The effects of exercise training on lipid metabolism and coronary heart disease

Abstract

Blood lipoproteins are formed by various amounts of cholesterol (C), triglycerides (TGs), phospholipids, and apolipoproteins (Apos). ApoA1 is the major structural protein of high-density lipoprotein (HDL), accounting for ~70% of HDL protein, and mediates many of the antiatherogenic functions of HDL. Conversely, ApoB is the predominant low-density lipoprotein (LDL) Apo and is an indicator of circulating LDL, associated with higher coronary heart disease (CHD) risk. Thus, the ratio of ApoB to ApoA1 (ApoB/ApoA1) is used as a surrogate marker of the risk of CHD related to lipoproteins. Elevated or abnormal levels of lipids and/or lipoproteins in the blood are a significant CHD risk factor, and several studies support the idea that aerobic exercise decreases CHD risk by partially lowering serum TG and LDL-cholesterol (LDL-C) levels and increasing HDL-C levels. Exercise also exerts an effect on HDL-C maturation and composition and on reverse C transport from peripheral cells to the liver to favor its catabolism and excretion. This process prevents atherosclerosis, and several studies showed that exercise training increases heart lipid metabolism and protects against cardiovascular disease. In these and other ways, it more and more appears that regular exercise, nutrition, and strategies to modulate lipid profile should be viewed as an integrated whole. The purpose of this review is to assess the effects of endurance training on the nontraditional lipid biomarkers, including ApoB, ApoA1, and ApoB/ApoA1, in CHD risk.

The Regulation of Fat Metabolism during Aerobic Exercise

“…When exercise intensity increases, there is a shift from FA to glucose oxidation with a reduction in the percentage of the total energy requirement derived from fat oxidation and a reciprocal increase in carbohydrate oxidation, which becomes the main energy source when exercise reaches above ~80% of VO 2max [ 58 , 65 , 66 , 67 ]. During exercise intensity at 65% of VO 2max , the contribution of plasma FAs decreases and the rate of IMTG increases and provides about 50% of the FA for total fat oxidation [ 20 , 68 , 69 ]. Thus, peripheral lipolysis and, consequently, the release rate of FFA into plasma, is stimulated at maximum at the lowest exercise intensity and progressively decreases with increasing exercise intensity up to a point where the concentration of plasma FFA during exercise at 85% of VO 2max appears significantly suppressed.…”

“…The increase of lipolysis and, consequently, the release rate of FFA in the plasma, is greater in endurance-trained, with respect to untrained subjects [ 63 ]. The majority of the studies have shown a decrement of TG after aerobic exercises, due to their mobilization from visceral and sub-cutaneous adipose tissues along with TG in the VLDL-C broken down to FFA by lipases [ 68 , 69 , 80 , 81 ]. It is well-known that marathon and middle-distance runners have different protocols of endurance training.…”

SARS-CoV-2 Acquisition and Immune Pathogenesis Among School-Aged Learners in Four Diverse Schools

“…20,21 Levels of HDL seem to be particularly sensitive to physical activity. 22,23 The mechanisms responsible for the significant association we found between low HDL levels and SARS-CoV-2 are at present unknown, but may be related to the association of overweight/obesity and chronic inflammation in children. 24 Increases in physical inactivity and weight in children have accompanied school closures over the past year.…”

Determinants of the Postprandial Triglyceride Response to a High-fat Meal in Healthy Overweight and Obese Adults.

“…This is a notable nding as habitual physical activity has not been found to be a key determinant of postprandial TG responses (3). Chronic exercise improves the overall fasting lipid pro le through modulation of apolipoprotein A1 expression and increase in HDL by way of increased lecithin-cholesterol acyltransferase activity (49). Acute exercise has been found to lower the magnitude of the postprandial lipemic response through decreased chylomicron appearance (22), increased oxidation of fatty acids post-exercise (50), decreased VLDL secretion from the liver, and increased LPL activity (22) though LPL activity in particular may be enhanced in men compared to women post-exercise ( 51).…”