Lucy K. Wasse

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 24h. 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 + or - 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 17,191 kJ, exercise 17,606 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.

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 YY(3-36) (PYY(3-36)) 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 VO(2) 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 PYY(3-36) decreased, in response to food restriction (two-way ANOVA, trial × 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 PYY(3-36) in determining divergent feeding responses to energy deficits imposed by food restriction and exercise.

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 x m(-2), (.)VO2max 55.9 +/- 1.8 mL x kg(-1) x 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 x 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.

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

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.

Influence of rest and exercise at a simulated altitude of 4,000 m on appetite, energy intake, and plasma concentrations of acylated ghrelin and peptide YY

The reason for high altitude anorexia is unclear but could involve alterations in the appetite hormones ghrelin and peptide YY (PYY). This study examined the effect of resting and exercising in hypoxia (12.7% O(2); ∼4,000 m) on appetite, energy intake, and plasma concentrations of acylated ghrelin and PYY. Ten healthy males completed four, 7-h trials in an environmental chamber in a random order. The four trials were control-normoxia, control-hypoxia, exercise-normoxia, and exercise-hypoxia. During exercise trials, participants ran for 60 min at 70% of altitude-specific maximal oxygen consumption (Vo(2max)) and then rested. Participants rested throughout control trials. A standardized meal was consumed at 2 h and an ad libitum buffet meal at 5.5 h. Area under the curve values for hunger (assessed using visual analog scales) tended to be lower during hypoxic trials than normoxic trials (repeated-measures ANOVA, P = 0.07). Ad libitum energy intake was lower (P = 0.001) in hypoxia (5,291 ± 2,189 kJ) than normoxia (7,718 ± 2,356 kJ; means ± SD). Mean plasma acylated ghrelin concentrations were lower in hypoxia than normoxia (82 ± 66 vs. 100 ± 69 pg/ml; P = 0.005) while PYY concentrations tended to be higher in normoxia (32 ± 4 vs. 30 ± 3 pmol/l; P = 0.059). Exercise suppressed hunger and acylated ghrelin and increased PYY but did not influence ad libitum energy intake. These findings confirm that hypoxia suppresses hunger and food intake. Further research is required to determine if decreased concentrations of acylated ghrelin orchestrate this suppression.

The influence of vigorous running and cycling exercise on hunger perceptions and plasma acylated ghrelin concentrations in lean young men

Vigorous running suppresses plasma acylated ghrelin concentrations but the limited literature on cycling suggests that acylated ghrelin is unchanged, perhaps because body mass is supported during cycling. It is important from a research and applied perspective to determine whether acylated ghrelin and hunger responses are exercise-mode specific. This study sought to examine this. Eleven recreationally active males fasted overnight and completed three 4-h trials: control, running, and cycling, in a random order. Participants rested throughout the control trial and ran or cycled at 70% of mode-specific maximal oxygen uptake for the first hour during exercise trials, resting thereafter. Hunger was measured every 0.5 h using visual analogue scales. Eight venous blood samples were collected to determine acylated ghrelin concentrations and a standardised meal was consumed at 3 h. Compared with the control trial, acylated ghrelin concentrations were suppressed to a similar extent at 0.5 and 1 h during the running (p < 0.005) and cycling (p < 0.001) trials. Area under the curve values for ghrelin concentration over time were lower during exercise trials versus control (Control: 606 ± 379; Running: 455 ± 356; Cycling: 448 ± 315 pg·mL(-1)·4 h(-1); mean ± SD, p < 0.05). Hunger values did not differ significantly between trials but an interaction effect (p < 0.05) indicated a tendency for hunger to be suppressed during exercise. Thus, at similar relative exercise intensities, plasma acylated ghrelin concentrations are suppressed to a similar extent during running and cycling.

Appetite and Energy Intake Responses to Acute Energy Deficits in Females versus Males.

ABSTRACT Purpose To explore whether compensatory responses to acute energy deficits induced by exercise or diet differ by sex. Methods In experiment one, 12 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 V˙O2max) and Food-Def trials. In experiment two, 10 men and 10 women completed two 7-h trials (control and exercise). Sixty minutes of running (∼70% of V˙O2max) was performed at the beginning of the exercise trial. The 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 approximately 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 in 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 seem 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.

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, 8h trials (exercise and control) in a randomised-crossover design. In the exercise trials participants consumed a breakfast snack and then rested for 1h before undertaking a 60 min run (72% of VO(2)max) on a treadmill. Participants then rested in the laboratory for 6h 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.

Effect of ambient temperature during acute aerobic exercise on short-term appetite, energy intake, and plasma acylated ghrelin in recreationally active males

Ambient temperature during exercise may affect energy intake regulation. Compared with a temperate (20 °C) environment, 1 h of running followed by 6 h of rest tended to decrease energy intake from 2 ad libitum meals in a hot (30 °C) environment but increase energy intake in a cool (10 °C) environment (p = 0.08). Core temperature changes did not appear to mediate this trend; whether acylated ghrelin is involved is unclear. Further research is warranted to clarify these findings.

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 to which 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-h 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 (V.O2peak)) and VIG (36-min running at 75% V.O2peak). In experiment two, nine healthy males completed three, 9-h conditions (control, 45-min running (EX45) and 90-min running (EX90)). Exercise was performed at 70% V.O2peak 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 1.5 h 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.