Cardiovascular Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
PLoS One. 2012;7(7):e41817. doi: 10.1371/journal.pone.0041817. Epub 2012 Jul 24.
Exercise confers numerous health benefits, many of which are thought to stem from exercise-induced mitochondrial biogenesis (EIMB) in skeletal muscle. The transcriptional coactivator PGC-1α, a potent regulator of metabolism in numerous tissues, is widely believed to be required for EIMB. We show here that this is not the case. Mice engineered to lack PGC-1α specifically in skeletal muscle (Myo-PGC-1αKO mice) retained intact EIMB. The exercise capacity of these mice was comparable to littermate controls. Induction of metabolic genes after 2 weeks of in-cage voluntary wheel running was intact. Electron microscopy revealed no gross abnormalities in mitochondria, and the mitochondrial biogenic response to endurance exercise was as robust in Myo-PGC-1αKO mice as in wildtype mice. The induction of enzymatic activity of the electron transport chain by exercise was likewise unperturbed in Myo-PGC-1αKO mice. These data demonstrate that PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle, in sharp contrast to the prevalent assumption in the field.
锻炼能带来诸多健康益处，其中许多益处被认为源于骨骼肌中的运动诱导的线粒体生物发生（EIMB）。过氧化物酶体增殖物激活受体γ 共激活因子 1α（PGC-1α）是许多组织中代谢的有力调节剂，被广泛认为是 EIMB 所必需的。我们在此表明事实并非如此。专门在骨骼肌中缺乏 PGC-1α 的基因工程小鼠（Myo-PGC-1αKO 小鼠）保留了完整的 EIMB。这些小鼠的运动能力与同窝对照相当。在笼内自愿轮跑 2 周后，代谢基因的诱导是完整的。电子显微镜检查显示线粒体没有明显异常，Myo-PGC-1αKO 小鼠和野生型小鼠的耐力运动引起的线粒体生物发生反应一样强烈。运动引起的电子传递链酶活性的诱导在 Myo-PGC-1αKO 小鼠中也未受到干扰。这些数据表明，PGC-1α 对于骨骼肌中的运动诱导的线粒体生物发生是可有可无的，这与该领域的普遍假设形成鲜明对比。
