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

Abstract

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.

Keywords

• chronic obstructive pulmonary disease;skeletal muscle dysfunction;mitochondrial damage;mitophagy;exercise rehabilitation training