
no change in TG and a significant increase in PYY and GLP-1 plasma levels with moderate-
intensity exercise (compared with rest), in normal-weight and obese men (29). Marzullo and
collaborators (2008) also showed no change in TG with maximal exercise, in normal-weight
and obese individuals, despite a significant suppression in AG (20). Finally, Westerterp-
Plantenga and collaborators (1997) reported a significant suppression in hunger and EI after
2h of cycling at 60% max workload in normal-weight and obese men (32).
5. Three recent reviews/meta-analysis, including obese individuals, have addressed the impact of
exercise on appetite (8, 23, 24). They have concluded that there is little or no evidence that
acute exercise affects energy or macronutrient intake, therefore, being able to produce a short-
term negative energy deficit (8, 23). Moreover, acute exercise is associated with positive
changes in appetite-related hormones, supressing levels of AG, while simultaneously
increasing levels of satiety peptides (PYY, GLP-1 and pancreatic polypeptide) (24).
6. High-intensity intermittent exercise, in which high intensity work is interspersed with low-
intensity work, has been shown to be a time saving and sustainable exercise method, even in
the untrained obese patient, with good results on body weight and composition,
cardiovascular fitness and insulin resistance (4). However, few studies have compared the
impact of different intensities of acute bouts of exercise on appetite, and they were performed
in trained normal-weight men (6, 7, 28) and did not standardise the energy expenditure of the
exercise bouts (6, 28). In a recently published study, Sim and colleagues (2013) reported a
lower ad libitum EI after high-intensity intermittent cycling (HIIC) and very-HIIC, compared
with control and a significantly lower AG plasma levels after very-HIIC compared with the
other conditions in overweight inactive men (26). However, this study included men only,
who were not obese, and exercise was performed in fasting. This has limitations concerning
5
generalization of the results to other populations and in conditions where exercise is
performed in the postprandial state, which is the case in the majority of the situations.
7. The primary objective of this study was to investigate the effects of acute isocaloric bouts of
HIIC and moderate-intensity continuous cycling (MICC) (250kcal) (and a short bout of HIIC
(average 9 minutes – 125kcal)), in comparison with a resting control condition, on the
postprandial release of appetite-regulating hormones, subjective feelings of appetite,
subsequent EI and food reward in overweight/obese individuals. We hypothesized that an
isocaloric session of HIIC would result in a larger reduction in AG and hunger, a larger
increase in satiety peptides and a greater reduction in subsequent EI compared with MICC
(and that the short-bout of HIIC would produce the same appetite changes as MICC).
8.
Methods:
Subjects
9. Twelve healthy but sedentary overweight/obese volunteers (five males and seven females),
not currently dieting to lose weight and weight stable on the previous 3 months (≤2kg
variation), were recruited for this study. Participants had an average (±SD) age of 33.4±10.0
years, an average (±SD) BMI of 32.3±2.7 kg/m2 and an average (±SD) VO2max of 30.5±4.9
ml/kg/min.
10. The exclusion criteria were as follows: a restraint score derived from the Three Factor Eating
Behaviour Questionnaire>12 (TFEQ) (30), history of coronary heart disease, type 1 or type 2
diabetes, anaemia, gout, depression or other psychological disorders, eating disorders, drug or
alcohol abuse within the last two years, current medication known to affect appetite or induce
weight loss and hypertension.
11. This study was conducted according to the guidelines laid down in the Declaration of Helsinki
and was approved by the regional Ethics Committee (Midt-Norge, Trondheim, Norway) (Ref.
6
2010/444-1). Written informed consent was obtained from all participants before enrolling in
the study.
Study design
12. This was a randomised cross-over study with four conditions. Participants acted as their own
controls and were assigned to the four experimental conditions: control, MICC, HIIC and S-
HIIC, 1 week apart, in a counter-balanced order.
Detailed protocol
13. Participants were asked to attend the Research Unit five times: one preliminary familiarisation
session and four experimental conditions: control, MICC and HIIC isocaloric sessions
designed to induce a 250kcal energy deficit and S-HIIC designed to induce an energy deficit
of 125kcal.
14. In order to reduce the inherent variability, participants were instructed to refrain from
exercising and from drinking alcohol and caffeine 24h prior to and on the day of each
experimental condition. Participants were also asked to record on a food diary everything they
ate and drank for dinner on the day before the first experimental condition and asked to
consume exactly the same type and amount of food for dinner on the day before the other
three conditions. Participants were interviewed in the morning of each experimental condition
in order to check their compliance with these requirements.
