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Journal ArticleDOI

Appetite-regulatory hormone responses on the day following a prolonged bout of moderate-intensity exercise

15 Mar 2015-Physiology & Behavior (Elsevier)-Vol. 141, pp 23-31

TL;DR: It is indicated that short-term energy deficits induced by exercise initially prompt a compensatory response by chronic but not acute hormonal regulators of appetite and energy balance within this 24h time-frame however there is no conscious recognition of the perturbation to energy balance.
Abstract: Exercise increases energy expenditure however acutely this does not cause compensatory changes in appetite or food intake. This unresponsiveness contrasts the rapid counter-regulatory changes seen after food restriction. The present investigation examined whether corrective changes in appetite-regulatory parameters occur after a time delay, namely, on the day after a single bout of exercise. Nine healthy males completed two, two-day trials (exercise & control) in a random order. On the exercise trial participants completed 90 min of moderate-intensity treadmill running on day one (10:30–12:00 h). On day two appetite-regulatory hormones and subjective appetite perceptions were assessed frequently in response to two test meals provided at 08:00 and 12:00 h. Identical procedures occurred in the control trial except no exercise was performed on day one. Circulating levels of leptin were reduced on the day after exercise (AUC 5841 ± 3335 vs. 7266 ± 3949 ng− 1·mL− 1 · 7 h, P = 0.012). Conversely, no compensatory changes were seen for circulating acylated ghrelin, total PYY, insulin or appetite perceptions. Unexpectedly, levels of acylated ghrelin were reduced on the exercise trial following the second test meal on day two (AUC 279 ± 136 vs. 326 ± 136 pg− 1·mL− 1 · 3 h, P = 0.021). These findings indicate that short-term energy deficits induced by exercise initially prompt a compensatory response by chronic but not acute hormonal regulators of appetite and energy balance. Within this 24 h time-frame however there is no conscious recognition of the perturbation to energy balance.
Topics: Appetite (56%)

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Appetite regulatory hormone responses on the day following a prolonged bout
of moderate-intensity exercise
James A. King
1,2
, Jack O. Garnham
1
, Andrew P. Jackson
1,2
, Benjamin M. Kelly
1
,
Soteris Xenophontos
1,2
, Myra A. Nimmo
1,2
1
School of Sport, Exercise & Health Sciences, Loughborough University,
Leicestershire, UK
2
NIHR Leicester-Loughborough Diet, Lifestyle & Physical Activity Biomedical
Research Unit, UK
Running Head: Latent Appetite Regulatory Responses Following Exercise
Correspondence
Dr James King
School of Sport, Exercise & Health Sciences
Loughborough University
Leicestershire
UK
LE11 3TU
E-mail: J.A.King@lboro.ac.uk
Phone: +44(0)1509 226324
Abstract
Key words: Exercise, Appetite Regulation, Gut Peptides

1
Abstract 1
Exercise increases energy expenditure however acutely this does not cause 2
compensatory changes in appetite or food intake. This unresponsiveness contrasts 3
the rapid counter regulatory changes seen after food restriction. The present 4
investigation examined whether corrective changes in appetite regulatory 5
parameters occur after a time delay, namely, on the day after a single bout of 6
exercise. Nine healthy males completed two, two-day trials (exercise & control) in a 7
random order. On the exercise trial participants completed 90 min of moderate 8
intensity treadmill running on day one (10:30 12:00 h). On day two appetite 9
regulatory hormones and subjective appetite perceptions were assessed frequently 10
in response to two test meals provided at 08:00 and 12:00 h. Identical procedures 11
occurred in the control trial except no exercise was performed on day one. 12
Circulating levels of leptin were reduced on the day after exercise (AUC 5841 ± 3335 13
vs. 7266 ± 3949 ng
-1
·mL
-1
·7 h, P = 0.012). Conversely, no compensatory changes 14
were seen for circulating acylated ghrelin, total PYY, insulin or appetite perceptions. 15
Unexpectedly, levels of acylated ghrelin were reduced on the exercise trial following 16
the second test meal on day two (AUC 279 ± 136 vs. 326 ± 136 pg
-1
·mL
-1
·3 h, P = 17
0.021). These findings indicate that short-term energy deficits induced by exercise 18
initially prompt a compensatory response by chronic but not acute hormonal 19
regulators of appetite and energy balance. Within this 24 h time-frame however there 20
is no conscious recognition of the perturbation to energy balance. 21
22
23
24
25
26

