Effect of Acute High Intensity Interval Exercise and Energy Balance on Plasma Acylated Ghrelin Concentrations

Ghrelin is an appetite-stimulating hormone produced mainly in the stomach and duodenum. Poor ghrelin control is often caused by obesity-related hyperinsulinemia, which fails to suppress ghrelin and results in excess appetite and higher body fat storage that perpetuates even greater fat accumulation. High intensity exercise has been shown to acutely decrease plasma acylated ghrelin concentrations in healthy weight individuals. However, the evidence for how exercise affects ghrelin in obese individuals is currently lacking. PURPOSE: To compare the effects of high intensity interval exercise on acute plasma acylated ghrelin levels in obese and non-obese males. METHODS: Eighteen subjects with a mean age of 29.8 yr. (± 7.6) were assessed for body fat percent (BF%), acylated ghrelin and hunger. Subjects included 9 non- obese men (BF% mean= 13.7 ± 3.6) and 9 obese men (BF% mean = 31.7 ± 4.7) who agreed to participate in this study. Using a crossover design, participants were randomly assigned to an exercise or control condition, with each subject acting as their own control. The exercise trial consisted of participants cycling at high intensity intervals for 20 minutes (not including the 5 minute warmup and cool down) at a rate of 65% to 85% of their heart rate reserve on a cycle ergometer followed by 60 minutes of rest. The control trial consisted of 90 minutes of rest. Blood samples (3-4ml) were collected at baseline, 0.5, 1, and 1.5 hours post-intervention. Acylated ghrelin concentrations were determined from plasma. Hunger was assessed using a 10-point Likert-type scale while blood samples were being drawn. Group means for plasma ghrelin concentrations between groups were analyzed using an independent t-test. The effect of exercise on ghrelin was analyzed using paired t-test. The relationship between perceived hunger and ghrelin was assessed using Pearson correlations. RESULTS: Baseline plasma ghrelin levels were significantly higher in the non-obese group when compared to the obese group (t = 3.43, p = .036). While exercise was effective in reducing plasma acylated ghrelin levels in the non-obese group (t = 2.34, p = .047), no significant changes were found in acylated ghrelin in the obese group between baseline or any time point following the exercise intervention. CONCLUSIONS: The low resting levels of plasma ghrelin concentrations exhibited by the obese subjects, when compared to non-obese subjects, may result in long fasting periods that lead to hypoglycemia and a hyperinsulinemic response at the next eating opportunity. Furthermore, the lack of reduction in ghrelin following exercise may result in an overconsumption of energy. Both the sustained ghrelin with associated excess energy intake and the hyperinsulinemia may result in sustained or increased fat storage in obese individuals