Prescribing Aerobic Exercise for the Regulation of Postprandial Lipid Metabolism
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Prescribing Aerobic Exercise for the Regulation of Postprandial Lipid Metabolism Current Research and Recommendations Christos S. Katsanos Department of Surgery, The University of Texas Medical Branch, Galveston, Texas, USA
Abstract
Prolonged presence of elevated plasma triglycerides (TGs) during the postprandial period has been suggested to increase the risk for coronary artery disease. Aerobic exercise attenuates postprandial lipaemia and this has generally been described as a short-term effect of the exercise. Effects of exercise on postprandial lipaemia have mostly been investigated, and documented, with large exercise-induced energy expenditures (i.e. 1000 kcal). The exact mechanisms involved in the attenuation of postprandial lipaemia with exercise are not completely understood, but it appears that at least two mechanisms are involved: a decrease in TG secretion by the liver and an increase in plasma TG clearance by the muscle. Changes in the metabolism of other lipids, such as those in high-density lipoprotein cholesterol, have been documented only when the exercise is performed some hours before the fat meal. Although factors such as the physical fitness and percentage body fat of an individual are likely to also be involved, the most important factors determining the magnitude of the attenuation in postprandial lipaemia appear to be the magnitude of the exercise-induced energy expenditure and the intensity of exercise. To date, the evidence suggests that healthy individuals can generally induce favourable changes in postprandial lipaemia with aerobic exercise that: (i) is completed during the period extending from 16 hours before a meal through 1.5 hours after a meal; (ii) is of moderate intensity; and (iii) results in an energy expenditure of approximately 500 kcal (or more).
It is well documented from epidemiological studies conducted during the past several decades that there is a positive relationship between an abnormal lipid and lipoprotein metabolism and the development and progression of atherosclerosis and coronary artery disease (CAD). For example, high levels of total cholesterol (TC) have long been known to be associated with CAD.[1,2] Also, there is a positive association between low-density lipoprotein choles-
terol (LDL-C) and CAD, and an inverse relationship between high-density lipoprotein cholesterol (HDLC) and CAD. During the last two decades, research efforts have focused on exploring the association between plasma triglyceride (TG) levels and CAD. Although this association was initially a matter of debate, which primarily originated from the statistical approach used to determine individual lipid effects on CAD,
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the overall evidence now strongly suggests that TG levels are significant and independent predictors of CAD.[3-5] It has been known for some time that individuals with CAD demonstrate abnormally higher postprandial TG levels compared with controls,[6] and it has now been suggested that nonfasting
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