运动诱导线粒体生物合成的分子机制研究

Molecular Mechanism of Exercise Training-induced Mitochondrial Biogenesis

耐力训练不但能增加线粒体数量,也能提高线粒体池或线立体网络的功能或效率。线粒体容易损害,与核DNA相比,线粒体DNA受氧化应激和年龄的影响,易于缺失。骨骼肌细胞产生新的线粒体,维持健康,清除受损的线粒体,非常重要。骨骼肌一个最重要的适应是增强代谢的能力,提高运动成绩和健康。主要的基本机制涉及线粒体网络结构的调节,通过PGC-1α调节,生成和增加新的线粒体;通过线粒体自噬,清除受损或失调的线粒体。重构线粒体网络结构是运动诱导一个重要的适应。通过这一动力性过程,生成新的、健康的线粒体,替代老的、不健康的线粒体,增强运动后骨骼肌线粒体的数量和质量。

Endurance exercise seems to not only increase the number of organelles efficiency of the mitochondrial pool/network. However, mitochondria are subject to but also improve the function damage , and the mitochondrial DNA is especially susceptible to deletions caused by oxidative stress and aging compared with nuclear DNA. There- fore, it is imperative that muscle cells have means not only to generate new mitochondria but also maintain the healthy ones and remove the damaged/dysfunctional ones. In skeletal muscle, one of the most important adaptations is enhanced metabolic capacity, which helps improve performance and health. The primary underlying mechanisms involve the regulation of the mitochondrial network. The mechanisms involved in the generation and addition of new mitochondria, which is now known to be regulated by PGC-lot. The remodeling of the mitochondrial network through elimination of damaged/dysfunctional mitochondria through mitophagy are all of importance in exercise-in- duced adaptation. This dynamic process of replacing old unhealthy mitochondria with new healthy mitochondria un- derscores enhanced quantity and quality of mitochondria in skeletal muscle after exercise training.