F L Burton1, D Malkova, M J Caslake, J M R Gill. 1. Institute of Diet, Exercise and Lifestyle, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK.
Abstract
BACKGROUND: The extent to which exercise-induced changes to postprandial metabolism are dependant on the associated energy deficit is not known. OBJECTIVE: To determine the effects of exercise, with and without energy replacement, on postprandial metabolism. DESIGN: Each subject underwent three 2-day trials in random order. On day 1 of each trial subjects rested (control), walked at 50% maximal oxygen uptake to induce a net energy expenditure of 27 kJ kg(-1) body mass (energy-deficit) or completed the same walk with the net energy expended replaced (energy-replacement). On day 2 subjects completed an 8.5-h metabolic assessment. For 3 days prior to day 2, subjects consumed an isocaloric diet, avoided planned exercise (apart from exercise interventions) and alcohol. SUBJECTS: A total of 13 overweight/obese men (age: 40+/-8 years, body mass index: 31.1+/-3.0 kg m(-2)). MEASUREMENTS: Postprandial triglyceride, insulin, glucose, non-esterified fatty acid and 3-hydroxybutyrate concentrations and substrate utilization rates were determined. RESULTS: Energy-deficit lowered postprandial triglyceride concentrations by 14 and 10% compared with control and energy-replacement (P<0.05 for both). Energy-deficit increased postprandial 3-hydroxybutyrate concentrations by 40 and 19% compared with control and energy-replacement (P<0.05 for both). Postprandial insulin concentrations were 18 and 10% lower for energy-deficit and energy-replacement compared with control and 10% lower for energy-deficit than energy-replacement (P<0.05 for all). Postprandial fat oxidation increased by 30 and 14% for energy-deficit and energy-replacement compared to control and was 12% higher for energy-deficit than energy-replacement (P<0.05 for all). CONCLUSION:Exercise with energy replacement lowered postprandial insulinaemia and increased fat oxidation. However an exercise-induced energy deficit augmented these effects and was necessary to lower postprandial lipaemia.
RCT Entities:
BACKGROUND: The extent to which exercise-induced changes to postprandial metabolism are dependant on the associated energy deficit is not known. OBJECTIVE: To determine the effects of exercise, with and without energy replacement, on postprandial metabolism. DESIGN: Each subject underwent three 2-day trials in random order. On day 1 of each trial subjects rested (control), walked at 50% maximal oxygen uptake to induce a net energy expenditure of 27 kJ kg(-1) body mass (energy-deficit) or completed the same walk with the net energy expended replaced (energy-replacement). On day 2 subjects completed an 8.5-h metabolic assessment. For 3 days prior to day 2, subjects consumed an isocaloric diet, avoided planned exercise (apart from exercise interventions) and alcohol. SUBJECTS: A total of 13 overweight/obesemen (age: 40+/-8 years, body mass index: 31.1+/-3.0 kg m(-2)). MEASUREMENTS: Postprandial triglyceride, insulin, glucose, non-esterified fatty acid and 3-hydroxybutyrate concentrations and substrate utilization rates were determined. RESULTS:Energy-deficit lowered postprandial triglyceride concentrations by 14 and 10% compared with control and energy-replacement (P<0.05 for both). Energy-deficit increased postprandial 3-hydroxybutyrate concentrations by 40 and 19% compared with control and energy-replacement (P<0.05 for both). Postprandial insulin concentrations were 18 and 10% lower for energy-deficit and energy-replacement compared with control and 10% lower for energy-deficit than energy-replacement (P<0.05 for all). Postprandial fat oxidation increased by 30 and 14% for energy-deficit and energy-replacement compared to control and was 12% higher for energy-deficit than energy-replacement (P<0.05 for all). CONCLUSION: Exercise with energy replacement lowered postprandial insulinaemia and increased fat oxidation. However an exercise-induced energy deficit augmented these effects and was necessary to lower postprandial lipaemia.
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