目的：探讨低氧复合运动对线粒体含量的影响及线粒体生物合成和自噬在其中的作用。方法：雄性SD大鼠随机分为常氧对照（ NC）组、常氧运动（ NT）组、低氧对照（ HC）组和低氧复合运动（ HT）组。低氧干预为常压低氧帐篷，11．3％氧浓度持续暴露4周。运动干预为跑台训练（5°，15 m/min），60 min/d，每周5 d，共4周。JC-1荧光探针检测线粒体膜电位；萤光素酶法检测线粒体ATP合成能力；Western blotting 检测骨骼肌过氧化物酶体增殖物激活受体γ辅激活因子1（PGC-1α）、线粒体转录因子A（Tfam）、Bcl-2/腺病毒E1B 19kD相互作用蛋白3（Bnip3）、苄氯素1（beclin-1）、细胞色素C氧化酶亚基IV（COXIV）和电压依赖性阴离子通道1（VDAC-1）蛋白表达量。结果：HC组与NC组比较，线粒体膜电位、ATP合成能力及COXIV、VDAC-1、PGC-1α和Tfam蛋白表达显著降低（P＜0.05或P＜0.01），Bnip3和beclin-1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合成能力及COXIV、VDAC-1、PGC-1α、Tfam、Bnip3和beclin-1蛋白表达均显著升高（ P＜0.05或P＜0.01）。结论：慢性低氧暴露提高了线粒体自噬但抑制了线粒体生物合成，导致线粒体含量减少。低氧复合运动促进低氧状态下骨骼肌线粒体自噬，并促进线粒体生物合成，从而提高线粒体含量及功能。%[ABSTRACT]AIM:Toinvestigatetheeffectofhypoxiacombinedwithexercisetrainingonmitochondrialcon-tent, and the role of mitochondrial biogenesis and mitophagy in this process .METHODS:Male Sprague-Dawley rats were randomly divided into 4 groups:normoxia control (NC) group, normoxia+training (NT) group, hypoxia+control (HC) group, and hypoxia+training (HT) group.The hypoxic animals were housed in normobaric hypoxic tent (11.3 % oxy-gen) for consecutive 4 weeks.The exercise training animals were exercised on a motor-driven rodent treadmill (5°) at a speed of 15 m/min, 60 min/d, 5 d/week for 4 weeks.Mitochondrial membrane potential was determined using JC-1 fluo-rescent probe .ATP synthesis capacity was determined using a bioluminescence technique .The protein expression of cyto-chrome C oxidase IV (COXIV), voltage-dependent anion channel-1 (VDAC-1), peroxisome proliferator-activated receptor gamma cofactor 1 alpha (PGC-1α), mitochondrial transcription factor A (Tfam),Bcl-2/adenovirus E1B 19 kD-interacting protein 3 (Bnip3) and beclin-1 in the muscles was detected by Western blotting .RESULTS:Compared with NC group, hypoxia attenuated mitochondrial membrane potential , ATP synthesis capacity , and the expression of COXIV , VDAC-1, PGC-1αand Tfam.Furthermore, hypoxia increased the expression of Bnip 3 and beclin-1.Compared with HC group , the exercise training elevated mitochondrial membrane potential , ATP synthesis capacity , and the expression of COXIV , VDAC-1, PGC-1α, Tfam, Bnip3 and beclin-1.CONCLUSION:A combination of reduced mitochondrial biogenesis and increased mitophagy seems to be responsible for the decrease in mitochondrial content after hypoxia .Exercise training with hypoxia elevates mitochondrial content and function in hypoxia , which may be mediated by appropriate increase and co-reg-ulation of mitochondrial biogenesis and mitophagy .
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