Ziaaldini Mohammad Mosaferi, Marzetti Emanuele, Picca Anna, Murlasits Zsolt
Sport Physiology Department, Ferdowsi University of Mashhad, Mashhad, Iran.
Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart, Rome, Italy.
Front Med (Lausanne). 2017 Oct 4;4:167. doi: 10.3389/fmed.2017.00167. eCollection 2017.
Aging is a complex process characterized by progressive multisystem derangement predisposing individuals to increased risk of developing negative health outcomes. Sarcopenia is the age-related decline of muscle mass and function/strength and represents a highly prevalent correlate of aging. Several factors have been indicated to play a role in the onset and progression of sarcopenia; however, its pathophysiology is still unclear. Physical exercise is to date one of the few strategies able to improve muscle health in old age through multiple metabolic and transcriptional adaptations. Although the benefits of different exercise modalities on the function and structure of aged myocytes is acknowledged, the cellular and molecular mechanisms underlying such effects are not yet fully identified. Here, we briefly overview the current knowledge on the biochemical pathways associated with the onset and progression of sarcopenia. We subsequently describe the effects of exercise on relevant signaling pathways involved in sarcopenia pathophysiology.
衰老过程复杂,其特征是多系统渐进性紊乱,使个体出现负面健康结果的风险增加。肌肉减少症是与年龄相关的肌肉质量和功能/力量下降,是衰老的一个高度普遍的相关因素。已有多种因素被指出在肌肉减少症的发生和发展中起作用;然而,其病理生理学仍不清楚。体育锻炼是迄今为止少数能够通过多种代谢和转录适应来改善老年人肌肉健康的策略之一。尽管不同运动方式对老年心肌细胞功能和结构的益处已得到认可,但其潜在的细胞和分子机制尚未完全明确。在此,我们简要概述目前关于与肌肉减少症发生和发展相关的生化途径的知识。随后,我们将描述运动对肌肉减少症病理生理学中相关信号通路的影响。