耐力训练抑制急性低氧时骨骼肌线粒体生物能学变化:ROS和UCP3的作用(英文)

骨骼肌线粒体解耦联蛋白3（uncoupling protein3，UCP3）在低氧时的生理作用尚不清楚。本研究观察了大鼠在耐力训练前后，模拟急性高原低氧各时间点的骨骼肌线粒体UCP3 mRNA和蛋白表达、线粒体呼吸功能、活性氧（reactive oxygen species，ROS）产生速率以及锰超氧化物歧化酶（manganese superoxide dismutase，MnSOD）表达和活性的变化。急性低氧导致线粒体一系列生物能学功能障碍。未训练大鼠UCP3蛋白在4h时比静息时升高了60％，而MnSOD蛋白含量及活性在低氧暴露过程中无显著变化；UCP3蛋白上调通过降低电子传递链耦联程度抑制O2-产生，但同时降低了ATP合成效率。耐力训练显著抑制急性低氧诱导的骨骼肌UCP3蛋白上调（67％；S42％）。训练组大鼠的ROS产生速率在低氧2h、4h和6h时显著低于未训练组；MnSOD蛋白含量及活性分别较术训练组提高了50％和34％。训练组人鼠MnSOD上调可增加线粒体对ROS的耐受力，进而抑制UCP3蛋白表达，从而提高氧化磷酸化效率。急性低氧中，未训练组大鼠呼吸控制比（respiratory control ratio，RCR）和磷氧比（ADP to oxygen consumption ratio，P／O）显著降低，而训练组RCR和P／O保持相对稳定。以上结果提示：（1）模拟急性高原低氧可诱导UCP3 mRNA及蛋白表达升高，从而降低升高了的线粒体膜电位（△ψ），使ROS的产生减少；（2）耐力训练可抑制低氧诱导的UCP3表达上调，提高ROS酶学清除能力，从而提高线粒体氧化磷酸化效率。

Endurance training attenuates the bioenergetics alterations of rat skeletal muscle mitochondria submitted to acute hypoxia:Role of ROS and UCP3

The physiological significance of skeletal muscle mitochondrial uncoupling protein 3(UCP3) in hypoxia is elusive.In the current study,UCP3 mRNA and protein expressions were investigated along with mitochondrial respiratory function,reactive oxygen species(ROS) generation,as well as manganese superoxide dismutase(MnSOD) expression in rat skeletal muscle with or without endurance training after an acute and severe hypobaric hypoxia exposure for different time.Acute hypoxia induced a series of impairments in s...