Zderic Theodore W, Schenk Simon, Davidson Christopher J, Byerley Lauri O, Coyle Edward F
Dept. of Kinesiology and Health Education, Bellmont Hall 222, The University of Texas at Austin, Austin, TX 78712, USA.
Am J Physiol Endocrinol Metab. 2004 Dec;287(6):E1195-201. doi: 10.1152/ajpendo.00302.2004. Epub 2004 Aug 17.
We have recently reported that, during moderate intensity exercise, low muscle glycogen concentration and utilization caused by a high-fat diet is associated with a marked increase in fat oxidation with no effect on plasma glucose uptake (R(d) glucose). It is our hypothesis that this increase in fat oxidation compensates for low muscle glycogen, thus preventing an increase in R(d) glucose. Therefore, the purpose of this study was to determine whether low muscle glycogen availability increases R(d) glucose under conditions of impaired fat oxidation. Six cyclists exercised at 50% peak O(2) consumption (Vo(2 peak)) for 1 h after 2 days on either a high-fat (HF, 60% fat, 24% carbohydrate) or control (CON, 22% fat, 65% carbohydrate) diet to manipulate muscle glycogen to low and normal levels, respectively. Two hours before the start of exercise, subjects ingested 80 mg of propanolol (betaB), a nonselective beta-adrenergic receptor blocker, to impair fat oxidation during exercise. HF significantly decreased calculated muscle glycogen oxidation (P < 0.05), and this decrease was partly compensated for by an increase in fat oxidation (P < 0.05), accompanied by an increase in whole body lipolysis (P < 0.05), despite the presence of betaB. Although HF increased fat oxidation, plasma glucose appearance rate, R(d) glucose, and glucose clearance rate were also significantly increased by 13, 15, and 26%, respectively (all P < 0.05). In conclusion, when lipolysis and fat oxidation are impaired, in this case by betaB, fat oxidation cannot completely compensate for a reduction in muscle glycogen utilization, and consequently plasma glucose turnover increases. These findings suggest that there is a hierarchy of substrate compensation for reduced muscle glycogen availability after a high-fat, low-carbohydrate diet, with fat being the primary and plasma glucose the secondary compensatory substrate. This apparent hierarchy likely serves to protect against hypoglycemia when endogenous glucose availability is low.
我们最近报道，在中等强度运动期间，高脂饮食导致的低肌肉糖原浓度和利用率与脂肪氧化显著增加相关，而对血浆葡萄糖摄取（R(d)葡萄糖）无影响。我们的假设是，这种脂肪氧化的增加补偿了低肌肉糖原，从而防止R(d)葡萄糖增加。因此，本研究的目的是确定在脂肪氧化受损的情况下，低肌肉糖原可用性是否会增加R(d)葡萄糖。六名自行车运动员在高脂（HF，60%脂肪，24%碳水化合物）或对照（CON，22%脂肪，65%碳水化合物）饮食2天后，以50%峰值耗氧量（Vo(2 peak)）运动1小时，分别将肌肉糖原控制在低水平和正常水平。在运动开始前两小时，受试者摄入80毫克普萘洛尔（βB），一种非选择性β-肾上腺素能受体阻滞剂，以损害运动期间的脂肪氧化。HF显著降低了计算得出的肌肉糖原氧化（P < 0.05），尽管存在βB，但这种降低部分被脂肪氧化增加（P < 0.05）所补偿，同时全身脂肪分解增加（P < 0.05）。尽管HF增加了脂肪氧化，但血浆葡萄糖出现率、R(d)葡萄糖和葡萄糖清除率也分别显著增加了13%、15%和26%（均P < 0.05）。总之，当脂肪分解和脂肪氧化受损时，在这种情况下由βB引起，脂肪氧化不能完全补偿肌肉糖原利用率的降低，因此血浆葡萄糖周转率增加。这些发现表明，在高脂低碳水化合物饮食后，对于降低的肌肉糖原可用性存在底物补偿层次，脂肪是主要的补偿底物，血浆葡萄糖是次要的补偿底物。当内源性葡萄糖可用性较低时，这种明显的层次结构可能有助于预防低血糖。
