Abstract
A high level of physical activity is associated with a lower cardiovascular risk in adult and elderly subjects. Several mechanisms are involved. Physical activity induces an increase in energy output. The contribution of fats to muscle energy metabolism increases with exercise duration. It decreases with exercise intensity. EPOC contributes by about 10% to the total energy cost of exercise. This supplementary energy expenditure is principally covered with fat oxidation, this being related to GH release. Part of energy expended during intermittent exercise is supplied by fat oxidation. The used lipids are taken from the muscular triacylglycerol stores and from the circulating FFA and lipoprotein triacylglycerols. Hydrolysis of triacylglycerols is achieved by LPL. Endurance training induces an increased contribution from fat to the exercise energy need. This results from increased muscle capillary density, enhanced activity of LPL and of the enzymes controlling beta-oxydation. The increased energy expenditure results in a reduced fat mass, which accounts for a decreased plasma triacylglycerol level. Endurance activity requiring approximately an expenditure of 60 kJ.kg-1 per week usually produces favourable lipoprotein changes. Level of post-prandial lipemia is lowered. These alterations disappear within the first two days of recovery.
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CITATION STYLE
Hashimoto, T. (2013). Lipid metabolism and exercise. The Journal of Physical Fitness and Sports Medicine, 2(2), 149–154. https://doi.org/10.7600/jpfsm.2.149
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