Abstract

PURPOSE: Post-exercise energy compensation (EC) through increased energy intake (EI) has been demonstrated to lead to lower than anticipated weight reduction with physical activity. The physiological mechanisms mediating the increase in EI remain to be fully elucidated. This study sought to determine the mechanisms, independent of bodyweight, that are involved in exercise-induced EC, specifically assessing the homeostatic appetite control system including appetite-regulating hormones in rats. METHODS: Twelve-week-old male Sprague Dawley rats (n = 30) fed an AIN-93 M diet were randomized into 1 of 3 groups and completed an 8-week intervention: 1) inactive control (SED); 2) voluntary aerobic exercise through wheel running (EX); and 3) inactive, weight-matched to aerobic exercise (SED-WM). SED-WM was included to assess the weight-independent impact of exercise on appetite-regulating hormones. EI, running distance, and bodyweight were recorded daily. After 8 weeks, an oral glucose tolerance test was conducted and blood samples were taken to assess acyl-ghrelin, glucagon-like peptide-1, peptide YY, insulin, and leptin. At euthanasia, portal blood was collected to examine appetite-regulating hormones and fat pads were collected to assess body composition. RESULTS: Bodyweight increased in all 3 groups. There was a time x group interaction (P < 0.05) for bodyweight, such that bodyweight was initially reduced in EX, but no differences were present between SED and EX at the end of the study. A time x group interaction was observed for EI (P < 0.05), showing an early reduction in EI in EX relative to SED, followed by a steady increase in EI in EX. Relative fat mass was reduced in EX relative to SED (P < 0.05) and SED-WM (P < 0.05). Leptin concentration was lower in EX relative to SED-WM (P < 0.05). There was a positive correlation between total body fat and leptin concentration (r = 0.851, P < 0.05). No differences were present between groups for acyl-ghrelin and insulin concentrations. CONCLUSIONS: These findings show that EC through increased EI may be in part responsible for limiting weight reduction with increased physical activity. Based on our findings, a reduction in leptin with exercise appears to be a primary mediating factor contributing to an increase in EI. Funded by NSERC.

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