15. In the preliminary session, anthropometric data were collected and cardiovascular fitness
(VO2max) was measured on a cycle ergometer (Ergomedic 839E, Monark 2008, Sweden)
using the system Oxigen Pro (Viasys Healthcare, Hoechberg, Germany). The test started with
a 5 min warm up with a resistance of 50W and afterwards the workload was gradually
increased by 20W every 2 minutes and participants asked to maintain a cadence between 60-
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70 rpm. An expiratory exchange ratio (RER) of 1.05 or above, was set as the criterion for
achieving VO2max. Heart rate was continuously recorded during the test using a heart rate
(HR) monitor (Polar type 610; Polar Electro Oy). Maximal heart rate was defined by adding
five beats to the highest heart rate value obtained during the VO2max test.
16. For the four experimental conditions, participants were asked to arrive at approximately 8.00,
having fasted for at least 10 hours (water was permitted ad libitum during this time), and a
cannula was inserted into an antecubital vein. A fasting blood sample was taken and
participants were instructed to consume a standard breakfast (time = zero), consisting of
bread, orange juice, milk, cheese, and jam (600 kcal, 17% protein, 35% fat, and 48%
carbohydrate) within 10 min. After that, serial blood samples were taken at regular intervals
for a period of 3h (30, 60, 80, 100, 120, 150 and 180 minutes) and analysed for haemoglobin,
haematocrit, insulin, AG and PYY3-36 and GLP-1.
17. Participants were asked to rate their subjective feelings of hunger, fullness and desire to eat
using 10cm visual analogue scales (VAS) throughout each study morning, at different time
points (right before each blood sample), as previously described (11). The reward value of
food was measured using a computer-based behavioural procedure called the Leeds Food
Preference Questionnaire (LFPQ) (10), immediately before and after each condition. The
LFPQ provides measures of explicit liking (EL), implicit wanting (IW) and relative food
preference (FP) according to the shared sensory properties of foods.
18. Three hours after breakfast, participants were placed in individual rooms, presented with a
standardized lunch and instructed to rate the taste and palatability of the food presented (and
afterwards to eat as much or as little as they wanted, from the food presented). The
standardized ad libitum lunch test meal consisting of 10 ¼ of sandwiches, 300g of strawberry
yoghurt and 60g of crisps, in excess of expected consumption (1358kcal, 53g P, 61g fat, 133g
carbohydrates). Participants were asked in advance to rank four sandwiches’ fillings (ham,
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cheese, salami and liver paste) by order of preference. Participants were then offered their
second most liked option.
19. Participants were then allowed to leave the Research Unit, but were asked to use an
AiperMotion 440PC accelerometer (Aipermon GmbH & Co. KG, Munich, Germany) to
measure PA levels, until retiring to bed. They were also asked to write down everything they
ate and drank for the rest of the day in a food diary, to estimate cumulative EI over that day
(lunch plus subsequent EI till bedtime). Dietary analysis was performed using Mat på Data
5.0 program (Landsforeningen for kosthold og helse, Oslo, Norway).
Experimental conditions
20. During the resting condition, participants remained seated, but were allowed to read, write or
use a computer. During the exercise conditions, participants performed one of three exercise
sessions, one hour after breakfast. Water was allowed ad bibitum in all four conditions. Each
exercise session started with a 5 min warm-up and finished with a 5-min cool down. The
MICC consisted of cycling at 70% maxHR. The HIIC consisted of bouts of 8s sprinting (all
out) and 12 s of turning the pedals very slowly (20-30 rpm). Participants were asked to follow
a pre-recorded tape which prompted them to start and stop cycling so that the work:rest ratio
was 8s:12s. The resistance used was that needed to increase the participant’s HR to 85-90%
maxHR. The S-HIIC was the same as the HIIC but for only half duration. The duration of
each exercise session was individually designed (based on data collected during the VO2max
test), in order to induce a 250kcal (MICC and HIIC) or 125kcal (S-HIIC) energy deficit. HR
was measured continuously, during each exercise session, using a HR monitor (Polar F1 –
Polar Electro Oy, Kempele, Finland). Average duration of each exercise session was 27±6,
18±3 and 9±2 minutes for the MICC, HIIC and S-HIIC sessions, respectively. Average HR
9
during exercise was 133±8 (71±1% maxHR), 162±11 (86±2.5% maxHR) and 160±9
(85±3.5% maxHR) beats per minute, for the MICC, HIIC and S-HIIC sessions, respectively.
