Keramidas Michail E, Mekjavic Igor B, Eiken Ola
Department of Environmental Physiology, Swedish Aerospace Physiology Center, School of Technology and Health, Royal Institute of Technology, Stockholm, Sweden.
Department of Automation, Biocybernetics and Robotics, Jozef Stefan Institute, Ljubljana, Slovenia.
Exp Physiol. 2017 Jun 1;102(6):694-710. doi: 10.1113/EP086167.
What is the central question of this study? What are the distinct and interactive effects of a 10 day exposure to hypoxia and horizontal bedrest on the whole-body peak oxygen uptake and on the regional cerebral and skeletal muscle tissue oxygenation during upright cycle ergometry in male lowlanders? What is the main finding and its importance? A 10 day sustained exposure to hypoxia aggravates the bedrest-induced reduction in peak oxygen uptake during dynamic exercise engaging large muscle groups, but mitigates the skeletal muscle oxidative capacity impairment elicited by bedrest. The study examined the interactive effects of a 10 day exposure to hypoxia and bedrest on the whole-body peak oxygen uptake (V̇O2 peak ) during maximal exercise and on skeletal muscle and cerebral oxygenation during submaximal exercise. Nine males underwent three 10 day confinements, in a Latin-square order, as follows: (i) a normoxic bedrest [NBR; partial pressure of inspired O (PI,O2) = 134.2 ± 0.7 mmHg]; (ii) a hypoxic bedrest (HBR; PI,O2 = 102.9 ± 0.1 mmHg at day 1, 91.5 ± 1.2 mmHg at days 3-10); and (iii) a hypoxic ambulation (HAMB; PI,O2 as in HBR). Before, 1 (R+1) and 3 days (R+3) after each confinement, subjects performed exhaustive, incremental-load and moderate-intensity constant-load (CLTs) cycle-ergometry trials, while breathing either room air or a hypoxic gas mixture. During the CLTs, changes in the regional oxygenation of the cerebral frontal cortex and the vastus lateralis and intercostal muscles were monitored with near-infrared spectroscopy. At R+1, the confinement-related impairment in V̇O2 peak was greater after HBR than after NBR or HAMB, regardless of whether the trial was performed in room air or hypoxia (HBR, -16.2%; NBR, -8.3%; HAMB, -4.1%; P = 0.001). During the CLTs, bedrest aggravated the exercise-induced reduction in locomotor and respiratory muscle oxygenation (P ≤ 0.05); an effect that was less after HBR than after NBR (P ≤ 0.05). The hypoxic exercise-induced cerebral vasodilatory response was blunted by HBR, probably because of the marked hyperventilation-dependent hypocapnia, attendant to the sustained hypoxic stimulus. Hence, short-term exposure to hypoxia potentiates the reduction in V̇O2 peak , but it mitigates the impairment in skeletal muscle oxidative capacity induced by bedrest.
本研究的核心问题是什么？对于男性低地人，10天的低氧暴露与水平卧床休息对全身峰值摄氧量以及在直立周期运动测试期间局部脑和骨骼肌组织氧合的独特及交互作用是什么？主要发现及其重要性是什么？持续10天暴露于低氧环境会加剧卧床休息引起的涉及大肌肉群的动态运动中峰值摄氧量的降低，但会减轻卧床休息引起的骨骼肌氧化能力损害。该研究考察了10天的低氧暴露与卧床休息对最大运动时的全身峰值摄氧量（V̇O2峰值）以及次最大运动时骨骼肌和脑氧合的交互作用。9名男性按照拉丁方顺序进行了3次为期10天的限制活动，具体如下：（i）常氧卧床休息[NBR；吸入氧分压（PI,O2）=134.2±0.7mmHg]；（ii）低氧卧床休息（HBR；第1天PI,O2=102.9±0.1mmHg，第3 - 10天为91.5±1.2mmHg）；以及（iii）低氧行走（HAMB；PI,O2与HBR相同）。在每次限制活动前、活动后1天（R + 1）和3天（R + 3），受试者进行力竭性、递增负荷和中等强度恒定负荷（CLTs）的周期运动测试，同时呼吸室内空气或低氧混合气体。在CLTs期间，使用近红外光谱监测大脑额叶皮质、股外侧肌和肋间肌的局部氧合变化。在R + 1时，无论测试是在室内空气还是低氧环境下进行，HBR后V̇O2峰值的限制活动相关损害均大于NBR或HAMB后（HBR，-16.2%；NBR，-8.3%；HAMB，-4.1%；P = 0.001）。在CLTs期间，卧床休息加剧了运动引起的运动和呼吸肌氧合降低（P≤0.05）；HBR后的这种效应小于NBR后（P≤0.05）。低氧运动引起的脑血管舒张反应在HBR后减弱，可能是由于持续低氧刺激伴随的明显的过度通气依赖性低碳酸血症。因此，短期暴露于低氧环境会增强V̇O2峰值的降低，但会减轻卧床休息引起的骨骼肌氧化能力损害。
