Circadian and ultradian components of hunger in human non-homeostatic meal-to-meal eating.

UNLABELLED: A unifying physiological explanation of the urge to initiate eating is still not available as human hunger in meal-to-meal eating may not be under homeostatic control. We hypothesized that a central circadian and a gastrointestinal ultradian timing mechanism coordinate non-deprivation meal-to-meal eating. We examined hunger as a function of time of day, inter-meal (IM) energy expenditure (EE), and concentrations of proposed hunger-controlling hormones ghrelin, leptin, and insulin. METHODS: In two crossover studies, 10 postmenopausal women, BMI 23-26 kg/m(2) engaged in exercise (EX) and sedentary (SED) trials. Weight maintenance meals were provided at 6h intervals with an ad libitum meal at 13 h in study 1 and 21 h snack in study 2. EE during IM intervals was measured by indirect calorimetry and included EX EE of 801 kcal in study 1, and 766-1,051 kcal in study 2. Hunger was assessed with a visual analog scale and blood was collected for hormonal determination. RESULTS: Hunger displayed a circadian variation with acrophase at 13 and 19 h and was unrelated to preceding EE. Hunger was suppressed by EX between 10 and 16 h and bore no relationship to either EE during preceding IM intervals or changes in leptin, insulin, and ghrelin; however leptin reflected IM energy changes and ghrelin and insulin, prandial events. CONCLUSIONS: During non-deprivation meal-to-meal eating, hunger appears to be under non-homeostatic central circadian control as it is unrelated to EE preceding meals or concentrations of proposed appetite-controlling hormones. Gastrointestinal meal processing appears to intermittently suppress this control and entrain an ultradian hunger pattern.

Two bouts of exercise before meals, but not after meals, lower fasting blood glucose.

INTRODUCTION: Reduced counterregulatory responses to a next-day hypoglycemic challenge and hypoglycemia result from two spaced episodes of moderate-intensity exercise and have been characterized as exercise-associated autonomic failure. We hypothesized that this phenomenon is caused by postabsorptive state at the time of exercise rather than by autonomic failure. METHODS: Participants were nine healthy postmenopausal women in a crossover study. Two hours of treadmill exercise at 43% of maximal effort were performed twice a day, separated by 5 h, either 1 h before (Before-Meals trial) or 1 h after a meal (After-Meals trial). Plasma insulin, counterregulatory hormones (glucagon, growth hormone, cortisol), and metabolites (glucose, free fatty acids, ketones) were measured to evaluate the effects of nutritional timing. Analyses of HR and vagal tone were measured to assess autonomic function. RESULTS: Before-Meals exercise, but not After-Meals exercise, reduced postabsorptive plasma glucose by 20.2% during a 16-h period, without a change in counterregulatory response, and elicited postexercise ketosis. A 49% increase in insulin-glucagon ratio during meals, a 1 mM decline in glucagon glycemic threshold, and a reduced vagal tone during exercise were associated with Before-Meals but not with After-Meals trials. CONCLUSIONS: These results demonstrate that exercise performed in postabsorptive, but not in postprandial state, lowers glucoregulatory set point and glucagon glycemic threshold and is accompanied by reduced vagal tone, counterregulatory responses, and glucagon glycemic threshold and by increased insulin-glucagon ratio. Reduced counterregulatory response, altered neuroendocrine function, and sustained lowering of blood glucose are most likely the consequences of reduced carbohydrate availability during exercise.