Hormone and metabolite measurement
21. Venous blood was collected into regular EDTA tubes for the measurement of haemoglobin
and haematocrit and EDTA-coated tubes containing 500 KIU aprotinin (Pentapharm, Basel,
Switzerland)/ml whole blood for the measurement of insulin and gut peptides. Haemaglobin
and haematocrits were measured using standard haematological procedures. The other EDTA
tubes containing aprotinin were then centrifuged at 2000 g for 10 minutes and kept at –80° C
for later analyses. For the measurement of AG, 50 μl of a 1 N hydrochloric acid solution and
10 μl of Phenylmethylsulfonyl fluoride (Sigma, Schnelldorf, Germany) (10 mg/ml of
isopropanol) was added to each ml of plasma immediately after centrifugation. All samples
were batch analysed at the end of the study to reduce inter-assay variability.
22. Insulin, AG and PYY3-36 were quantified using human-specific RIA kits (Linco Research, St
Charles, USA) and GLP-1 using an in house RIA method. GLP-1 concentrations in plasma
were measured by RIA after extraction of plasma with 70 % ethanol (vol/vol, final
concentration) as previously described (20). Carboxy-terminal GLP-1 immunoreactivity was
determined using antiserum 89390 which has an absolute requirement for the intact amidated
carboxy-terminus of GLP-1 (7-36) amide and crossreacts less than 0.01% with carboxy-
terminally truncated fragments and 89% with GLP-1 (9-36) amide, the primary metabolite of
dipeptidyl-peptidase IV mediated degradation. The sum of the two components (total GLP-1
concentration) reflects the rate of secretion of the L-cell.
23. The sensitivity of the assays was 14 pmol/L for insulin, 7.8 pg/ml for AG, 1 pmol/L for GLP-
1 and 2 pmol/l for PYY3-36. All samples were assayed in duplicate and samples from the
10
same participant (all 4 legs) were analysed in the same batch. The intra-assay coefficient of
variation was of <10% for insulin and AG and <5% for GLP-1 and PYY3-36.
Statistical analysis
24. Statistical analysis was carried out using SPSS version 13.0 (SPSS Inc., Chicago, IL). All the
variables were checked regarding their normal distribution using the Shapiro-Wilk test and
data expressed as mean ± SEM, unless otherwise stated.
25. Differences in fasting/postprandial levels of metabolites and hormones and appetite sensations
between the experimental conditions were assessed by a repeated measure ANOVA using
experimental condition and time as independent variables. Due to significant differences in
hemoglobin plasma levels and hematocrit (see results section) among conditions, suggesting
hemoconcentration during the exercise legs, plasma levels of the appetite hormones measured
were adjusted for hematocrit (by multiplying by baseline hematocrit/hematocrit at a specific
time point). The area under the curve (AUC) for plasma levels of appetite related hormones
and subjective feeling of appetite was calculated from before to 180 min after breakfast using
the trapezoidal rule (baseline measurements were taken into account). Differences among
experimental conditions were assessed by repeated measures ANOVA. Post hoc analysis,
with Bonferroni adjustment, was used to perform multiple comparisons.
26. Relative energy intake (REI), at the lunch test meal, was calculated by subtracting the
estimated EE during the exercise and rest sessions (180 minutes) from their respective lunch
EI. EE during the three hours at the Research Unit was estimated based on the assumption that
participants were allowed to read, write, work with the computer, etc, corresponding to a
MET=1.3 (1). EE during the MICC and HIIC was the same as the control condition + 250kcal
and for the S-HIIC, the same as the control condition + 125kcal. Differences in absolute and
11
relative EI and macronutrient intake at lunch, and absolute energy and macronutrient intake
throughout the day among conditions, were assessed by repeated measured ANOVA. Post hoc
analysis, with Bonferroni adjustment, was used to perform multiple comparisons.
27. The reward value of food (explicit liking and implicit wanting response measures and relative
food preference) was analyzed using two 4x2 design ANOVA (experimental condition x time
(pre/post) for high fat relative to low fat food.
Results:
Hemoglobin and hematocrit
28. Hemoglobin plasma levels and hematocrit changes over time in the four conditions can be
seen in figure 1. There was a significant effect of time (P<0.0001) and a condition*time
interaction (P<0.0001) on both hemoglobin and hematocrit. Hemoglobin plasma levels
experienced a peak during exercise (quickly returning to control levels once the exercise
stopped) in the three exercise conditions (Figure 1a). A similar pattern was observed for
hematocrit (Figure 1b).
