Horowitz J F, Mora-Rodriguez R, Byerley L O, Coyle E F
The Human Performance Laboratory, Department of Kinesiology and Health Education and Division of Nutritional Sciences, The University of Texas at Austin, Austin, Texas 78712, USA.
Am J Physiol. 1999 May;276(5):E828-35. doi: 10.1152/ajpendo.1999.276.5.E828.
This study determined the effect of carbohydrate ingestion during exercise on the lipolytic rate, glucose disappearance from plasma (Rd Glc), and fat oxidation. Six moderately trained men cycled for 2 h on four separate occasions. During two trials, they were fed a high-glycemic carbohydrate meal during exercise at 30 min (0.8 g/kg), 60 min (0.4 g/kg), and 90 min (0.4 g/kg); once during low-intensity exercise [25% peak oxygen consumption (VO2 peak)] and once during moderate-intensity exercise (68% VO2 peak). During two additional trials, the subjects remained fasted (12-14 h) throughout exercise at each intensity. After 55 min of low-intensity exercise in fed subjects, hyperglycemia (30% increase) and a threefold elevation in plasma insulin concentration (P < 0.05) were associated with a 22% suppression of lipolysis compared with when subjects were fasted (5.2 +/- 0.5 vs. 6.7 +/- 1.2 micromol. kg-1. min-1, P < 0.05), but fat oxidation was not different from fasted levels at this time. Fat oxidation when subjects were fed carbohydrate was not reduced below fasting levels until 80-90 min of exercise, and lipolysis was in excess of fat oxidation at this time. The reduction in fat oxidation corresponded in time with the increase in Rd Glc. During moderate-intensity exercise, the very small elevation in plasma insulin concentration (approximately 3 microU/ml; P < 0.05) during the second hour of exercise when subjects were fed vs. when they were fasted slightly attenuated lipolysis (P < 0.05) but did not increase Rd Glc or suppress fat oxidation. These findings indicate that despite a suppression of lipolysis after carbohydrate ingestion during exercise, the lipolytic rate remained in excess and thus did not limit fat oxidation. Under these conditions, a reduction in fat oxidation was associated in time with an increase in glucose uptake.
本研究确定了运动期间摄入碳水化合物对脂肪分解速率、血浆葡萄糖消失率（Rd Glc）和脂肪氧化的影响。六名中度训练的男性在四个不同的场合进行了2小时的骑行。在两次试验中，他们在运动期间于30分钟（0.8克/千克）、60分钟（0.4克/千克）和90分钟（0.4克/千克）时摄入高血糖碳水化合物餐；一次是在低强度运动[25%峰值耗氧量（VO2峰值）]期间，一次是在中等强度运动（68%VO2峰值）期间。在另外两次试验中，受试者在每种强度的运动过程中都保持禁食（12 - 14小时）。与禁食时相比，在进食的受试者进行55分钟低强度运动后，高血糖（升高30%）和血浆胰岛素浓度升高三倍（P < 0.05）与脂肪分解受到22%的抑制相关（5.2±0.5对6.7±1.2微摩尔·千克-1·分钟-1，P < 0.05），但此时脂肪氧化与禁食水平无差异。当受试者摄入碳水化合物时，脂肪氧化直到运动80 - 90分钟才降至禁食水平以下，此时脂肪分解超过脂肪氧化。脂肪氧化的降低在时间上与Rd Glc的增加相对应。在中等强度运动期间，当受试者进食与禁食时相比，运动第二小时血浆胰岛素浓度非常小的升高（约3微单位/毫升；P < 0.05）略微减弱了脂肪分解（P < 0.05），但没有增加Rd Glc或抑制脂肪氧化。这些发现表明，尽管运动期间摄入碳水化合物后脂肪分解受到抑制，但脂肪分解速率仍然过高，因此并未限制脂肪氧化。在这些条件下，脂肪氧化的降低在时间上与葡萄糖摄取的增加相关。
