Responses of LDL and HDL particle size and distribution to omega-3 fatty acid supplementation and aerobic exercise

Abstract

The purpose of this investigation was to determine the independent and combined effects of aerobic exercise and omega-3 fatty acid (n-3fa) supplementation on lipid and lipoproteins. Sedentary, normoglycemic, nonsmoking men (n = 11) were assigned to perform rest and exercise before and during n-3fa supplementation. Exercise consisted of 3 consecutive days of treadmill walking at 65% maximum O(2) consumption for 60 min. Supplementation consisted of 42 days of 4.55 g/day of n-3fa. A two-way factorial ANOVA with repeated measures revealed significant reductions in total cholesterol (P = 0.001, -9.2%) and triglyceride (P = 0.007, -32.4%) concentrations postexercise. In addition, exercise increased LDL peak particle size (P = 0.001) from 26.2 to 26.4 nm, but not HDL size. The n-3fa supplementation resulted in a significant shift in the distribution of HDL-cholesterol (HDL-C) carried by HDL(2b+2a) (P = 0.001, 14.2%) and HDL(3a+3b) (P = 0.001, -22.8%), despite no significant changes in lipid and lipoprotein-cholesterol concentrations. The majority of the shift in HDL-C was noted in HDL(2b) (P = 0.001, 20.9%) and HDL(3a) (P < 0.001, -31.0%) particles. There were no combined effects of exercise and n-3fa supplementation on lipids and lipoproteins. Three consecutive days of aerobic exercise reduced triglyceride and total cholesterol concentrations with a concomitant increase in LDL peak particle size. In contrast, n-3fa supplementation shifted HDL-C from HDL(3) particles to HDL(2) particles, despite no significant changes in HDL(2)-C and HDL(3)-C concentrations. Exercise and n-3fa supplementation do not synergistically improve serum lipids and lipoproteins, but rather independently affect the metabolism of lipids and lipoproteins.

Lipoprotein subfractions and dietary intake of n-3 fatty acid: the Genetics of Coronary Artery Disease in Alaska Natives study

“…In turn, the accelerated catabolism increases the availability of triglycerides for exchange with the HDL compartment; this mechanism might explain our observed increasing large and decreasing small and medium HDL concentrations and higher particle size with higher intakes of n23 fatty acids. This finding is also consistent with previous studies of n23 fatty acid supplementation showing that the cholesterol content shifts from HDL3 particles to the larger HDL2 particles (27). In the presence of enhanced catabolism of large VLDLs, reduced cholesteryl ester transfer protein activity (28) would be expected to reduce the triglyceride and cholesterol ester exchange with HDL.…”

Combined dyslipidemia in childhood

“…[127][128][129] These lifestyle change interventions have been shown to significantly reduce TG, non-HDL-C and TG/HDL-C ratio, and lead to an improvement in LDL subpopulation pattern. 130,131 There are no trials of CDO evaluating clinical cardiovascular events in response to lifestyle changes initiated in childhood. However, better vascular health in adults can be related to healthy childhood risk status and behaviors, as shown in the Bogalusa Heart Study and in the Cardiovascular Risk in Young Finns study, where sustained low-risk status and healthy diet from childhood to adulthood was associated with thinner cIMT.…”

Effects of Peroxisome Proliferator-Activated Receptors, Dietary Fat Intakes and Gene–Diet Interactions on Peak Particle Diameters of Low-Density Lipoproteins

“…Diets higher in saturated fats have generally been related to larger more buoyant LDL particles than diets rich in monounsaturated or polyunsaturated fats [8]. Other studies have reported an increase in LDL size after supplementation with docosahexaenoic acid [9], but results are inconsistent [10]. …”