Appetite-related hormones
29. Plasma levels of insulin, AG, PYY3-36 and GLP-1 overtime in the different conditions can be
seen in figure 2.
30. A significant effect of time (P<0.0001) and a condition*time interaction (P<0.0001) were
observed on insulin plasma levels, but no main effect of condition (P>0.05) (Figure 2a).
Insulin plasma levels showed a peak at t=30 minutes and decreased gradually afterwards in
the control rest condition. In the exercise conditions, a pronounced reduction was observed
12
during the exercise period (60-80 minutes), with an increase being observed shortly
afterwards. No significant effect of condition was observed on insulin AUC (see
supplementary table 1).
31. A significant effect of time (P<0.0001) and condition (P<0.001), but no interaction, were
observed on AG plasma levels (Figure 2b). AG plasma levels decreased after breakfast
consumption with a nadir between 60-100 minutes and experienced a gradual increase
afterwards. Moreover, AG plasma levels were significantly reduced in the MICC and HIIC
conditions (P<0.05) (but not S-HIIC), compared with control. No significant difference was
observed in AG plasma levels between the MICC and HIIC conditions. A significant effect of
condition was observed on AG AUC (P=0.001), with AG AUC being significantly lower in
the MIIC and HIIC compared with control (P=0.02 and P=0.037, respectively) (see
supplementary table 1).
32. A significant effect of time (P<0.0001), but no effect of condition or interaction, was
observed on PYY3-36 plasma levels (Figure 2c), which increased gradually following breakfast
consumption. No significant effect of condition was observed on PYY AUC (see
supplementary table 1).
33. A significant effect of time (P<0.0001) and a condition*time interaction (P<0.0001), but no
main effect of condition (P>0.05), were observed on GLP-1 plasma levels. GLP-1 plasma
levels peaked at around 30 minutes and decreased afterwards in the control rest condition.
GLP-1 plasma levels were higher in the exercise conditions, compared with the control rest
condition, during and in the post-exercise period. No significant effect of condition was
observed on GLP-1 AUC (see supplementary table 1).
13
Subjective feelings of appetite and subsequent food intake
34. Subjective feelings of appetite can be seen in figure 3.
35. There was a significant effect of time (P<0.0001), but no effect of condition or interaction on
hunger and fullness ratings (figure 3a and 3b). For desire to eat, there was a significant effect
of time (P<0.001) and a time*condition interaction (P<0.05), but no main effect of condition
(figure 3c). Desire to eat ratings decreased immediately after breakfast consumption and
decreased afterwards and were lower in the exercise conditions compared with rest, during the
exercise period. No significant effect of condition was observed for hunger, fullness or desire
to eat AUC (see table, SDC1. AUC for subjective feelings of appetite and appetite-related
hormones in the different conditions).
36. Energy and macronutrient intake at lunch, after each condition, and throughout the day can be
seen in table 1. There were no significant differences in absolute energy or macronutrient
intake, at lunch or throughout the day, among conditions. There was a significant effect of
condition on REI at lunch (P<0.0001). Post hoc analysis showed that REI in the control
condition was significantly higher than in the exercise conditions (P<0.0001 for MICC,
P=0.002 for HIIC and P=0.01 for S-HIIC). REI after MIIC was also significantly lower than
after the S-HIIC (P<0.0001).
Physical activity levels throughout the day after each experimental condition
37. Time spent on different activities, throughout the day, in the different conditions can be seen
in table 2. No significant differences were observed on sedentary time or time spent walking
or fast walking among conditions. A significant effect of condition was observed on time
spent active (P=0.029). Further post hoc analysis, however, did not reveal any significant
difference in active time among conditions.
14
Food Reward
38. Explicit liking, implicit wanting and relative preference scores can be seen in table 3. Mean
scores were positive in all experimental conditions indicating that HF foods were more
rewarding, on average, than LF foods. There were no significant differences in the reward
value of high fat foods between conditions or over time (and no interaction between condition
and time) according to measures of explicit liking, implicit wanting or relative preference.
Discussion:
39. To the best of our knowledge, this is the first study to evaluate the role of exercise intensity on
appetite responses to acute bouts of exercise in overweight/obese individuals. Our hypothesis
that an isocaloric session of HIIC would result in a larger reduction in AG and hunger, a
larger increase in satiety peptides and a greater reduction in subsequent EI compared with
MICC was not confirmed.
