运动康复训练调节线粒体损伤对慢性阻塞性肺疾病骨骼肌功能障碍的影响

Effect of Exercise Rehabilitation Training Regulating Mitochondrial Damage on Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease

慢性阻塞性肺疾病(COPD)是一种异质性的慢性呼吸系统疾病,骨骼肌功能障碍作为COPD常见的并发症之一,主要临床表现为肌力和肌耐力下降、肌纤维类型改变、骨骼肌质量降低。线粒体损伤是引起骨骼肌功能障碍的关键因素之一。线粒体不仅为骨骼肌提供能量,同时也参与活性氧(ROS)产生、自噬和蛋白质周转,对维持骨骼肌正常功能具有重要意义。本研究阐述COPD骨骼肌功能障碍的线粒体改变、COPD骨骼肌功能障碍的线粒体损伤作用机制以及运动康复训练对COPD骨骼肌线粒体损伤的潜在影响,旨在进一步明确线粒体和骨骼肌功能间的关系,为优化COPD骨骼肌功能障碍的运动康复方案提供参考。其中,COPD骨骼肌功能障碍的线粒体改变主要包括线粒体呼吸链受损、线粒体自噬激增和线粒体生物发生减少3个方面;COPD骨骼肌功能障碍的线粒体损伤作用机制主要包括增加骨骼肌降解、减少骨骼肌生成和干扰骨骼肌分化;运动康复训练对COPD骨骼肌线粒体损伤的潜在影响主要包括运动康复训练可修复COPD患者骨骼肌线粒体呼吸链、调控COPD患者骨骼肌线粒体自噬和促进COPD骨骼肌线粒体生物发生。下一步研究仍需探讨线粒体对维持骨骼肌正常功能结构的关键作用、COPD骨骼肌功能障碍的发生原理以及运动康复训练调节线粒体损伤改善COPD骨骼肌功能障碍的具体作用机制,以期为运动康复训练干预COPD骨骼肌功能障碍提供参考依据。

Chronic obstructive pulmonary disease(COPD)is a heterogeneous chronic respiratory condition,and skeletal muscle dysfunction is one of its common complications,mainly clinically manifested as decreased muscle strength and endurance,altered muscle fiber type and decreased skeletal muscle mass.Mitochondrial damage is one of the key factors causing skeletal muscle dysfunction.Mitochondria not only provide energy for skeletal muscle,but also participate in reactive oxygen species(ROS)production,autophagy and protein turnover,which is of great significance to maintain the normal function of skeletal muscle.This study elucidated the mitochondrial changes in skeletal muscle dysfunction in patients with COPD,the mechanism of mitochondrial damage in skeletal muscle dysfunction in patients with COPD,and the potential effects of exercise rehabilitation training on mitochondrial damage in skeletal muscle in patients with COPD,in order to further clarify the relationship between mitochondria and skeletal muscle function,and to provide a reference for optimizing the exercise rehabilitation program for skeletal muscle dysfunction in COPD.The mitochondrial changes of skeletal muscle dysfunction in COPD mainly include impairment of the mitochondrial respiratory chain,a surge in mitochondrial autophagy,and a decreased in mitochondrial biogenesis.The mechanisms underlying mitochondrial damage of skeletal muscle dysfunction in COPD mainly include increasing skeletal muscle degradation,decreasing of skeletal muscle production and interfering with skeletal muscle differentiation.The potential effects of exercise rehabilitation training regulating mitochondrial damage in COPD skeletal muscle mainly include repairing the respiratory chain of skeletal muscle mitochondria in COPD patients,regulating mitophagy of skeletal muscle mitochondria,and promote the mitochondrial biogenesis of skeletal muscle in patients with COPD.Future research still needs to explore the key role of mitochondria in maintaining the normal functional structure of skeletal muscle,the mechanism of COPD skeletal muscle dysfunction,and the specific mechanism of exercise rehabilitation training in regulating mitochondrial damage to improve COPD skeletal muscle dysfunction,so as to provide a reference for exercise rehabilitation training in COPD skeletal muscle dysfunction.