Effects of exercise on postprandial metabolism, appetite responses and feeding behaviour

Exaggerated metabolic perturbations during the postprandial period are likely to play a role in the development of vascular and metabolic diseases. Elevated levels of postprandial triglycerides (TG) are associated with increased risk for atherosclerosis independently of other cardiovascular risk factors, and exaggerated postprandial insulin excursions are known to contribute to lipid dysmetabolism and chronic insulin resistance. This, together with the fact that free-living humans spend most of their time in the postprandial state, suggests that interventions focusing on the improvement of postprandial metabolism could play a role in the prevention and management of cardiovascular and metabolic diseases. Exercise has a potent role in improving postprandial metabolism, by effectively attenuating postprandial lipaemia and insulinemia, as well as increasing fat oxidation, all of which providing positive outcomes for the prevention and treatment of metabolic disorders. It is however unclear the extent to which these beneficial effects of exercise persist when food is consumed ad libitum. In addition, the effects of exercise on appetite regulation and food intake require further elucidation. It is possible that exercise may provoke compensatory adaptations in food intake in an effort to restore energy balance, through physiological and/or behavioural responses. This has implications for the efficacy of exercise in the regulation of a healthy body weight. Therefore, the overall aim of this thesis is to describe the effects of exercise on postprandial metabolism, appetite responses and feeding behaviour in overweight/obese men. The first two experimental chapters of this thesis (Chapters 3 and 4) aimed to investigate the effects of single vs. repeated exercise sessions (~700 kcal per session) on postprandial metabolism, energy intake, appetite and gut peptide responses in response to ad libitum feeding. Ten sedentary, overweight/obese men underwent: i) no-exercise control; ii) one exercise session (Day 3); and iii) three exercise sessions over three consecutive days (Days 1-3); prior to a 7-h metabolic assessment day (Day 4). Energy substrate utilisation, postprandial TG, insulin, acylated ghrelin, PYY3-36 as well as appetite responses and ad-libitum energy intake (breakfast, lunch, dinner) were determined. The findings of this study showed that the beneficial effects of a single exercise session on postprandial metabolism on postprandial metabolic responses persisted when meals were consumed ad libitum, but were not augmented by inducing a larger energy deficit by exercising on consecutive days. Furthermore, while a single exercise session did not elicit compensatory responses in appetite and energy intake, exercising on consecutive days led to a partial compensation (~24%) in energy intake as well as increased hunger sensation. Gut peptide responses were unaltered by exercise. The next chapter (Chapter 5) aimed to determine the effects of exercise timing relative to meal ingestion on postprandial metabolism, appetite responses, and ad libitum energy intake. Ten, sedentary overweight men exercised for an hour (~400 kcal) before or after consuming a standardised breakfast meal, followed by an 8.5 h metabolic assessment period. Energy substrate utilisation, postprandial TG, insulin, as well as appetite responses and ad-libitum energy intake (lunch, dinner) were determined. The findings indicated that exercise performed prior to a breakfast meal and exercise performed after a breakfast meal waas similarly beneficial in improving postprandial metabolism. Exercise timing relative to meal ingestion also did not influence appetite responses and ad libitum energy intake. In the final experimental chapter (Chapter 6), a pilot study was designed to examine the effects of acute exercise on non-metabolic factors related to appetite using a computer-based assessment. Twenty-seven men and women walked for an hour on the treadmill or rested on a control day. Appetite-related measures were assessed before and immediately after exercise, and hourly for 2 hours post exercise. The findings showed that an acute bout of moderate intensity exercise had an anorexigenic effect; characterised by diminished hunger and lower prospective food intake (ideal portion size) compared to no exercise. Although not a primary aim, this study discovered a novel association between loss aversion and prospective food intake and food liking. The collective findings of this thesis suggest that exercise attenuates postprandial TG and enhances fat oxidation in response to ad libitum feeding, indicating that exercise’s benefits can be extended into the ‘real world’ setting. The beneficial effects of exercise on postprandial metabolism are also independent of its timing relative to meal ingestion. In line with evidence in the literature, an acute bout of aerobic exercise does not induce compensatory responses in terms of energy intake and increased appetite, supporting the role of exercise in weight management. Other than physiological factors, the behavioural and cognitive aspects related to feeding can play a role in mediating compensatory responses to exercise and this requires further investigation