Effect of exercise and different environmental conditions on appetite, food intake and the appetite-regulatory hormones, ghrelin and peptide YY

The role of gut hormones in the regulation of appetite and food intake is well established. The studies presented within this thesis have examined the effects of exercise and different environmental conditions on gut hormones (acylated ghrelin and total peptide YY), appetite and food intake. Forty-two young (mean ± SEM; 22.6 ± 0.4 y), healthy and generally lean (body mass index 23.7 ± 0.3 kg m2) males were recruited into four studies. In study one, 60 minutes of high intensity (70 % of O2 max) running and cycling exercise suppressed concentrations of the appetite-stimulating hormone acylated ghrelin to a similar extent. Study two revealed that after 60 minutes running in the heat (30 °C), hunger is lower in the pre-prandial period, and energy intake lower over the 7 h trial duration compared with a similar trial conducted in temperate (20 °C) conditions. Acylated ghrelin was suppressed during running in the temperate and hot environment but this did not appear to mediate the lower energy intake observed during the hot trial. In study three, energy intake tended to be higher after 60 minutes running in a cool environment (10 °C) compared with a temperate (20 °C) environment. During and shortly after running in the cold, perceived ratings of fullness and satisfaction were lower. Acylated ghrelin concentrations appeared to be suppressed to a lesser extent during running in the cold which could mediate the elevated energy intake observed at the first meal. However, energy intake was also higher at the second meal in the cold trial when acylated ghrelin concentrations were higher in the temperate trial. Study four showed that energy intake and acylated ghrelin concentrations were lower, and total PYY tended to be lower, in normobaric hypoxia suggesting a possible role for acylated ghrelin, but not PYY, in mediating the decrease in energy intake observed in hypoxia. This thesis confirms that exercise transiently suppresses acylated ghrelin concentrations regardless of the environmental conditions (temperature and altitude) exercise is performed in. The findings support anecdotal reports that appetite and energy intake are suppressed in the heat and stimulated in the cold. These responses may be partly mediated by acylated ghrelin immediately after running but other mechanisms are likely involved thereafter. Acute hypoxic exposure suppresses acylated ghrelin concentrations; an observation which may explain the decreased energy intake in hypoxia

Acute exercise increases feeding latency in healthy normal weight young males but does not alter energy intake

This study investigated the acute influence of exercise on eating behaviour in an ecologically valid setting whereby healthy active males were permitted complete ad libitum access to food. Ten healthy males completed two, 8 h trials (exercise and control) in a randomised-crossover design. In the exercise trials participants consumed a breakfast snack and then rested for 1 h before undertaking a 60 min run (72% of V˙O2 max) on a treadmill. Participants then rested in the laboratory for 6 h during which time they were permitted complete ad libitum access to a buffet meal. The timing of meals, energy/macronutrient intake and eating frequency were assessed. Identical procedures were completed in the control trial except no exercise was performed. Exercise increased the length of time (35 min) before participants voluntarily requested to eat afterwards. Despite this, energy intake at the first meal consumed, or at subsequent eating episodes, was not influenced by exercise (total trial energy intake: control 7426 kJ, exercise 7418 kJ). Neither was there any difference in macronutrient intake or meal frequency between trials. These results confirm that food intake remains unaffected by exercise in the immediate hours after but suggest that exercise may invoke a delay before food is desired

Influence of prolonged treadmill running on appetite, energy intake and circulating concentrations of acylated ghrelin

The effects of prolonged treadmill running on appetite, energy intake and acylated ghrelin (an appetite stimulating hormone) were examined in 9 healthy males over the course of 24 h. Participants completed 2 experimental trials (exercise and control) in a randomised - crossover fashion. In the exercise trial participants ran for 90 min at 68.8 ± 0.8% of maximum oxygen uptake followed by 8.5 h of rest. Participants returned to the laboratory on the following morning to provide a fasting blood sample and ratings of appetite (24 h measurement). No exercise was performed on the control trial. Appetite was measured within the laboratory using visual analogue scales and energy intake was assessed from ad libitum buffet meals. Acylated ghrelin was determined from plasma using an ELISA assay. Exercise transiently suppressed appetite and acylated ghrelin but each remained no different from control values in the hours afterwards. Furthermore, despite participants expending 5324 kJ during exercise there was no compensatory increase in energy intake (24 h energy intake; control 17191 kJ, exercise 17606 kJ). These findings suggest that large energy deficits induced by exercise do not lead to acute compensatory responses in appetite, energy intake or acylated ghrelin

Influence of brisk walking on appetite, energy intake, and plasma acylated ghrelin