2
Introduction 27
The relationship between exercise and appetite regulation has important implications 28
regarding the role of exercise in weight management (33). In recent years, 29
advancements in scientific understanding regarding the psycho-biological regulation 30
of appetite and food intake have ignited research interest around the interaction 31
between exercise, appetite regulation and energy balance (47). Within this sphere, 32
one particular issue that has received significant attention is the impact of exercise 33
on hormonal mediators of appetite which are central components of the body’s 34
homeostatic system governing energy balance and weight control (28, 49). 35
36
The body’s appetite regulatory system includes several peptides of gastro-intestinal, 37
pancreatic and adipose tissue origin, which communicate acute nutrient status and 38
chronic energy availability to the central nervous system (28). Leptin and insulin act 39
as chronic mediators of energy balance, with circulating concentrations being 40
present in proportion to stored energy within adipose tissue (40). Additionally, on a 41
meal to meal basis, food intake is regulated by a selection of gastrointestinal 42
peptides, most notably acylated ghrelin, peptide-YY (PYY), glucagon-like peptide-1 43
(GLP-1), cholecystokinin (CCK) and oxyntomodulin (44). Ghrelin is secreted from the 44
stomach and remains unique as the only circulating appetite stimulating hormone. 45
Circulating concentrations of ghrelin rise and fall before and after meals, data which 46
implicates ghrelin as meal initiating signal (12, 13). Conversely, each of the other 47
short-acting peptides has an inhibitory effect on appetite. Most prominent is PYY 48
which is secreted chiefly from the distal intestine and colon in direct proportion to the 49
energy content of an ingested meal (1, 37). Within key appetite regulatory brain 50
centres these afferent signals are integrated and the summed response initiated 51

3
which impacts directly up on appetite and eating, as well as thermogenesis and 52
substrate metabolism (43). 53
54
The last 10 years has seen an explosion of research exploring the links between 55
appetite and appetite regulatory hormones in the context of exercise (47, 49). 56
Research has demonstrated that single bouts of exercise have a marked impact on 57
the circulating levels of appetite regulatory hormones with changes occurring rapidly 58
after the initiation of exercise. Notably however, these alterations appear to be 59
transient. For example, circulating levels of acylated ghrelin are distinctly suppressed 60
during exercise of moderate intensity or higher (10, 29, 31). This perturbation 61
however is absent within 30 min after exercise. Similarly, circulating concentrations 62
of PYY increase during moderate to high intensity exercise however customary 63
levels are re-established shortly thereafter (9, 51). Each of these responses is 64
consistent with an appetite inhibitory profile which may in part contribute to a well 65
characterised inhibition of appetite at moderate-high exercise intensities, a 66
phenomena which has been termedexercise induced anorexia’ (32). 67
68
Studies have shown that acute energy deficits induced by food restriction lead to 69
rapid and quite striking compensatory alterations to appetite and appetite regulatory 70
hormones (27, 31). Intuitively, it may be expected that energy deficits induced by 71
exercise would lead to similar changes in appetite regulatory parameters in an effort 72
to maintain energy balance. Paradoxically, several studies have failed to observe 73
any compensatory changes in circulating appetite hormones (acylated ghrelin or 74
PYY) even after bouts of exercise associated with high levels of energy expenditure 75
and over several hours of observation afterwards (29, 31, 51). It remains possible 76

4
that compensatory appetite regulatory changes may occur over a greater period of 77
time than what has previously been examined i.e. beyond the day that exercise is 78
completed on. 79
80
To test this hypothesis the current study assessed circulating levels of key appetite 81
regulatory hormones (acylated ghrelin, total PYY, leptin & insulin) and subjective 82
appetite perceptions on the day after a single bout of exercise with a large 83
associated energy deficit. We hypothesised that meal stimulated acylated ghrelin 84
(suppression) and PYY (elevation) responses would be attenuated on the day after 85
exercise whilst circulating levels of leptin would be reduced. Furthermore, we thought 86
that these changes would be associated with higher subjective ratings of appetite. 87
88
Materials & Methods 89
Participants 90
After receiving local ethical advisory committee approval nine young, healthy male 91
volunteers (age 22 ± 1.2 y; BMI 22.6 ± 1.8 kg·m
2
; waist circumference 74.4 ± 1.8 cm; 92
estimated basal metabolic rate 7247 ± 405 kJ;
2
OV
max 60.6 ± 7.6 mL·kg·min
-1
) 93
gave their written informed consent to participate. Participants were weight stable (< 94
2 kg change in body mass in the last three months), non-smokers, free of cardio-95
metabolic disease, had a BMI within the healthy range (18.5 24.9 kg·m
2
) and were 96
not taking any medications or supplements. Participants were recreationally active 97
i.e. typically games players, but were not accustomed to undertaking endurance 98
exercise regularly. 99
100
101

Citations
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01 Jan 2004-Nature
Abstract: Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.

