Effects of moderate exercise on VLDL1 and Intralipid kinetics in overweight/obese middle-aged men

Prior moderate exercise reduces plasma triglyceride (TG)-rich lipoprotein concentrations, mainly in the large very low-density lipoprotein (VLDL1) fraction, but the mechanism responsible is unclear. We investigated the effects of brisk walking on TG-rich lipoprotein kinetics using a novel method. Twelve overweight/obese middle-aged men underwent two kinetic studies, involving infusion of Intralipid to block VLDL1catabolism, in random order. On the afternoon prior to infusion, subjects either walked on a treadmill for 2 h at ∼50% maximal oxygen uptake or performed no exercise. Multiple blood samples were taken during and after infusion for separation of Intralipid (Sf400) and VLDL1(Sf60–400). VLDL1-TG and -apoB production rates were calculated from their linear rises during infusion; fractional catabolic rates (FCR) were calculated by dividing linear rises by fasting concentrations. Intralipid-TG FCR was determined from the postinfusion exponential decay. Exercise reduced fasting VLDL1-TG concentration by 30% ( P = 0.007) and increased TG enrichment of VLDL1particles [30% decrease in cholesteryl ester (CE)/TG ratio ( P = 0.007); 26% increase in TG/apoB ratio ( P = 0.059)]. Exercise also increased VLDL1-TG, VLDL1-apoB, and Intralipid-TG FCRs by 82, 146, and 43%, respectively (all P &lt; 0.05), but had no significant effect on VLDL1-TG or -apoB production rates. The exercise-induced increase in VLDL1-apoB FCR correlated strongly with the exercise-induced changes in VLDL1CE/TG ( r = −0.659, r = 0.020) and TG/apoB ( r = 0.785, P = 0.002) ratios. Thus, exercise-induced reductions in VLDL1concentrations are mediated by increased catabolism, rather than reduced production, which may be facilitated by compositional changes to VLDL1particles that increase their affinity for clearance from the circulation.</jats:p