40. In one of the few studies performed in obese individuals, Ueda and colleagues (2009) showed
that 60 minutes of cycling at 50% VO2max leads to a significant suppression in insulin, a
significant increase in PYY and GLP-1, and no changes in TG or subjective appetite feelings
in obese men (29). It is difficult to ascertain why, in the present study, exercising at an even
higher intensity was unable to increase PYY3-36 plasma levels. However, given the larger
exercise-induced energy deficit in Ueda and colleagues (2009) study, compared with ours
(~600kcal compared with 250kcal), it is possible that a larger energy deficit would be needed
to induce an increase in the postprandial release of PYY. Moreover, it is difficult to compare
studies which measured total PYY (PYY1-36) with studies measuring its active component
PYY3-36, since it remains unknown the conversion rate of total PYY (PYY1-36) to PYY3-36 and
only PYY3-36 has satiety properties.
15
41. In contrast to the majority of the studies performed in normal-weight individuals (18), a
transient suppression of hunger during exercise was not observed in the present study.
However, subjective feelings of desire to eat were lower during exercise (compared with rest),
regardless of the exercise condition. Westerterp-Plantenga and colleagues (1997), in a study
including both normal-weight and obese men, reported a significant suppression of hunger
after 2h of cycling at 60% of max workload (compared with a resting condition).
Unfortunately, analysis was not performed separately in obese men (32). Again, it is possible
that the larger exercise-induced EE in that study, compared with ours, has contributed to the
differences in outcome.
42. Absolute energy and macronutrient intake at the lunch test meal was similar regardless of the
experimental condition. However, REI was negative and significantly lower after the exercise
conditions compared with control. No significant differences were observed in absolute
energy and macronutrient intake throughout the day among conditions. However, taking into
account that sedentary and active time also did not differ among conditions, a lower REI and
subsequent negative EB, would be expected after acute exercise. This is in accordance with
Ueda and colleagues (2009) study, where a reduction in absolute and relative EI after 60
minutes of cycling at 50%VO2max, was reported in obese men (29).
43. Few studies have investigated the impact of exercise intensity on appetite. Ueda and
colleagues (2009) (28) looked at the impact of cycling at 50% or 75%VO2max (or rest) for 30
min on PYY3-36 and GLP-1 plasma levels, in normal-weight trained men. They reported a
larger increase in PYY3–36 plasma levels at higher intensity, despite a similar increase in GLP-
1 levels and a similar reduction in absolute EI and hunger feelings in both exercise conditions
(28). Kissileff and colleagues (1990) looked at the impact of strenuous (90 W) or moderate
(30 W) intensity cycling for 40 minutes (or rested) on food intake 15 minutes afterwards, in
normal-weight or overweight women. Food intake after exercise was significantly less after
16
the strenuous than after the moderate exercise in the normal-weight women but was similar in
obese women (17). The above evidence seems to suggest that high intensity exercise would,
not only, induce a larger suppression in orexigenic signals (AG), but also a larger release of
satiety signals (PYY3-36). However, the two last mentioned studies (17, 28) used non-
isocaloric bouts of exercise. Therefore, it is impossible to ascertain if the differences are due
to exercise intensity or to the larger energy deficit induced by the high-intensity exercise bout.
A recently published study in trained normal-weight men, using isocaloric bouts of HIIC and
MICC showed a significant suppression of hunger and a significant increase in PYY3-36
concentrations during/after exercise, especially during the HIIT, and no difference in ad
libitum EI (7).
44. In the present study, in overweight/obese individuals, using isocaloric bouts of moderate and
high intensity exercise, no significant impact of exercise intensity was observed on appetite
hormones, subjective feelings of appetite or EI. Exercise intensity, by itself, does not seem, at
least in overweight/obese individuals, to have an impact on appetite. In a recently published
study, Sim and colleagues (2013) randomly assigned overweight sedentary men to isocaloric
bouts of MICC (60% VO2peak), HIIC (60 s at 100% VO2peak: 240 s at 50% VO2peak), very-HIIC
(15 s at 170% VO2peak:60 s at 32% VO2peak) and control in a counterbalanced order. They
showed, as in our study, no differences in subjective appetite among conditions, but a lower
ad libitum EI after HIIC and very-HIIC compared with control and significantly lower AG
plasma levels after very-HIIC compared with the other conditions (26). However, that study
recruited overweight men and the exercise was performed in fasting. Moreover, the much
higher exercise intensity employed in that study, compared to ours, at levels that would be
difficult to sustain in the obese population, is likely to explain the different outcomes.
