Bersiner Käthe, Park So-Young, Schaaf Kirill, Yang Woo-Hwi, Theis Christian, Jacko Daniel, Gehlert Sebastian
Department for Biosciences of Sports, Institute of Sports Science, University of Hildesheim, Hildesheim, Germany.
Graduate School of Sports Medicine, CHA University, Pocheon, Republic of Korea.
Phys Act Nutr. 2023 Jun;27(2):78-95. doi: 10.20463/pan.2023.0021. Epub 2023 Jun 30.
Skeletal muscle regulates health and performance by maintaining or increasing strength and muscle mass. Although the molecular mechanisms in response to resistance exercise (RE) significantly target the activation of protein synthesis, a plethora of other mechanisms and structures must be involved in orchestrating the communication, repair, and restoration of homeostasis after RE stimulation. In practice, RE can be modulated by variations in intensity, continuity and volume, which affect molecular responses and skeletal muscle adaptation. Knowledge of these aspects is important with respect to planning of training programs and assessing the impact of RE training on skeletal muscle.
In this narrative review, we introduce general aspects of skeletal muscle substructures that adapt in response to RE. We further highlighted the molecular mechanisms that control human skeletal muscle anabolism, degradation, repair and memory in response to acute and repeated RE and linked these aspects to major training variables.
Although RE is a key stimulus for the activation of skeletal muscle anabolism, it also induces myofibrillar damage. Nevertheless, to increase muscle mass accompanied by a corresponding adaptation of the essential substructures of the sarcomeric environment, RE must be continuously repeated. This requires the permanent engagement of molecular mechanisms that re-establish skeletal muscle integrity after each RE-induced muscle damage.
Various molecular regulators coordinately control the adaptation of skeletal muscle after acute and repeated RE and expand their actions far beyond muscle growth. Variations of key resistance training variables likely affect these mechanisms without affecting muscle growth.
骨骼肌通过维持或增加力量和肌肉质量来调节健康和运动表现。尽管抗阻运动(RE)后的分子机制主要靶向蛋白质合成的激活,但在RE刺激后,众多其他机制和结构必定参与协调通信、修复和内环境稳态的恢复。实际上,RE可通过强度、连续性和运动量的变化进行调节,这些变化会影响分子反应和骨骼肌适应性。了解这些方面对于训练计划的制定以及评估RE训练对骨骼肌的影响至关重要。
在本篇叙述性综述中,我们介绍了骨骼肌亚结构在响应RE时发生适应性变化的一般情况。我们进一步强调了在急性和重复RE刺激下控制人类骨骼肌合成代谢、降解、修复和记忆的分子机制,并将这些方面与主要训练变量联系起来。
尽管RE是激活骨骼肌合成代谢的关键刺激因素,但它也会导致肌原纤维损伤。然而,为了增加肌肉质量并伴随肌节环境基本亚结构的相应适应性变化,必须持续重复进行RE。这需要在每次RE诱导的肌肉损伤后重新建立骨骼肌完整性的分子机制持续发挥作用。
各种分子调节因子协同控制急性和重复RE后骨骼肌的适应性变化,其作用远远超出肌肉生长的范畴。关键抗阻训练变量的变化可能会影响这些机制,但不影响肌肉生长。