Groennebaek Thomas, Vissing Kristian
Section for Sport Science, Department of Public Health, Aarhus UniversityAarhus, Denmark.
Front Physiol. 2017 Sep 15;8:713. doi: 10.3389/fphys.2017.00713. eCollection 2017.
Skeletal muscle metabolic and contractile properties are reliant on muscle mitochondrial and myofibrillar protein turnover. The turnover of these specific protein pools is compromised during disease, aging, and inactivity. Oppositely, exercise can accentuate muscle protein turnover, thereby counteracting decay in muscle function. According to a traditional consensus, endurance exercise is required to drive mitochondrial adaptations, while resistance exercise is required to drive myofibrillar adaptations. However, concurrent practice of traditional endurance exercise and resistance exercise regimens to achieve both types of muscle adaptations is time-consuming, motivationally demanding, and contended to entail practice at intensity levels, that may not comply with clinical settings. It is therefore of principle interest to identify effective, yet feasible, exercise strategies that may positively affect both mitochondrial and myofibrillar protein turnover. Recently, reports indicate that traditional high-load resistance exercise can stimulate muscle mitochondrial biogenesis and mitochondrial respiratory function. Moreover, fatiguing low-load resistance exercise has been shown capable of promoting muscle hypertrophy and expectedly entails greater metabolic stress to potentially enhance mitochondrial adaptations. Consequently, fatiguing low-load resistance exercise regimens may possess the ability to stimulate muscle mitochondrial adaptations without compromising muscle myofibrillar accretion. However, the exact ability of resistance exercise to drive mitochondrial adaptations is debatable, not least due to some methodological challenges. The current review therefore aims to address the evidence on the effects of resistance exercise on skeletal muscle mitochondrial biogenesis, content and function. In prolongation, a perspective is taken on the specific potential of low-load resistance exercise on promoting mitochondrial adaptations.
骨骼肌的代谢和收缩特性依赖于肌肉线粒体和肌原纤维蛋白的更新。在疾病、衰老和缺乏运动的情况下，这些特定蛋白池的更新会受到损害。相反，运动可以增强肌肉蛋白更新，从而抵消肌肉功能的衰退。根据传统的共识，需要耐力运动来驱动线粒体适应性变化，而需要抗阻运动来驱动肌原纤维适应性变化。然而，同时进行传统的耐力运动和抗阻运动方案以实现两种类型的肌肉适应性变化既耗时，对动机要求也高，并且有人认为在强度水平上的训练可能不符合临床环境。因此，确定可能对线粒体和肌原纤维蛋白更新产生积极影响的有效且可行的运动策略具有重要的理论意义。最近，有报告表明传统的高负荷抗阻运动可以刺激肌肉线粒体生物合成和线粒体呼吸功能。此外，疲劳性低负荷抗阻运动已被证明能够促进肌肉肥大，并且预计会带来更大的代谢压力，从而可能增强线粒体适应性变化。因此，疲劳性低负荷抗阻运动方案可能具有刺激肌肉线粒体适应性变化而不影响肌肉肌原纤维增生的能力。然而，抗阻运动驱动线粒体适应性变化的确切能力存在争议，尤其是由于一些方法学上的挑战。因此，本综述旨在阐述抗阻运动对骨骼肌线粒体生物合成、含量和功能影响的相关证据。此外，还探讨了低负荷抗阻运动在促进线粒体适应性变化方面的具体潜力。
