Burton F L, Malkova D, Caslake M J, Gill J M R
Institute of Diet, Exercise and Lifestyle, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, UK.
Int J Obes (Lond). 2008 Mar;32(3):481-9. doi: 10.1038/sj.ijo.0803754. Epub 2007 Nov 13.
The extent to which exercise-induced changes to postprandial metabolism are dependant on the associated energy deficit is not known.
To determine the effects of exercise, with and without energy replacement, on postprandial metabolism.
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.
A total of 13 overweight/obese men (age: 40+/-8 years, body mass index: 31.1+/-3.0 kg m(-2)).
Postprandial triglyceride, insulin, glucose, non-esterified fatty acid and 3-hydroxybutyrate concentrations and substrate utilization rates were determined.
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).
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.
运动引起的餐后代谢变化在多大程度上依赖于相关的能量不足尚不清楚。
确定有无能量补充时运动对餐后代谢的影响。
每位受试者按随机顺序进行三次为期2天的试验。在每次试验的第1天，受试者休息（对照）、以50%最大摄氧量步行以诱导净能量消耗为27 kJ·kg-1体重（能量不足）或在补充消耗的净能量的情况下完成相同的步行（能量补充）。在第2天，受试者完成8.5小时的代谢评估。在第2天之前的3天里，受试者食用等热量饮食，避免有计划的运动（运动干预除外）和饮酒。
总共13名超重/肥胖男性（年龄：40±8岁，体重指数：31.1±3.0 kg·m-2）。
测定餐后甘油三酯、胰岛素、葡萄糖、非酯化脂肪酸和3-羟基丁酸浓度以及底物利用率。
与对照和能量补充相比，能量不足使餐后甘油三酯浓度分别降低了14%和10%（两者P<0.05）。与对照和能量补充相比，能量不足使餐后3-羟基丁酸浓度分别增加了40%和19%（两者P<0.05）。与对照相比，能量不足和能量补充时餐后胰岛素浓度分别降低了18%和10%，与能量补充相比，能量不足时餐后胰岛素浓度降低了10%（所有P<0.05）。与对照相比，能量不足和能量补充时餐后脂肪氧化分别增加了30%和14%，与能量补充相比，能量不足时餐后脂肪氧化高12%（所有P<0.05）。
补充能量的运动可降低餐后胰岛素血症并增加脂肪氧化。然而，运动引起的能量不足增强了这些作用，并且是降低餐后血脂的必要条件。
