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Cardiovascular disease is a leading cause of mortality and morbidity worldwide. One of the key factors mediating cardiovascular disease risk, and the underlying atherogenic disease process, is disturbances to metabolism in the postprandial state, particularly with respect to lipoprotein metabolism. A number of studies have demonstrated that prior exercise can reduce postprandial triglyceride (TG) concentrations, with recent evidence indicating that increased clearance from the circulation of large very low density lipoproteins (VLDL1) plays an important role. However, it was unclear how exercise facilitated this potentially beneficial effect and this was the focus of the present work. The first experimental study in this thesis demonstrated, in 10 overweight/obese men, that 90 minutes of prior moderate exercise increased the affinity of VLDL1 for TG hydrolysis by lipoprotein lipase by 2.2-fold in the fasted state (p = 0.02) and 2.6-fold in the postprandial state (p = 0.001), but did not significantly alter the affinity of chylomicrons, a novel observation that adds to understanding of the mechanism by which exercise lowers TG concentrations. Postprandial responses to meal ingestion depend on the macronutrient composition of the food ingested. In the second experimental chapter, postprandial responses to ingestion of a test meal containing 75g glucose, or 75g fat, or a combination of 75g glucose and 75g fat were compared in 10 overweight/obese men. The main finding was that co-ingestion of fat with the glucose load reduced the postprandial glucose response, but not insulin response, compared with glucose ingestion alone. Co-ingestion of fat with the glucose load also substantially reduced the postprandial suppression of non-esterified fatty acids (NEFA) compared to glucose only ingestion. Postprandial TG responses were similar when only fat was consumed compared with co-ingestion of fat and glucose, but postprandial VLDL1 concentrations were lower in the latter condi

Cardiovascular disease is a leading cause of mortality and morbidity worldwide. One of the key factors mediating cardiovascular disease risk, and the underlying atherogenic disease process, is disturbances to metabolism in the postprandial state, particularly with respect to lipoprotein metabolism. A number of studies have demonstrated that prior exercise can reduce postprandial triglyceride (TG) concentrations, with recent evidence indicating that increased clearance from the circulation of large very low density lipoproteins (VLDL1) plays an important role. However, it was unclear how exercise facilitated this potentially beneficial effect and this was the focus of the present work. The first experimental study in this thesis demonstrated, in 10 overweight/obese men, that 90 minutes of prior moderate exercise increased the affinity of VLDL1 for TG hydrolysis by lipoprotein lipase by 2.2-fold in the fasted state (p = 0.02) and 2.6-fold in the postprandial state (p = 0.001), but did not significantly alter the affinity of chylomicrons, a novel observation that adds to understanding of the mechanism by which exercise lowers TG concentrations. Postprandial responses to meal ingestion depend on the macronutrient composition of the food ingested. In the second experimental chapter, postprandial responses to ingestion of a test meal containing 75g glucose, or 75g fat, or a combination of 75g glucose and 75g fat were compared in 10 overweight/obese men. The main finding was that co-ingestion of fat with the glucose load reduced the postprandial glucose response, but not insulin response, compared with glucose ingestion alone. Co-ingestion of fat with the glucose load also substantially reduced the postprandial suppression of non-esterified fatty acids (NEFA) compared to glucose only ingestion. Postprandial TG responses were similar when only fat was consumed compared with co-ingestion of fat and glucose, but postprandial VLDL1 concentrations were lower in the latter condi

Cardiovascular disease is a leading cause of mortality and morbidity worldwide. One of the key factors mediating cardiovascular disease risk, and the underlying atherogenic disease process, is disturbances to metabolism in the postprandial state, particularly with respect to lipoprotein metabolism. A number of studies have demonstrated that prior exercise can reduce postprandial triglyceride (TG) concentrations, with recent evidence indicating that increased clearance from the circulation of large very low density lipoproteins (VLDL1) plays an important role. However, it was unclear how exercise facilitated this potentially beneficial effect and this was the focus of the present work. The first experimental study in this thesis demonstrated, in 10 overweight/obese men, that 90 minutes of prior moderate exercise increased the affinity of VLDL1 for TG hydrolysis by lipoprotein lipase by 2.2-fold in the fasted state (p = 0.02) and 2.6-fold in the postprandial state (p = 0.001), but did not significantly alter the affinity of chylomicrons, a novel observation that adds to understanding of the mechanism by which exercise lowers TG concentrations. Postprandial responses to meal ingestion depend on the macronutrient composition of the food ingested. In the second experimental chapter, postprandial responses to ingestion of a test meal containing 75g glucose, or 75g fat, or a combination of 75g glucose and 75g fat were compared in 10 overweight/obese men. The main finding was that co-ingestion of fat with the glucose load reduced the postprandial glucose response, but not insulin response, compared with glucose ingestion alone. Co-ingestion of fat with the glucose load also substantially reduced the postprandial suppression of non-esterified fatty acids (NEFA) compared to glucose only ingestion. Postprandial TG responses were similar when only fat was consumed compared with co-ingestion of fat and glucose, but postprandial VLDL1 concentrations were lower in the latter condi