Timing of Meals and Exercise Affects Hormonal Control of Glucoregulation, Insulin Resistance, Substrate Metabolism, and Gastrointestinal Hormones, but Has Little Effect on Appetite in Postmenopausal Women.

The current prevalence of obesity in the US is strongly associated with excessive food intake and insufficient physical activity. This study examined whether changing the timing of exercise before or after two daily meals could alter human appetite for food. Fifty-four healthy postmenopausal women were matched by body weight and assigned to two groups: (1) two bouts of 2-h moderate-intensity exercise ending one hour before each weight-maintenance meal (XM, n = 23), (2) two-hour moderate-intensity exercise starting 1 h after each weight-maintenance meal (MX, n = 23), and one sedentary control (SED) arm (n = 8). Measurements included appetite ratings, circulating glucose, free fatty acids (FFAs), a ketone body D-ß-hydroxybutyrate (BHB), glucoregulatory hormones insulin and glucagon, and gastrointestinal hormones associated with food digestion and absorption and implicated in appetite sensations. XM group increased concentrations of FFAs and BHB during exercise and increased insulin and homeostatic assessment of insulin resistance (HOMA-IR) during postprandial periods. MX group reduced postprandial insulin and HOMA-IR by about 50% without a major change in plasma glucose. There was brief suppression of hunger and an increase in satiation in both exercise groups near the end of the first postprandial period. The time course of hunger was unrelated to the perturbations in fuel metabolism, depletion of liver glycogen, and not correlated with concentration changes in hunger-stimulating hormone ghrelin during XM exercise before meals. Similarly, there was no correlation between the time course of fullness during exercise after meals with the postprandial secretion of gastrointestinal hormones including cholecystokinin (CCK) that has been linked to satiation. Hunger and satiation appear to depend on oral intake and gastrointestinal processing of nutrients and are not affected by metabolic and hormonal consequences of the timing of exercise with respect to meals. Moderate-intensity exercise performed shortly after meals induces a rapid and highly effective lowering of insulin resistance.

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.

Appetite responds to changes in meal content, whereas ghrelin, leptin, and insulin track changes in energy availability.

CONTEXT: It is uncertain how between-meal variations in energy availability and physiological changes in ghrelin, leptin, and insulin affect appetite. OBJECTIVE: The aim of the study was to examine the influence on human appetite of the meal size and its nutrient content or changes in energy availability and concentrations of ghrelin, leptin, and insulin. DESIGN: We conducted a crossover study manipulating meal size and energy availability through exercise energy expenditure and iv nutrient replacement (TPN). SETTING: The study was performed at a Clinical Research Center. PARTICIPANTS: Ten healthy postmenopausal women (age, 59.7 +/- 1.5 yr; mean body mass index, 26 kg/m(2)) were studied. INTERVENTIONS: We conducted trials based on different morning meal size (418 vs. 2090 KJ), presence or absence of exercise energy expenditure (2273 to 2361 KJ), energy replacement by TPN (1521 to 1538 KJ), and a midday ad libitum meal. MAIN OUTCOME MEASURES: Changes in hunger, fullness, midday ad libitum food consumption, and concentrations of ghrelin, leptin, insulin, and metabolic fuels were measured. We also performed midday meal tests for the presence of caloric compensation. RESULTS: Appetite was influenced by the size and energy content of the meals, but not by variation in energy availability which also did not trigger consummatory compensation. Exercise reduced hunger and increased fullness. Ghrelin, leptin, and insulin responded to changes in energy availability but not to meal size. Appetite was unaffected by physiological changes in ghrelin, leptin, or insulin. CONCLUSIONS: During rest, appetite is influenced by the size and energy content of meals, but it bears no homeostatic relationship to between-meal changes in energy availability due to small meals, exercise, or TPN, or concentrations of ghrelin, leptin, and insulin.

Exercise energy expenditure is not consciously detected due to oro-gastric, not metabolic, basis of hunger sensation.

We tested the hypothesis that exercise energy expenditure (EEE) will elicit reflex metabolic compensations but no increases in hunger. Exercise expended 800 kcal once when fasted and at another time in a post-prandial state. During fasting exercise, pre-meal ratings of hunger were unaffected by EEE, but plasma concentrations of ghrelin, growth hormone and free fatty acids were higher than in the absence of EEE. We propose that the perception of hunger is based on the vagal, lateral hypothalamic and cortical projections of oral and gastro-intestinal (GI) stimuli and that EEE triggers neuroendocrine compensations and influences hunger indirectly by affecting GI functions.