Department of Health, Exercise Science, and Recreation Management, Kevser Ermin Applied Physiology Laboratory, The University of Mississippi, University, MS, United States.
Department of Health, Exercise Science, and Recreation Management, Kevser Ermin Applied Physiology Laboratory, The University of Mississippi, University, MS, United States.
Med Hypotheses. 2019 Apr;125:51-56. doi: 10.1016/j.mehy.2019.02.030. Epub 2019 Feb 13.
Skeletal muscle hypertrophy commonly occurs with repeated bouts of resistance exercise as well as following the administration of exogenous drugs. This increase in muscle size is thought to be mechanistically important for the increase in muscle function. However, at present, there is no experimental evidence that would support any paradigm in which muscle hypertrophy is a mechanism for increasing strength with exercise. Therefore, it seems reasonable to also question the importance of changes in muscle size for changes in muscle strength (function) following exogenous drugs as well as aging, where both muscle size and strength decrease. The purpose of this paper is to discuss whether changes in muscle size contribute to changes in voluntary strength following exercise, pharmaceutical interventions, and aging. We also aim to provide potential mechanisms (central and peripheral) for the change in strength as well as outline study designs to better address this question. Herein, we suggest that there are dissociations between changes in muscle size and strength following exercise, anabolic drug administration, and aging (to a point). These dissociations occur throughout the literature, suggesting that these changes may be completely separate phenomena. We are not dismissing the potential importance of maintaining muscle mass, particularly in clinical populations. What we are suggesting, however, is that muscle function may not necessarily be improved by these exercise or pharmacological induced increases in muscle size. Exploring mechanisms and explanations beyond just changes in muscle size may improve therapy targeted at improving muscle function.
骨骼肌肥大通常发生在反复进行抗阻运动以及外源性药物给药之后。肌肉大小的这种增加被认为对肌肉功能的增加具有机械重要性。然而，目前没有实验证据支持任何一种观点，即肌肉肥大是通过运动增加力量的机制。因此，质疑外源性药物以及衰老（肌肉大小和力量均下降）对肌肉力量（功能）变化中肌肉大小变化的重要性似乎也是合理的。本文旨在讨论运动、药物干预和衰老后肌肉大小的变化是否有助于自愿力量的变化。我们还旨在提供力量变化的潜在机制（中枢和外周），并概述研究设计以更好地解决这个问题。在这里，我们建议在运动、合成代谢药物给药和衰老后（在一定程度上），肌肉大小和力量的变化之间存在分离。这些分离现象在整个文献中都有出现，表明这些变化可能是完全独立的现象。我们并不是要否定维持肌肉质量的潜在重要性，特别是在临床人群中。然而，我们所建议的是，肌肉功能不一定会通过这些运动或药物诱导的肌肉大小增加而得到改善。探索除肌肉大小变化之外的机制和解释，可能会改善针对改善肌肉功能的治疗方法。
