Graduate School of Sports and Health Science, Ritsumeikan University, Kusatsu, Shiga, Japan.
Research Fellow of Japan Society for the Promotion of Science, Chiyodaku, Japan.
Physiol Rep. 2020 Jul;8(13):e14457. doi: 10.14814/phy2.14457.
Endurance exercise in hypoxia promotes carbohydrate (CHO) metabolism. However, detailed CHO metabolism remains unclear. The purpose of this study was to evaluate the effects of endurance exercise in moderate hypoxia on exogenous glucose oxidation at the same energy expenditure or relative exercise intensity.
Nine active healthy males completed three trials on different days, consisting of 30 min of running at each exercise intensity: (a) exercise at 65% of normoxic maximal oxygen uptake in normoxia [NOR, fraction of inspired oxygen (F O ) = 20.9%, 10.6 ± 0.3 km/h], (b) exercise at the same relative exercise intensity with NOR in hypoxia (HYPR, F O = 14.5%, 9.4 ± 0.3 km/h), and (c) exercise at the same absolute exercise intensity with NOR in hypoxia (HYPA, F O = 14.5%, 10.6 ± 0.3 km/h). The subjects consumed C-labeled glucose immediately before exercise, and expired gas samples were collected during exercise to determine C-excretion (calculated by CO / CO ).
The exercise-induced increase in blood lactate was significantly augmented in the HYPA than in the NOR and HYPR (p = .001). HYPA involved a significantly higher respiratory exchange ratio (RER) during exercise compared with the other two trials (p < .0001). In contrast, exogenous glucose oxidation ( C-excretion) during exercise was significantly lower in the HYPA than in the NOR (p = .03). No significant differences were observed in blood lactate elevation, RER, or exogenous glucose oxidation between NOR and HYPR.
Endurance exercise in moderate hypoxia caused a greater exercise-induced blood lactate elevation and RER compared with the running exercise at same absolute exercise intensity in normoxia. However, exogenous glucose oxidation ( C-excretion) during exercise was attenuated compared with the same exercise in normoxia.
低氧耐力运动促进碳水化合物（CHO）代谢。然而，详细的 CHO 代谢仍不清楚。本研究的目的是评估在相同能量消耗或相对运动强度下，中度低氧耐力运动对外源性葡萄糖氧化的影响。
9 名活跃的健康男性在不同的日子里完成了三项试验，包括在每个运动强度下进行 30 分钟的跑步：（a）在常氧下以 65%的最大摄氧量进行运动[NOR，吸入氧气分数（F O ）= 20.9%，10.6±0.3km/h]，（b）在相同的相对运动强度下在低氧中进行运动（HYPR，F O = 14.5%，9.4±0.3km/h），和（c）在相同的绝对运动强度下在低氧中进行运动（HYPA，F O = 14.5%，10.6±0.3km/h）。受试者在运动前立即消耗 C 标记的葡萄糖，并且在运动期间收集呼出气体样本以确定 C 排泄量（通过 CO / CO 计算）。
与 NOR 和 HYPR 相比，HYPA 中的运动诱导的血乳酸升高显著增加（p = 0.001）。与其他两个试验相比，HYPA 在运动期间的呼吸交换率（RER）显著更高（p<0.0001）。相比之下，与 NOR 相比，HYPA 中的运动期间外源性葡萄糖氧化（C 排泄）明显较低（p=0.03）。NOR 和 HYPR 之间在外源性葡萄糖氧化升高、RER 或血乳酸升高方面没有观察到显著差异。
与在常氧下进行相同绝对运动强度的跑步运动相比，中度低氧耐力运动引起更大的运动诱导的血乳酸升高和 RER。然而，与在常氧下进行相同运动相比，运动期间的外源性葡萄糖氧化（C 排泄）减弱。