Purpose: This study examined the effect of an acute bout of brisk walking on appetite, energy intake, and the appetite-stimulating hormone-acylated ghrelin. Methods: Fourteen healthy young males (age 21.9 +/- 0.5 yr, body mass index 23.4 +/- 0.6 kg.m(-2), (V) over dotO(2max) 55.9 +/- 1.8 mL.kg(-1).min(-1); mean +/- SEM) completed two 8-h trials (brisk walking and control) in a randomized counterbalanced fashion. The brisk walking trial commenced with 60 min of subjectively paced brisk walking on a level-motorized treadmill after which participants rested for 7 h. Participants rested for the duration of the control trial. Ad libitum buffet meals were offered twice during main trials (1.5-2 and 5-5.5 h). Appetite (hunger, fullness, satisfaction, and prospective food consumption) was assessed at 30-min intervals throughout. Levels of acylated ghrelin, glucose, insulin, and triacylglycerol were determined from plasma. Results: Sixty minutes of brisk walking (7.0 +/- 0.1 km.h(-1)) yielded a net (exercise minus resting) energy expenditure of 2008 +/- 134 kJ, yet it did not significantly influence appetite, energy/macronutrient intake, or the plasma concentration of acylated ghrelin either during or after exercise (P > 0.05). Participants did not compensate for energy expended during walking, therefore a deficit in energy was induced (1836 kJ, 439 kcal) relative to control. Conclusions: This study demonstrates that, despite inducing a moderate energy deficit, an acute bout of subjectively paced brisk walking does not elicit compensatory responses in acylated ghrelin, appetite, or energy intake. This finding lends support for a role of brisk walking in weight management

Exercise and ghrelin. A narrative overview of research

Since its discovery in 1999, ghrelin has been implicated in a multiplicity of physiological activities. Most notably, ghrelin has an important influence on energy metabolism and after the identification of its potent appetite stimulating effects ghrelin has been termed the ‘hunger hormone.’ Exercise is a stimulus which has a significant impact on energy homeostasis and consequently a substantial body of research has investigated the interaction between exercise and ghrelin. This narrative review provides an overview of research relating to the acute and chronic effects of exercise on circulating ghrelin (acylated, unacylated and total). To enhance study comparability, the scope of this review is limited to research undertaken in adult humans and consequently studies involving children and animals are not discussed. Although there is significant ambiguity within much of the early research, our review suggests that acute exercise transiently interferes with the production of acylated ghrelin. Furthermore, the consensus of evidence indicates that exercise training does not influence circulating ghrelin independent of weight loss. Additional research is needed to verify and extend the available literature, particularly by uncovering the mechanisms governing acute exercise-related changes and characterising responses in other populations such as females, older adults, and the obese

Acute effect of exercise intensity and duration on acylated ghrelin and hunger in men

Acute exercise transiently suppresses the orexigenic gut hormone acylated ghrelin, but the extent exercise intensity and duration determine this response is not fully understood. The effects of manipulating exercise intensity and duration on acylated ghrelin concentrations and hunger were examined in two experiments. In experiment one, nine healthy males completed three, 4-hour conditions (control, moderate-intensity running (MOD) and vigorous-intensity running (VIG)), with an energy expenditure of ~2.5 MJ induced in both MOD (55 min running at 52% peak oxygen uptake (VO2peak)) and VIG (36 min running at 75% VO2peak). In experiment two, nine healthy males completed three, 9-hour conditions (control, 45 min running (EX45) and 90 min running (EX90)). Exercise was performed at 70% VO2peak. In both experiments, participants consumed standardised meals, and acylated ghrelin concentrations and hunger were quantified at predetermined intervals. In experiment one, delta acylated ghrelin concentrations were lower than control in MOD (ES=0.44, P=0.01) and VIG (ES=0.98, P<0.001); VIG was lower than MOD (ES=0.54, P=0.003). Hunger ratings were similar across the conditions (P=0.35). In experiment two, delta acylated ghrelin concentrations were lower than control in EX45 (ES=0.77, P<0.001) and EX90 (ES=0.68, P<0.001); EX45 and EX90 were similar (ES=0.09, P=0.55). Hunger ratings were lower than control in EX45 (ES=0.20, P=0.01) and EX90 (ES=0.27, P=0.001); EX45 and EX90 were similar (ES=0.07, P=0.34). Hunger and delta acylated ghrelin concentrations remained suppressed at 1.5h in EX90 but not EX45. In conclusion, exercise intensity, and to a lesser extent duration, are determinants of the acylated ghrelin response to acute exercise

Differential acylated ghrelin, peptide YY3-36, appetite, and food intake responses to equivalent energy deficits created by exercise and food restriction

