Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada ; Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.
PLoS One. 2013 Dec 6;8(12):e81879. doi: 10.1371/journal.pone.0081879. eCollection 2013.
Mitochondrial oxidative stress is a complex phenomenon that is inherently tied to energy provision and is implicated in many metabolic disorders. Exercise training increases mitochondrial oxidative capacity in skeletal muscle yet it remains unclear if oxidative stress plays a role in regulating these adaptations. We demonstrate that the chronic elevation in mitochondrial oxidative stress present in Sod2 (+/-) mice impairs the functional and biochemical mitochondrial adaptations to exercise. Following exercise training Sod2 (+/-) mice fail to increase maximal work capacity, mitochondrial enzyme activity and mtDNA copy number, despite a normal augmentation of mitochondrial proteins. Additionally, exercised Sod2 (+/-) mice cannot compensate for their higher amount of basal mitochondrial oxidative damage and exhibit poor electron transport chain complex assembly that accounts for their compromised adaptation. Overall, these results demonstrate that chronic skeletal muscle mitochondrial oxidative stress does not impact exercise induced mitochondrial biogenesis, but impairs the resulting mitochondrial protein function and can limit metabolic plasticity.
线粒体氧化应激是一种复杂的现象，与能量供应密切相关，并与许多代谢紊乱有关。运动训练可以增加骨骼肌中线粒体的氧化能力，但目前尚不清楚氧化应激是否在调节这些适应中发挥作用。我们的研究表明，Sod2（ +/-）小鼠中线粒体氧化应激的慢性升高会损害运动引起的线粒体功能和生化适应。运动训练后，Sod2（ +/-）小鼠的最大工作能力、线粒体酶活性和 mtDNA 拷贝数均不能增加，尽管线粒体蛋白正常增加。此外，运动后的 Sod2（ +/-）小鼠不能补偿其更高的基础线粒体氧化损伤，表现出较差的电子传递链复合物组装，这是其适应能力受损的原因。总的来说，这些结果表明，慢性骨骼肌线粒体氧化应激不会影响运动引起的线粒体生物发生，但会损害线粒体蛋白的功能，并可能限制代谢的可塑性。