45. Few studies on the effects of exercise on appetite have included measures of food reward.
Finlayson et al (2009) reported an increase in implicit wanting for foods varying in fat content
17
and sweet taste, after moderate intensity cycling (compared to no exercise), but only in those
participants who increased their EI after exercise (9). Taylor & Oliver (2009) reported that
exercise transiently decreased cravings for chocolate (compared with rest) (27). In the present
study, we found no difference in liking, implicit wanting or relative preference for high fat
food relative to low fat food. These findings suggest that the overall mean pattern of food
reward was stable. However, the large standard deviation of scores indicates a broad range of
between-subject variability.
46. Our study presents with both strengths and limitations. The main strength of our study is its
design (crossover) and the fact that we measured several aspects of appetite (subjective
feelings, plasma levels of several appetite-related hormones, EI and food reward). As a
limitation, we have not accounted for phase of menstrual cycle, known to impact on energy
and macronutrient intake (22) and food reward (21, 22). However, given our design
(crossover randomised with 4 legs), we believe phase of menstrual cycle had a minor impact
on our results. Even though we aimed to look at the impact of exercise intensity on appetite,
the MICC and HIIC differed both in intensity and continous/discontinuous. However, given
that the intervals of active resting in the HIIC were so short (12s), the HR was all the time at
85-90% maxHR. It would be impossible to perform continuous high intensity exercise
inducing an energy expenditure of 250kcal in this patient group (inactive overweight/obese
individuals). Our protocol with exercise (or rest) being performed one hour after breakfast
and, the lunch test meal being presented three hours after breakfast, was used in order to
simulate a typical day, since exercise is usually performed in the postprandial state. Several
other studies looking at the impact of acute exercise on appetite have used a similar order of
events (19, 28, 29, 32).
47. In conclusion, our findings show that in overweight/obese individuals, acute isocaloric bouts
of moderate or high-intensity exercise lead to a similar appetite response. Both suppress
18
insulin and AG and increase the postprandial release of GLP-1, without affecting PYY3-36
plasma levels and have no impact on hunger or fullness, despite reducing desire to eat. This
together with a significant reduction in REI in all exercise conditions, and no changes in
activities patterns throughout the day, strengthen previous findings in normal-weight
individuals that acute exercise, even at high intensity, is able to induce a negative EB, without
stimulating physiological compensatory adaptations at the level of the appetite control system.
Acknowledgements:
48. Catia Martins was supported by a PostDoctoral grant from the Liaison Committee between
the Central Norway Regional Health Authority (RHA) and the Norwegian University of
Science and Technology (NTNU). We would like to thank all the participants that took part in
this study for their time and enthusiasm and Mrs. Sissel Salater for her help with cannulation.
The results of the present study do not constitute endorsement by ACSM.
Conflict of interest:
49. The authors declare that there is no conflict of interest that would prejudice the impartiality of
this scientific work.
19
References:
1. Ainsworth BE, Haskell WL, Herrmann SD et al. 2011 Compendium of Physical
Activities: a second update of codes and MET values. Med. Sci. Sports Exerc.
2011;43(8):1575-81.
2. Bellisle F. Food choice, appetite and physical activity. Public Health Nutr.
1999;2(3A):357-61.
3. Blundell JE. Perspective on the Central Control of Appetite. Obesity.
2006;14(Supplement):160S-3S.
4. Boutcher SH. High-intensity intermittent exercise and fat loss. Obesity.
2011;2011:868305.
5. Broom DR, Stensel DJ, Bishop NC, Burns SF, Miyashita M. Exercise-induced
suppression of acylated ghrelin in humans. J. Appl. Physiol. 2007;102(6):2165-71.
6. Deighton K, Barry R, Connon CE, Stensel DJ. Appetite, gut hormone and energy
intake responses to low volume sprint interval and traditional endurance exercise. Eur.
J. Appl. Physiol. 2013;113(5):1147-56.
7. Deighton K, Karra E, Batterham RL, Stensel DJ. Appetite, energy intake, and PYY3-
36 responses to energy-matched continuous exercise and submaximal high-intensity
exercise. Appl Physiol Nutr Metab. 2013;38(9):947-52.
8. Donnelly JE, Herrmann SD, Lambourne K, Szabo AN, Honas JJ, Washburn RA. Does
increased exercise or physical activity alter ad-libitum daily energy intake or
macronutrient composition in healthy adults? A systematic review. PLoS One.
2014;9(1):e83498.
