中文摘要：

目的：观察慢性低氧及低氧联合运动对骨骼肌线粒体自噬的影响,并探讨低氧诱导因子-1α（HIF-1α）在其中的作用。方法：56只健康雄性SD大鼠随机分为：常氧对照组（NC）、低氧对照组（HC）、低氧联合运动组（HT,n=8）、低氧＋二甲基亚砜（DMSO）组（HC＋D）、低氧＋HIF-1α抑制剂YC-1组（HC＋Y）、低氧联合运动＋DMSO组（HT＋D）和低氧联合运动＋HIF-1α抑制剂YC-1组（HT＋Y）。低氧干预为常压低氧帐篷,模拟11.3%氧浓度。运动干预为低氧帐篷内53%VO2max跑台训练,1h/d。HIF-1α抑制剂组采用YC-1腹腔注射,4mg/kg,1次/d。DMSO组注射等体积1%DMSO。上述干预均持续4周。结果：HC组与NC组比较,线粒体膜电位、ATP合成活力显著降低（P〈0.05）,活性氧族（ROS）生成速率、PINK1、Parkin、Bnip3和HIF-1α蛋白表达显著升高（P〈0.05）。HT组与HC组比较,线粒体膜电位、ATP合成活力、Parkin、Bnip3和HIF-1α表达显著升高（P〈0.05）,ROS生成速率和PINK1表达显著降低（P〈0.05）。YC-1干预HC和HT组,均造成线粒体膜电位、ATP合成活力、Bnip3和HIF-1α表达显著降低（P〈0.05）,ROS生成速率和PINK1表达显著升高（P〈0.05）。结论：低氧联合运动可通过HIF-1α途径促进了低氧诱导的Bnip3介导的线粒体自噬保护机制,从而提高骨骼肌线粒体的质量。

英文摘要：

Objective： To observe the effects of chronic hypoxia alone and hypoxia combined with exercise training on mitochondrial autophagy, and to identify the roles of hypoxia-inducible factor-1α （HIF-1α）. Method： A total 56 health male Sprague-Dawley rats were randomly divided into seven groups： normoxia control group （NC）, hypoxia control group （HC）, hypoxia combined training group （HT）, dimethyl sulfoxide（DMSO） injection and hypoxia control group （HC＋D）, inhibitor of HIF-1α YC-1 injection and hypoxia control group （HC＋Y）, DMSO injection and hypoxia training group （HT＋D）, and YC-1 injection and hypoxia training group （HT＋Y）. The hypoxia rats were subjected to hypoxia exposure in normobaric hypoxic tent. The exercise training rats were administered exercise on a motor-driven rodent treadmill in normobaric hypoxic tent. Rats in HIF-1α inhibitor YC-1 groups received peritoneal injection of the YC-1 DMSO solution at 4mg/kg body weight once a day. Rats in DMSO groups received equivolume injections of the 1% DMSO solution. All interventions were administered for continuous 4 weeks. Result： Comparing with NC group, in HC group, mitochondrial membrane potential and ATP synthesis activity showed dramatic decrease （P〈0.05）, and reactive oxygen species（ROS） generation, PINK1, Parkin, Bnip3, HIF-1α protein expression elevated significantly （P〈0.05）. Comparing with HC group in HT group, mitochondrial membrane potential, ATP synthesis activity, Parkin, Bnip3, HIF-1α protein expressions improved significantly （P〈0.05）, and ROS generation, PINK1 protein expression markedly decreased （P〈0.05）. Both in HC and HT rats, YC-1 administration significantly depressed mitochondrial membrane potential, ATP synthesis activity, Bnip3, HIF-1α protein expression （P〈0.05）, and markedly elevated ROS generation, PINK1 protein expression （P〈0.05）. Conclusion： Hypoxia combined with exercise training could significantly promote hypoxia stress induced mito