Lipids are important substrates for oxidation at rest and during exercise. Aerobic exercise mediates a delayed onset decrease in total and VLDL-triglyceride (TG) plasma concentration. However, the acute effects of exercise on VLDL-TG oxidation and turnover remain unclear. Here, we studied the acute effects of 90 min of moderate-intensity exercise in healthy women and men. VLDL-TG kinetics were assessed using a primed constant infusion of ex vivo labeled [1-(14)C]triolein VLDL-TG. Fractional VLDL-TG-derived fatty acid oxidation was measured from (14)CO(2) specific activity in expired air. VLDL-TG concentration was unaltered during exercise and early recovery, whereas non-VLDL-TG concentration decreased significantly.VLDL-TG secretion rate decreased significantly during exercise and remained suppressed during recovery. Total VLDL-TG oxidation rate was unaffected by exercise. However, the contribution of VLDL-TG oxidation to total energy expenditure fell from 14 ± 9% at rest to 3 ± 4% during exercise. We conclude that VLDL-TG fatty acids are quantitatively important oxidative substrates under basal postabsorptive conditions but remain unaffected during 90-min moderate-intensity exercise and, thus, become relatively less important during exercise. Lower VLDL secretion rate during exercise may contribute to the decrease in TG concentrations during and after exercise.

Aims/hypothesis Type 2 diabetes is characterised by insulin resistance and increased post-absorptive secretion of VLDLtriacylglycerol (VLDL-TAG). Whether postprandial suppression of endogenous VLDL-TAG secretion is abnormala finding that would link hyperlipidaemia and type 2 diabetes-remains unclear. Methods Eight type 2 diabetic men and eight healthy men were studied before and after a fat-free test meal (40% of resting energy expenditure). VLDL-TAG kinetics were assessed using a primed-constant infusion of ex vivo labelled [1-14 C]triolein VLDL-TAG using non-steadystate calculations. Results Type 2 diabetic men had a higher basal VLDL-TAG secretion rate and concentration than healthy men (mean±SD secretion rate 137±61 vs 78±30 μmol/min, respectively [p00.03]; median concentration 1.03 [range 0.58-1.75] vs 0.33 [0.13-1.14]mmol/l, respectively [p<0.01]). Postprandially, the VLDL-TAG secretion rate decreased in healthy men (p<0.01), but remained unchanged in diabetic men (p00.47). The VLDL-TAG concentration increased in diabetic men and decreased in healthy men postprandially (p<0.05). The difference in VLDL-TAG secretion rate between the two groups approached significance (p00.06) and the relative change in VLDL-TAG secretion rate was significantly different (p00.01) between the two groups. Basal VLDL-TAG clearance was significantly lower in diabetic men (diabetic men 133 [49-390]ml/min; healthy controls 215 ml/min [p<0.05]). After meal ingestion, clearance decreased in healthy men (p00.03), but was unchanged in diabetic men (p00.58). Conclusions/interpretation Obese type 2 diabetic men have impaired postprandial suppression of VLDL-TAG secretion compared with lean healthy men, contributing to their postprandial lipaemia and hypertriacylglycerolaemia.