Endocrine Abstracts (2008) 16 S22.1

Mechanisms for the delayed effects of exercise on lipid and lipoprotein metabolism

Faidon Magkos


Department of Nutrition and Dietetics, Harokopio University, Athens, Greece.


Increased plasma triglyceride (TG) concentration is an important risk factor for cardiovascular disease. Regular aerobic exercise is associated with lower plasma TG concentrations and lower cardiovascular risk. The cardioprotective effect of endurance-type physical activity is therefore likely, to some extent at least, linked to the hypotriglyceridemic effect of aerobic exercise. It has long been recognized that the TG-lowering effect of exercise manifests in response to a single bout of aerobic activity with little, if any, evidence for chronic physiologic adaptations after repeated exercise sessions, i.e., training.

Results from several recent studies investigating the metabolism of very low density lipoproteins (VLDL) by using stable isotope labeled tracers have shed light on the mechanisms whereby exercise lowers plasma TG concentrations. Prolonged exercise of moderate intensity (2 h at 60% of maximal oxygen consumption), performed in the evening, lowers plasma and VLDL-TG concentrations the next morning (~15 h after exercise cessation). This is due to increased VLDL-TG plasma clearance rate, i.e., accelerated removal of VLDL-TG from the circulation, without any changes in VLDL-TG secretion rate by the liver. On the contrary, the hepatic secretion of VLDL-apolipoprotein B-100 (apoB-100) is suppressed by exercise. This suggests secretion of fewer but TG-richer VLDL particles after exercise, which may facilitate their intravascular hydrolysis by lipoprotein lipase. Interestingly, exercise fails to affect VLDL-TG secretion by the liver even though it greatly enhances free fatty acid (FFA) availability, i.e., the major precursor for hepatic TG synthesis, as indicated by the much higher FFA concentration and FFA rate of appearance in plasma after exercise, which could not be matched by the smaller increase in fatty acid oxidation rate.

The effects of exercise leading to hypotriglyceridemia are dose-dependent, since moderate-duration exercise (1 h at 60% of maximal oxygen consumption) does not affect VLDL-TG and VLDL-apoB-100 concentrations and kinetics. Nevertheless, such exercise is still sufficient to promote a great increase in FFA concentration and FFA rate of appearance in plasma, with no concomitant increase in fatty acid oxidation, clearly indicating that under these circumstances, FFA availability in plasma is not a major determinant of VLDL-TG secretion by the liver.

Evidence also suggests that systemic factors considered important for the regulation of VLDL-TG, VLDL-apoB-100, and plasma FFA metabolism, such as insulin, growth hormone, cytokines and adipokines, do not appear to mediate the effects of exercise on hepatic VLDL metabolism. Likewise, sex (men or women), the mode of aerobic exercise (running or cycling), and the type of exercise (endurance or resistance) do not emerge as important regulators of VLDL-TG and VLDL-apoB-100 metabolism response to exercise.

Collectively, recent data indicates that exercise-induced hypotriglyceridemia results from increased removal rate of VLDL-TG from the circulation, which may be facilitated by the secretion of fewer but TG-richer (and therefore likely larger) VLDL particles after exercise. The major determinant of this response appears to be the energy expenditure of exercise, whereas the role of traditional regulators of hepatic VLDL metabolism, such as insulin and the availability of plasma FFA, remains obscure.

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