Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.
Laboratory of Investigation of Chronic Diseases, Department of Physiological Sciences, Federal University of Santa Catarina, Florianópolis, Brazil.
Am J Physiol Cell Physiol. 2022 Jun 1;322(6):C1068-C1084. doi: 10.1152/ajpcell.00425.2021. Epub 2022 Apr 27.
Decreased skeletal muscle contractile activity (disuse) or unloading leads to muscle mass loss, also known as muscle atrophy. The balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB) is the primary determinant of skeletal muscle mass. A reduced mechanical load on skeletal muscle is one of the main external factors leading to muscle atrophy. However, endocrine and inflammatory factors can act synergistically in catabolic states, amplifying the atrophy process and accelerating its progression. In addition, older individuals display aging-induced anabolic resistance, which can predispose this population to more pronounced effects when exposed to periods of reduced physical activity or mechanical unloading. Different cellular mechanisms contribute to the regulation of muscle protein balance during skeletal muscle atrophy. This review summarizes the effects of muscle disuse on muscle protein balance and the molecular mechanisms involved in muscle atrophy in the absence or presence of disease. Finally, a discussion of the current literature describing efficient strategies to prevent or improve the recovery from muscle atrophy is also presented.
骨骼肌收缩活动（废用）或去负荷会导致肌肉质量损失，又称肌肉萎缩。肌肉蛋白合成（MPS）和肌肉蛋白分解（MPB）之间的平衡是骨骼肌质量的主要决定因素。骨骼肌机械负荷的降低是导致肌肉萎缩的主要外部因素之一。然而，在分解代谢状态下，内分泌和炎症因子可以协同作用，放大萎缩过程并加速其进展。此外，老年人表现出与年龄相关的合成代谢抵抗，这使他们在经历身体活动减少或机械去负荷的时期时更容易受到更明显的影响。不同的细胞机制有助于调节骨骼肌萎缩过程中的肌肉蛋白平衡。这篇综述总结了肌肉废用对肌肉蛋白平衡的影响，以及在没有或存在疾病的情况下肌肉萎缩所涉及的分子机制。最后，还讨论了目前描述有效预防或改善肌肉萎缩恢复的文献。
