低氧训练影响运动能力，但机制并不十分清楚。前期结果提示AMPKα2转基因(TG)鼠游泳至力竭的时间明显长于野生型（WT）鼠，低氧训练显著促进AMPKα2 TG鼠骨骼肌的谷胱甘肽（GSH）氧化还原平衡状态。以此为线索，核因子E2相关因子2（Nrf2）/抗氧化反应元件（ARE）通路引起我们的关注。 在前期工作和文献的基础上，本项目采用离体和在体实验，通过引进Nrf2 基因敲除（KO）鼠,并建立AMPKα2 TG 鼠与Nrf2 KO鼠的杂交鼠，而后利用WT、AMPKα2 TG、AMPKα2 KO、Nrf2 KO鼠和AMPKα2 TG/Nrf2 KO杂交鼠，探讨①低氧训练对Nrf2/ARE介导的抗氧化通路影响；②低氧训练中AMPKα2对Nrf2/ARE通路调控作用；③AMPKα2调控Nrf2/ARE通路对低氧训练后运动能力影响，揭示AMPKα2调控Nrf2/ARE通路对骨骼肌的保护作用及机制。

o Hypoxic training affacts movement ability,but the mechanism is not clear.Early results showed that the AMPKα2 transgenic(TG) mice had longer swimming time than wild type(WT) mice , hypoxic training improved the glutathione(GSH) redox state in skeletal muscles of AMPKα2 TG mice. On the basis of prophase work and references, the hypothesis of hypoxic training inducing AMPKα2 to regulate Nrf2/ARE signaling pathway for protection of skeletal muscles were investigated .Experiments in vitro and in vivo by WT,AMPKα2 TG,AMPKα2 KO,Nrf2 KO mice and AMPKα2 TG/Nrf2 KO hybrid mice were used in the project. And then, the molecular mechanisms about effects of hypoxic training on Nrf2/ARE signaling pathway , hypoxic training inducing AMPKα2 to regulate Nrf2/ARE pathway and the effect of the AMPKα2 regulating Nrf2/ARE pathway on the movement ability were studied.