Ghrelin is an orexigenic hormone secreted from endocrine cells in the stomach and other tissues. Acylation of ghrelin is essential for appetite regulation. Vigorous exercise induces appetite suppression, but this does not appear to be related to suppressed concentrations of total ghrelin. This study examined the effect of exercise and feeding on plasma acylated ghrelin and appetite. Nine male subjects aged 19-25 yr participated in two, 9-h trials (exercise and control) in a random crossover design. Trials began at 0800 in the morning after an overnight fast. In the exercise trial, subjects ran for 60 min at 72% of maximum oxygen uptake between 0800 and 0900. After this, they rested for 8 h and consumed a test meal at 1100. In the control trial, subjects rested for 9 h and consumed a test meal at 1100. Area under the curve values for plasma acylated ghrelin concentration (assessed from venous blood samples) were lower over the first 3 h and the full 9 h of the exercise trial compared with the control trial: 317+/-135 vs. 510+/-186 pg.ml(-1).3 h and 917+/-342 vs. 1,401+/-521 pg.ml(-1).9 h (means+/-SE) respectively (P<0.05). Area under the curve values for hunger (assessed using a visual scale) were lower over the first 3 h of the exercise trial compared with the control trial (P=0.013). These findings demonstrate that plasma acylated ghrelin concentration and hunger are suppressed during running.

• NOTICE: this is the author's version of a work that was accepted for publication in the journal, Appetite. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. Abstract: 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.Professor H.R Bertoud Louisiana State University Baton Rouge LA USA Dear Professor Berthold, Thank you for inviting us to re-submit our paper to be considered for publication in Appetite. We have carefully considered the comments from the reviewers and have formulated responses to the points raised. Our responses, and the necessary changes (highlighted in yellow) are included within the revised document. We thank you once more for considering our manuscript and we look forward to hearing from you in due course. We thank each reviewers for reading our paper and for their constructive comments. We feel that we can adequately address the issues raised by each reviewer therefore, in an effort to do so, below we have listed the comments from each reviewer followed by our responses. Reviewer # 1 comment 1Studies on exercise and compensation in the short term have already taken place and have shown no compensation in energy intake once REI is calculated; therefore what is the rationale for undertaking this study, and for the particular hypothesis? Response to comment of the reviewerReviewer #1 is quite right, studies to date have shown no compensation in energy intake after accounting for relative energy intake (REI). However, previous studies have not induced such a large energy deficit during a single bout of exercise. Moreover, previous studies have not examined appetite and energy intak...

Exercise facilitates weight control, partly through effects on appetite regulation. Single bouts of exercise induce a short-term energy deficit without stimulating compensatory effects on appetite, whilst limited evidence suggests that exercise training may modify subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. However, a large variability in responses exists between individuals. This article reviews the evidence relating to how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses. The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations. The effect of these individual characteristics and behaviours on appetite-related hormone responses to exercise remains equivocal. These findings support the continued promotion of exercise as a strategy for inducing short-term energy deficits irrespective of adiposity and sex, as well as the ability of exercise to positively influence energy balance over the longer term. Future well-controlled studies are required to further ascertain the potential mediators of appetite responses to exercise.

Background:This study examined the effect of accumulating short bouts of exercise on postprandial plasma triacylglycerol and resting blood pressure in healthy young men.Methods:Nineteen subjects underwent two 2-d trials in a randomized counterbalanced order. On day 1, subjects either rested or performed multiple 6 min running bouts (30 min rest between each) until they had accumulated an energy expenditure of 4.2 MJ (1000 kcal). On day 2, subjects rested and consumed test meals for breakfast and lunch. Blood pressure was measured throughout days 1 and 2. Venous blood samples were obtained throughout day 2.Results:Systolic and diastolic blood pressure was lower for the exercise compared with the control trial on day 1. Postprandial plasma triacylglycerol concentrations and systolic blood pressure were lower throughout day 2 on the exercise compared with the control trial.Conclusion:Accumulating short bouts of exercise throughout the day may modify cardiovascular disease risk.

The purpose of this study was to investigate the effects of curcumin supplementation on exercise-induced oxidative stress in humans. 10 male participants, ages 26.8±2.0 years (mean±SE), completed 3 trials in a random order: (1) placebo (control), (2) single (only before exercise) and (3) double (before and immediately after exercise) curcumin supplementation trials. Each participant received oral administration of 90 mg of curcumin or the placebo 2h before exercise and immediately after exercise. Each participant walked or ran at 65% of V˙2max on a treadmill for 60min. Blood samples were collected pre-exercise, immediately after exercise and 2h after exercise. The concentrations of serum derivatives of reactive oxygen metabolites measured immediately after exercise were significantly higher than pre-exercise values in the placebo trial (308.8±12.9 U. CARR, P<0.05), but not in the single (259.9±17.1 U. CARR) or double (273.6±19.7 U. CARR) curcumin supplementation trials. Serum biological antioxidant potential concentrations measured immediately after exercise were significantly elevated in the single and double curcumin supplementation trials compared with pre-exercise values (P<0.05). These findings indicate that curcumin supplementation can attenuate exercise-induced oxidative stress by increasing blood antioxidant capacity.