20
9. Finlayson G, Bryant E, Blundell JE, King NA. Acute compensatory eating following
exercise is associated with implicit hedonic wanting for food. Physiol. Behav.
2009;97(1):62-7.
10. Finlayson G, King N, Blundell J. The role of implicit wanting in relation to explicit
liking and wanting for food: implications for appetite control. Appetite.
2008;50(1):120-7.
11. Flint A, Raben A, Blundell JE, Astrup A. Reproducibility, power and validity of visual
analogue scales in assessment of appetite sensations in single test meal studies. Int. J.
Obes. Relat. Metab. Disord. 2000;24(1):38-48.
12. Haapanen N, Miilunpalo S, Pasanen M, Oja P, Vuori I. Association between leisure
time physical activity and 10-year body mass change among working-aged men and
women. Int. J. Obes. 1997;21:288-96.
13. King JA, Miyashita M, Wasse LK, Stensel DJ. Influence of prolonged treadmill
running on appetite, energy intake and circulating concentrations of acylated ghrelin.
Appetite. 2010;54(3):492-8.
14. King JA, Wasse LK, Broom DR, Stensel DJ. Influence of brisk walking on appetite,
energy intake, and plasma acylated ghrelin. Med. Sci. Sports Exerc. 2010;42(3):485-
92.
15. King NA, Hopkins M, Caudwell P, Stubbs RJ, Blundell JE. Individual variability
following 12 weeks of supervised exercise: identification and characterization of
compensation for exercise-induced weight loss. Int. J. Obes. 2008;32:177-84.
16. King NA, Tremblay A, Blundell JE. Effects of exercise on appetite control:
implications for energy balance. Med. Sci. Sports Exerc. 1997;29(8):1076-89.
17. Kissileff HR, Pi-Sunyer FX, Segal K, Meltzer S, Foelsch PA. Acute effects of exercise
on food intake in obese and nonobese women. Am. J. Clin. Nutr. 1990;52:240-5.
21
18. Martins C, Morgan L, Truby H. A review of the effects of exercise on appetite
regulation: an obesity perspective. Int. J. Obes. 2008;32(9):1337-47.
19. Martins C, Morgan LM, Bloom SR, Robertson MD. Effects of exercise on gut
peptides, energy intake and appetite. J. Endocrinol. 2007;193(2):251-8.
20. Marzullo P, Salvadori A, Brunani A et al. Acylated ghrelin decreases during acute
exercise in the lean and obese state Clin. Endocrinol. (Oxf). 2008;69:970-1.
21. McNeil J, Cameron JD, Finlayson G, Blundell JE, Doucet E. Greater overall olfactory
performance, explicit wanting for high fat foods and lipid intake during the mid-luteal
phase of the menstrual cycle. Physiol. Behav. 2013;112-113:84-9.
22. McNeil J, Doucet E. Possible factors for altered energy balance across the menstrual
cycle: a closer look at the severity of PMS, reward driven behaviors and leptin
variations. Eur. J. Obstet. Gynecol. Reprod. Biol. 2012;163(1):5-10.
23. Schubert MM, Desbrow B, Sabapathy S, Leveritt M. Acute exercise and subsequent
energy intake. A meta-analysis. Appetite. 2013;63(0):92.
24. Schubert MM, Sabapathy S, Leveritt M, Desbrow B. Acute exercise and hormones
related to appetite regulation: a meta-analysis. Sports Med. 2014;44(3):387-403.
25. Shaw K, Gennat H, O'Rourke P, Del Mar C. Exercise for overweight or obesity. The
Cochrane database of systematic reviews. 2006;(4):CD003817.
26. Sim AY, Wallman KE, Fairchild TJ, Guelfi KJ. High-intensity intermittent exercise
attenuates ad-libitum energy intake. Int. J. Obes. 2013 June 4:doi:
10.1038/ijo.2013.102. [Epub ahead of print].
27. Taylor AH, Oliver AJ. Acute effects of brisk walking on urges to eat chocolate, affect,
and responses to a stressor and chocolate cue. An experimental study. Appetite.
2009;52(1):155-60.
22
28. Ueda SY, Yoshikawa T, Katsura Y, Usui T, Fujimoto S. Comparable effects of
moderate intensity exercise on changes in anorectic gut hormone levels and energy
intake to high intensity exercise. J. Endocrinol. 2009;203(3):357-64.