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Abstract: The physiological control of appetite regulation involves circulating hormones with orexigenic (appetite-stimulating) and anorexigenic (appetite-inhibiting) properties that induce alterations in energy intake via perceptions of hunger and satiety. As the effectiveness of exercise to induce weight loss is a controversial topic, there is considerable interest in the effect of exercise on the appetite-regulating hormones such as acylated ghrelin, peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and pancreatic polypeptide (PP). Research to date suggests short-term appetite regulation following a single exercise session is likely affected by decreases in acylated ghrelin and increases in PYY, GLP-1, and PP. Further, this exercise-induced response may be intensity-dependent. In an effort to guide future research, it is important to consider how exercise alters the circulating concentrations of these appetite-regulating hormones. Potential mechanisms include blood redistribution, sympathetic nervous system activity, gastrointestinal motility, cytokine release, free fatty acid concentrations, lactate production, and changes in plasma glucose and insulin concentrations. This review of relevant research suggests blood redistribution during exercise may be important for suppressing ghrelin, while other mechanisms involving cytokine release, changes in plasma glucose and insulin concentrations, SNS activity, and muscle metabolism likely mediate changes in the anorexigenic signals PYY and GLP-1. Overall, changes in appetite-regulating hormones following acute exercise appear to be intensity-dependent, with increasing intensity leading to a greater suppression of orexigenic signals and greater stimulation of anorexigenic signals. However, there is less research on how exercise-induced responses in appetite-regulating hormones differ between sexes or different age groups. A better understanding of how exercise intensity and workload affect appetite across the sexes and life stages will be a powerful tool in developing more successful strategies for managing weight.

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Cites background from "Appetite-regulatory hormone respons..."

  • ...On the other hand, an energy deficiency achieved via increased exercise energy expenditure suppresses ghrelin and increases PYY, GLP-1, and PP serum concentrations in the hours following exercise [98–100] and even suppresses serum ghrelin concentrations the day after exercise [101]....

    [...]


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TL;DR: The hypothesis that the magnitude of the body's lean tissue is related to absolute levels of EI in a sample of inactive adolescents with obesity is supported.
Abstract: There has been renewed interest in examining the relationship between specific components of energy expenditure and the overall influence on energy intake (EI). The purpose of this cross-sectional analysis was to determine the strongest metabolic and anthropometric predictors of EI. It was hypothesized that resting metabolic rate (RMR) and skeletal muscle mass would be the strongest predictors of EI in a sample of overweight and obese adolescents. 304 post-pubertal adolescents (91 boys, 213 girls) aged 16.1 (±1.4) years with body mass index at or above the 95th percentile for age and sex OR at or above the 85th percentile plus an additional diabetes risk factor were measured for body weight, RMR (kcal/day) by indirect calorimetry, body composition by magnetic resonance imaging (fat free mass (FFM), skeletal muscle mass, fat mass (FM), and percentage body fat), and EI (kcal/day) using 3 day food records. Body weight, RMR, FFM, skeletal muscle mass, and FM were all significantly correlated with EI (p < 0.00...

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Cites background from "Appetite-regulatory hormone respons..."

  • ...To be sure, in the controlled setting of the laboratory and without exogenous pharmacologic administration of appetite hormones, very small effects or null findings are commonplace when trying to elucidate the role that these common appetite signals have in hunger, satiety, and energy balance in humans (Doucet and Cameron 2007; Gibbons et al. 2013; Sysko et al. 2013; King et al. 2015)....

    [...]

  • ...…administration of appetite hormones, very small effects or null findings are commonplace when trying to elucidate the role that these common appetite signals have in hunger, satiety, and energy balance in humans (Doucet and Cameron 2007; Gibbons et al. 2013; King et al. 2015; Sysko et al. 2013)....

    [...]


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