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Reductions in postprandial lipemia have been observed following aerobic exercise of sufficient energy expenditure. Increased excess postexercise oxygen consumption (EPOC) has been documented when comparing high- versus low-intensity exercise. The contribution of EPOC energy expenditure to alterations in postprandial lipemia has not been determined. The purpose of this study was to evaluate the effects of low- and high-intensity exercise on postprandial lipemia in healthy, sedentary, overweight and obese men (age, 43 ± 10 years; peak oxygen consumption, 31.1 ± 7.5 mL·kg·min; body mass index, 31.8 ± 4.5 kg/m) and to determine the contribution of EPOC to reductions in postprandial lipemia. Participants completed 4 conditions: nonexercise control, low-intensity exercise at 40%-50% oxygen uptake reserve (LI), high-intensity exercise at 70%-80% oxygen uptake reserve (HI), and HI plus EPOC re-feeding (HI+EERM), where the difference in EPOC energy expenditure between LI and HI was re-fed in the form of a sports nutrition bar (Premier Nutrition Corp., Emeryville, Calif., USA). Two hours following exercise participants ingested a high-fat (1010 kcals, 99 g sat fat) test meal. Blood samples were obtained before exercise, before the test meal, and at 2, 4, and 6 h postprandially. Triglyceride incremental area under the curve was significantly reduced following LI, HI, and HI+EERM when compared with nonexercise control (p < 0.05) with no differences between the exercise conditions (p > 0.05). In conclusions, prior LI and HI exercise equally attenuated postprandial triglyceride responses to the test meal. The extra energy expended during EPOC does not contribute significantly to exercise energy expenditure or to reductions in postprandial lipemia in overweight men.

The objectives of the present investigation were to determine the effects of exercise intensity on the blood lipid response to a high-fat test meal in sedentary, overweight men, and to determine the contribution of excess post-exercise oxygen consumption (EPOC) to changes in postprandial lipemia. Seven men (Age = 43 + 10 years; BMI = 31.8 + 4.5 kg/m2; Waist = 107.2 + 14.9 cm; and VO2peak = 31.7 + 7.5 ml/kg/min) participated in 4 experimental conditions: control, low-intensity (LI = 40-50% of VO2 reserve), highintensity (HI = 70-80% of VO2 reserve), and HI exercise plus EPOC re-feeding (HI + EERM) where the difference in EPOC following LI and HI was re-fed in the form of a commercially available meal bar. Exercise sessions were isocaloric (500 calories) and completed in the morning after a 12-hour overnight fast. Blood samples were taken before and after exercise, immediately before, and 2, 4, and 6 hours after a high-fat test meal (1010 calories, 100 g fat, 99 g saturated fat, 17 g carbohydrate, 3 g protein). Serum samples were measured for triglycerides (TG), lipoprotein cholesterol, non-esterified fatty acids (NEFA), glucose and insulin and were analyzed using 2-way repeated-measures ANOVAs. Repeated measures ANOVAs were used to examine triglyceride and insulin total (AUCT) and incremental (AUCI) areas under the curve. Comparisonwise significance was set at p < 0.05. Compared to control, TG were lower at 4 hours after both exercise intensities and remained lower at 6 hours after LI only. LI and HI significantly reduced postprandial triglyceride AUCI by 31 and 27%. AUCI and AUCT were similar between exercise intensities and changes in other dependent variables were of similar magnitude and direction in all conditions. The lower postprandial TG observed after exercise was not diminished in the HI+EERM trial. The results of this study indicate that similar significant reductions in postprandial triglycerides occur with LI and HI exercise with and without replacement of EPOC calories. In sedentary overweight men, EPOC does not contribute substantially to energy expenditure or reductions in postprandial lipemia.