29. Ueda SY, Yoshikawa T, Katsura Y, Usui T, Nakao H, Fujimoto S. Changes in gut
hormone levels and negative energy balance during aerobic exercise in obese young
males. J. Endocrinol. 2009;201(1):151-9.
30. van Strien T, Frijters JER, Bergers GPA, Defares PB. The Dutch Eating Behavior
Questionnaire (DEBQ) for assessment of restrained, emotional, and external eating
behavior. Int. J. Eat. Disord. 1986;5(2):259-315.
31. Varo JJ, Martinez-Gonzalez MA, De Irala-Estevez J, Kearney J, Gibney M, Martinez
JA. Distribution and determinants of sedentary lifestyles in the European Union. Int. J.
Epidemiol. 2003;32(1):138-46.
32. Westerterp-Plantenga MS, Verwegen CR, Ijedema MJ, Wijckmans NE, Saris WH.
Acute effects of exercise or sauna on appetite in obese and nonobese men. Physiol.
Behav. 1997;62(6):1345-54.
33. World Health Organization [Internet]. Obesity and overweight. Fact sheet N°311
[cited 2013 Nov 12]. Available from:
http://www.who.int/mediacentre/factsheets/fs311/en/
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Figures legend:
Figure 1a. Hemoglobin plasma level profiles (g/dl), after a 600kcal breakfast, for: control (♦),
moderate intensity continuous cycling (MICC) (□), high intensity intermittent cycling (▲) and
short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12 subjects. Repeated
measures ANOVA showed a significant effect of time (P<0.0001) and a significant
condition*time interaction (P<0.0001).
Figure 1b. Hematocrit level profiles after a 600kcal breakfast for: control (♦), moderate
intensity continuous cycling (MICC) (□), high intensity intermittent cycling (▲) and short-
duration HIIC (SHIIC) (X). Values represent means ± SEM for 12 subjects. Repeated
measures ANOVA showed a significant effect of time (P<0.0001) and a significant
condition*time interaction (P<0.0001).
Figure 2a. Insulin plasma level profiles (pmol/L) after a 600kcal breakfast for: control (♦),
moderate intensity continuous cycling (MICC) (□), high intensity intermittent cycling (▲) and
short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12 subjects. Repeated
measures ANOVA showed a significant effect of time (P<0.0001) and a significant
condition*time interaction (P<0.0001).
24
Figure 2b. Acylated ghrelin plasma level profiles (pg/ml), after a 600kcal breakfast, for:
control (♦), moderate intensity continuous cycling (MICC) (□), high intensity intermittent
cycling (▲) and short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12
subjects. Repeated measures ANOVA showed a significant effect of time (P<0.0001) and
condition (p<0.001), but no interaction
Figure 2c. PYY plasma level profiles (pmol/L), after a 600kcal breakfast for: control (♦),
moderate intensity continuous cycling (MICC) (□), high intensity intermittent cycling (▲) and
short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12 subjects. Repeated
measures ANOVA showed a significant effect of time (P<0.0001), but no effect of condition
or interaction.
Figure 2d. GLP-1 plasma level profile (pmol/L), after a 600kcal breakfast, for: control (♦),
moderate intensity continuous cycling (MICC) (□), high intensity intermittent cycling (▲) and
short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12 subjects. Repeated
measures ANOVA showed a significant effect of time (P<0.0001) and a significant
condition*time interaction (P<0.0001).
Figure 3a. Profiles of subjective feelings of hunger (cm), after a 600kcal breakfast, for:
control (♦), moderate intensity continuous cycling (MICC) (□), high intensity intermittent
cycling (▲) and short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12
subjects. Repeated measures ANOVA showed a significant effect of time (P<0.0001), but no
effect of condition or interaction.
25
Figure 3b. Profiles of subjective feelings of fullness (cm), after a 600kcal breakfast, for:
control (♦), moderate intensity continuous cycling (MICC) (□), high intensity intermittent
cycling (▲) and short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12
subjects. Repeated measures ANOVA showed a significant effect of time (P<0.0001), but no
effect of condition or interaction.
Figure 3c. Profiles of subjective feelings of desire to eat (cm), after a 600kcal breakfast, for:
control (♦), moderate intensity continuous cycling (MICC) (□), high intensity intermittent
cycling (▲) and short-duration HIIC (SHIIC) (X). Values represent means ± SEM for 12
subjects. Repeated measures ANOVA showed a significant effect of time (P<0.0001), and a
time*condition interaction (p<0.05).
26
Table . SDC1. AUC for subjective feelings of appetite and appetite-related hormones in the
different conditions