Watt Matthew J, Heigenhauser G J F, Stellingwerff Trent, Hargreaves Mark, Spriet Lawrence L
Department of Human Biology and Nutritional Sciences, University of Guelph, Ontario N1G 2W1, Canada.
J Physiol. 2002 Nov 1;544(3):949-56. doi: 10.1113/jphysiol.2002.026757.
This study investigated the effect of reduced acetylcarnitine availability on oxidative metabolism during the transition from rest to steady-state exercise. Eight male subjects completed two randomised exercise trials at 68 % of the peak rate of O(2) uptake (V((O(2)),peak)). On one occasion subjects ingested 1 g (kg body mass)(-1) glucose 75 min prior to exercise (CHO), whereas the other trial acted as a control (CON). Muscle samples were obtained pre- and 75 min post-ingestion, and following 1 and 10 min of exercise. Plasma glucose and insulin were elevated (P < 0.05), and plasma free fatty acids (FFA) were lower at the onset of exercise in CHO. Acetylcarnitine (CON, 4.8 +/- 1.8; CHO, 1.5 +/- 0.9 mmol (kg dry mass (d.m.))(-1), P < 0.05) and acetyl CoA (CON, 13.2 +/- 2.3; CHO, 6.3 +/- 0.6 micromol (kg d.m.)(-1), P < 0.05) were lower at rest, whereas pyruvate dehydrogenase activation (PDHa) was greater in CHO compared with CON (CON, 0.78 +/- 0.07; CHO, 1.44 +/- 0.19 mmol min(-1) (kg wet mass (w.m.))(-1)). Respiratory exchange ratio (RER) was significantly elevated during exercise in CHO. The acetyl groups increased at similar rates at the onset of exercise (1 min) and there was no difference in substrate phosphorylation as determined from lactate accumulation and phosphocreatine degradation between trials. Subsequently, oxidative metabolism during the transition from rest to steady-state exercise was not affected by prior carbohydrate ingestion. Although exercise resulted in the rapid activation of PDH in both trials, PDHa was greater at 1 min in CHO (CON, 2.36 +/- 0.22; CHO, 2.91 +/- 0.18 mmol min(-1) (kg w.m.)(-1)). No differences in muscle metabolite levels and PDHa were observed after 10 min of moderate exercise between trials. In summary, at rest, carbohydrate ingestion induced multiple metabolic changes which included decreased acetylcarnitine availability and small increases in PDHa. The prior changes in PDHa and acetylcarnitine availability had no effect on substrate phosphorylation and oxidative metabolism at the onset of exercise. These data suggest that acetylcarnitine availability is unlikely to be the site of metabolic inertia during the transition from rest to steady-state moderate intensity exercise.
本研究调查了在从静息状态过渡到稳态运动过程中，乙酰肉碱可用性降低对氧化代谢的影响。八名男性受试者以摄氧量峰值（V̇(O₂)peak）的68%完成了两项随机运动试验。一次，受试者在运动前75分钟摄入1 g·kg⁻¹体重的葡萄糖（CHO），而另一次试验作为对照（CON）。在摄入前、摄入后75分钟以及运动1分钟和10分钟后采集肌肉样本。CHO组运动开始时血浆葡萄糖和胰岛素升高（P < 0.05），血浆游离脂肪酸（FFA）降低。静息时乙酰肉碱（CON组，4.8±1.8；CHO组，1.5±0.9 mmol·kg⁻¹干质量（d.m.），P < 0.05）和乙酰辅酶A（CON组，13.2±2.3；CHO组，6.3±0.6 μmol·kg⁻¹ d.m.，P < 0.05）较低，而与CON组相比，CHO组丙酮酸脱氢酶激活（PDHa）更大（CON组，0.78±0.07；CHO组，1.44±0.19 mmol·min⁻¹·kg⁻¹湿质量（w.m.））。CHO组运动期间呼吸交换率（RER）显著升高。运动开始时（1分钟）乙酰基团以相似速率增加，且试验间根据乳酸积累和磷酸肌酸降解确定的底物磷酸化无差异。随后，从静息状态过渡到稳态运动期间的氧化代谢不受先前碳水化合物摄入的影响。尽管两次试验中运动均导致PDH快速激活，但CHO组1分钟时的PDHa更大（CON组，2.36±0.22；CHO组，2.91±0.18 mmol·min⁻¹·kg⁻¹ w.m.）。试验间中度运动10分钟后，未观察到肌肉代谢物水平和PDHa的差异。总之，静息时，碳水化合物摄入引起多种代谢变化，包括乙酰肉碱可用性降低和PDHa小幅增加。运动开始时，PDHa和乙酰肉碱可用性的先前变化对底物磷酸化和氧化代谢无影响。这些数据表明，在从静息状态过渡到稳态中等强度运动过程中，乙酰肉碱可用性不太可能是代谢惰性的位点。
