Effects of exercise, with and without an associated energy deficit, on postprandial metabolism and appetite regulation.
PhD thesis, University of Glasgow.
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In 1979, Donald Zilversmit published a landmark paper suggesting a role for postprandial metabolism in the development and progression of atherosclerosis, and in subsequent years, a number of postprandial metabolic perturbations have been highlighted as potential risk factors for atherosclerotic development. Interventions inducing favourable changes in postprandial metabolism may, therefore, have an important role in the management and control of cardiovascular disease and its associated risk factors. Acute exercise is one such intervention, successfully attenuating postprandial lipaemia and insulinaemia, enhancing endothelial function, reducing arterial stiffness and increasing postprandial fat oxidation. It also appears that exercise might facilitate a tighter coupling between energy intake and expenditure, mediating more stable and healthy body weights, perhaps by inducing changes in appetite, energy intake and circulating concentrations of 'hunger' hormones. It does, however, remain unclear as to what extent these changes are mediated by exercise per se, or the associated energy deficit and thus what effects exercise coupled with a state of energy balance would have on postprandial metabolism, appetite control and feeding behaviour. The aim of this thesis was, therefore, to investigate the immediate and delayed effects of exercise, coupled with a state of energy balance, on postprandial metabolism and appetite regulation.
Thirteen overweight, pre-menopausal women were recruited to compare the immediate effects of a state of energy balance coupled with a high (exercise) or low (rest) energy turnover. Using a one-day model, each volunteer completed a 60-minute, moderate intensity treadmill walk prior to ingesting a test breakfast and a 6-hour metabolic assessment period and a control trial during which no exercise was performed before breakfast. During the 6-hour observation period postprandial lipaemia, insulinaemia and glycaemia, total ghrelin and acylated ghrelin concentrations, pulse wave velocity and energy substrate utilisation were determined. Subjective ratings of appetite and food palatability and energy and macronutrient intakes at an ad libitum buffet meal were also recorded. Thirteen overweight and obese, middle-aged men were recruited to investigate the delayed effects of exercise withe energy balance, using a two-day model, on postprandial metabolism and appetite control. On the afternoon of day-one, each volunteer completed one of three intervention trials, a moderate intensity treadmill walk inducing a net energy expenditure of 17kJ.kg[supercript -1]. body mass, exactly the same walk with the net energy expenditure replaced or they performed no exercise. The following day, an 8.5-hour metabolic observation period was completed during which time postprandial lipaemia, insulinaemia and glycaemia, letpin and total gherin concentrations, pulse wave velocity, energy substrate utilisation and subjective ratings of appetite were recorded in response to two separate oral fat tolerance tests.
The findings from these studies showed exercise, coupled with a state of energy balance, to have no significant effect, immediate or delayed, on postprandial lipaemia suggesting and exercise-induced deficit was required to lower postprandial triglyceride concentrations. A significant attenuation was, however, observed in postprandial insulin concentrations on the day following exercise with energy balance, indicitive of enhanced insulin sensitivity. Both immediate and delayed increases in postprandial fat oxidation were observed following exercise, which led to lower (ie. more negative) fat balances. This could potentially have important implications for the future management and regulation of the overweight and obese state. The role for exercise with energy balance in attenuating pulse wave velocity speeds remains equivocal with no immediate effect observed on postprandial central or peripheral pulse wave velocity, whilst significantly lower peripheral pulse wave velocity speeds were observed after a delay of some hours post-exercise. With regard to appetite regulation, exercise coupled with a state of energy balance does appear to reduce postprandial leptin concentrations on the following day, whilst total gherlin remains resistant to any exercise-induced changes either immediatley or some hours later. An exciting find does, however, show acylated ghrelin concentrations to be significantly lower following exercise with energy balance, a response that may, to some extent, mediate subsequent changes in appetite. Changes in subjective ratings of appetite were transient, lasting just one to two hours after exercise with energy balance and energy and macronutrient intake at an ad libitum buffet meal consumed six hours after exercise with energy balance was not significantly altered.
The combined findings of this thesis suggest that exercise, coupled with a state of energy balance, induces favourable changes in postprandial insulinaemia, fat oxidation and peripheral pulse wave velocity, all of which may have important implications for lowering future risk of cardiovascular disease. Exercise performed in a state of energy balance may also contribute to the improved regulation of body weight, through effects on fat oxidation and balance and potentially via changes in 'hunger' hormones and appetite ratings, although the latter, in particular, requires further investigation.
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