Context: Acute energy deficits imposed by food restriction increase appetite and energy intake; however, these outcomes remain unchanged when energy deficits are imposed by exercise.Objective: Our objective was to determine the potential role of acylated ghrelin and peptide YY3-36 (PYY3-36) in mediating appetite and energy intake responses to identical energy deficits imposed by food restriction and exercise.Design: Twelve healthy males completed three 9-h trials (exercise deficit, food deficit, and control) in a randomized counterbalanced design. Participants ran for 90 min (70% of VO2 max) at the beginning of the exercise deficit trial and then rested for 7.5 h. Participants remained sedentary throughout the food deficit and control trials. Test meals were consumed by participants at 2 and 4.75 h in all trials. The amount provided in the food deficit trial was restricted so that an energy deficit (equivalent to that imposed by exercise) was induced relative to control. Participants were permitted access to a buffet meal at 8 h.Results: The energy deficits imposed by food restriction (4820 +/- 151 kJ) and exercise (4715 +/- 113 kJ) were similar. Appetite and ad libitum energy intake responded in a compensatory fashion to food restriction yet were not influenced by exercise. Plasma acylated ghrelin concentrations increased, whereas PYY3-36 decreased, in response to food restriction (two-way ANOVA, trial x time interaction, P < 0.001 for each). Exercise did not induce such compensatory responses.Conclusions: These findings suggest a mediating role of acylated ghrelin and PYY3-36 in determining divergent feeding responses to energy deficits imposed by food restriction and exercise. (J Clin Endocrinol Metab 96: 1114-1121, 2011

Appetite and energy intake responses to acute energy deficits in females versus males

PURPOSE: To explore whether compensatory responses to acute energy deficits induced by exercise or diet differ by sex. METHODS: In experiment one, twelve healthy women completed three 9 h trials (control, exercise-induced (Ex-Def) and food restriction induced energy deficit (Food-Def)) with identical energy deficits being imposed in the Ex-Def (90 min run, ∼70% of VO2 max) and Food-Def trials. In experiment two, 10 men and 10 women completed two 7 h trials (control and exercise). Sixty min of running (∼70% of VO2 max) was performed at the beginning of the exercise trial. Participants rested throughout the remainder of the exercise trial and during the control trial. Appetite ratings, plasma concentrations of gut hormones and ad libitum energy intake were assessed during main trials. RESULTS: In experiment one, an energy deficit of ∼3500 kJ induced via food restriction increased appetite and food intake. These changes corresponded with heightened concentrations of plasma acylated ghrelin and lower peptide YY3-36. None of these compensatory responses were apparent when an equivalent energy deficit was induced by exercise. In experiment two, appetite ratings and plasma acylated ghrelin concentrations were lower in exercise than control but energy intake did not differ between trials. The appetite, acylated ghrelin and energy intake response to exercise did not differ between men and women. CONCLUSIONS: Women exhibit compensatory appetite, gut hormone and food intake responses to acute energy restriction but not in response to an acute bout of exercise. Additionally, men and women appear to exhibit similar acylated ghrelin and PYY3-36 responses to exercise-induced energy deficits. These findings advance understanding regarding the interaction between exercise and energy homeostasis in women

Individual variation in hunger, energy intake and ghrelin responses to acute exercise

Purpose: To characterise the immediate and extended impact of acute exercise on hunger, energy intake and circulating acylated ghrelin concentrations using a large dataset of homogenous experimental trials; and to describe the variation in responses between individuals. Methods: Data from 17 of our group’s experimental crossover trials were aggregated yielding a total sample of 192 young, healthy, males. In these studies, single bouts of moderate to high-intensity aerobic exercise (69 ± 5% VO2 peak; mean ± SD) were completed with detailed participant assessments occurring during and for several hours post-exercise. Mean hunger ratings were determined during (n = 178) and after (n = 118) exercise from visual analogue scales completed at 30 min intervals whilst ad libitum energy intake was measured within the first hour after exercise (n = 60) and at multiple meals (n = 128) during the remainder of trials. Venous concentrations of acylated ghrelin were determined at strategic time points during (n = 118) and after (n = 89) exercise. Results: At group-level, exercise transiently suppressed hunger (P < 0.010; Cohen’s d = 0.77) but did not affect energy intake. Acylated ghrelin was suppressed during exercise (P < 0.001; Cohen’s d = 0.10) and remained significantly lower than control (no exercise) afterwards (P < 0.024; Cohen’s d = 0.61). Between participants, there were notable differences in responses however a large proportion of this spread lay within the boundaries of normal variation associated with biological and technical assessment error. Conclusion: In young men, acute exercise suppresses hunger and circulating acylated ghrelin concentrations with notable diversity between individuals. Care must be taken to distinguish true inter-individual variation from random differences within normal limits