Kitaoka Yu, Ogasawara Riki, Tamura Yuki, Fujita Satoshi, Hatta Hideo
a Department of Sports Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.
b Faculty of Sport and Health Science, Ritsumeikan University, Kusatsu, Shiga, Japan.
Appl Physiol Nutr Metab. 2015 Nov;40(11):1137-42. doi: 10.1139/apnm-2015-0184. Epub 2015 Jul 14.
It is well known that resistance exercise increases muscle protein synthesis and muscle strength. However, little is known about the effect of resistance exercise on mitochondrial dynamics, which is coupled with mitochondrial function. In skeletal muscle, mitochondria exist as dynamic networks that are continuously remodeling through fusion and fission. The purpose of this study was to investigate the effect of acute and chronic resistance exercise, which induces muscle hypertrophy, on the expression of proteins related to mitochondrial dynamics in rat skeletal muscle. Resistance exercise consisted of maximum isometric contraction, which was induced by percutaneous electrical stimulation of the gastrocnemius muscle. Our results revealed no change in levels of proteins that regulate mitochondrial fission (Fis1 and Drp1) or fusion (Opa1, Mfn1, and Mfn2) over the 24-h period following acute resistance exercise. Phosphorylation of Drp1 at Ser616 was increased immediately after exercise (P < 0.01). Four weeks of resistance training (3 times/week) increased Mfn1 (P < 0.01), Mfn2 (P < 0.05), and Opa1 (P < 0.01) protein levels without altering mitochondrial oxidative phosphorylation proteins. These observations suggest that resistance exercise has little effect on mitochondrial biogenesis but alters the expression of proteins involved in mitochondrial fusion and fission, which may contribute to mitochondrial quality control and improved mitochondrial function.
众所周知，抗阻运动可增加肌肉蛋白质合成和肌肉力量。然而，关于抗阻运动对线粒体动力学（与线粒体功能相关）的影响却知之甚少。在骨骼肌中，线粒体以动态网络的形式存在，通过融合和裂变不断重塑。本研究的目的是探讨急性和慢性抗阻运动（可诱导肌肉肥大）对大鼠骨骼肌中线粒体动力学相关蛋白质表达的影响。抗阻运动包括最大等长收缩，通过经皮电刺激腓肠肌诱导产生。我们的结果显示，急性抗阻运动后24小时内，调节线粒体裂变（Fis1和Drp1）或融合（Opa1、Mfn1和Mfn2）的蛋白质水平没有变化。运动后Drp1在Ser616位点的磷酸化立即增加（P < 0.01）。四周的抗阻训练（每周3次）增加了Mfn1（P < 0.01）、Mfn2（P < 0.05）和Opa1（P < 0.01）的蛋白质水平，而未改变线粒体氧化磷酸化蛋白。这些观察结果表明，抗阻运动对线粒体生物发生影响较小，但会改变参与线粒体融合和裂变的蛋白质表达，这可能有助于线粒体质量控制和改善线粒体功能。
