U.S. Army Research Institute of Environmental Medicine, Natick, MA, United States of America; Oak Ridge Institute of Science and Education, Oak Ridge, TN, United States of America.
U.S. Army Research Institute of Environmental Medicine, Natick, MA, United States of America.
Metabolism. 2019 Aug;97:1-8. doi: 10.1016/j.metabol.2019.05.003. Epub 2019 May 13.
Initiating aerobic exercise with low muscle glycogen content promotes greater fat and less endogenous carbohydrate oxidation during exercise. However, the extent exogenous carbohydrate oxidation increases when exercise is initiated with low muscle glycogen is unclear.
Determine the effects of muscle glycogen content at the onset of exercise on whole-body and muscle substrate metabolism.
Using a randomized, crossover design, 12 men (mean ± SD, age: 21 ± 4 y; body mass: 83 ± 11 kg; VO: 44 ± 3 mL/kg/min) completed 2 cycle ergometry glycogen depletion trials separated by 7-d, followed by a 24-h refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen stores. Participants then performed 80 min of steady-state cycle ergometry (64 ± 3% VO) while consuming a carbohydrate drink (95 g glucose +51 g fructose; 1.8 g/min). Substrate oxidation (g/min) was determined by indirect calorimetry and C. Muscle glycogen (mmol/kg dry weight), pyruvate dehydrogenase (PDH) activity, and gene expression were assessed in muscle.
Initiating steady-state exercise with LOW (217 ± 103) or AD (396 ± 70; P < 0.05) muscle glycogen did not alter exogenous carbohydrate oxidation (LOW: 0.84 ± 0.14, AD: 0.87 ± 0.16; P > 0.05) during exercise. Endogenous carbohydrate oxidation was lower and fat oxidation was higher in LOW (0.75 ± 0.29 and 0.55 ± 0.10) than AD (1.17 ± 0.29 and 0.38 ± 0.13; all P < 0.05). Before and after exercise PDH activity was lower (P < 0.05) and transcriptional regulation of fat metabolism (FAT, FABP, CPT1a, HADHA) was higher (P < 0.05) in LOW than AD.
Initiating exercise with low muscle glycogen does not impair exogenous carbohydrate oxidative capacity, rather, to compensate for lower endogenous carbohydrate oxidation acute adaptations lead to increased whole-body and skeletal muscle fat oxidation.
在低肌肉糖原含量下开始有氧运动可以促进运动中更多的脂肪和更少的内源性碳水化合物氧化。然而，当运动开始时肌肉糖原含量较低时，外源性碳水化合物氧化增加的程度尚不清楚。
确定运动开始时肌肉糖原含量对全身和肌肉底物代谢的影响。
采用随机交叉设计，12 名男性（平均±标准差，年龄：21±4 岁；体重：83±11 公斤；VO：44±3 ml/kg/min）完成了 2 次循环测力计糖原耗竭试验，间隔 7 天，然后进行 24 小时再喂养，以产生低（LOW；1.5 g/kg 碳水化合物，3.0 g/kg 脂肪）或足够（AD；6.0 g/kg 碳水化合物，1.0 g/kg 脂肪）的糖原储备。然后，参与者在稳定状态下进行 80 分钟的踏车运动（64±3%VO），同时饮用碳水化合物饮料（95 g 葡萄糖+51 g 果糖；1.8 g/min）。通过间接测热法和 C 来确定底物氧化（g/min）。肌肉糖原（mmol/kg 干重）、丙酮酸脱氢酶（PDH）活性和基因表达在肌肉中进行评估。
在 LOW（217±103）或 AD（396±70；P<0.05）肌肉糖原含量下开始稳定状态运动并没有改变运动中的外源性碳水化合物氧化（LOW：0.84±0.14，AD：0.87±0.16；P>0.05）。LOW 时内源性碳水化合物氧化较低，脂肪氧化较高（LOW：0.75±0.29 和 0.55±0.10；均 P<0.05），而 AD 时则较高（1.17±0.29 和 0.38±0.13；均 P<0.05）。运动前后，LOW 时 PDH 活性较低（P<0.05），脂肪代谢的转录调节（FAT、FABP、CPT1a、HADHA）较高（P<0.05）。
在低肌肉糖原含量下开始运动不会损害外源性碳水化合物氧化能力，相反，为了补偿内源性碳水化合物氧化的降低，急性适应会导致全身和骨骼肌脂肪氧化增加。
