Skeletal muscle dysfunction (SMD) is a prevalent extrapulmonary complication and a significant independent prognostic factor in patients with chronic obstructive pulmonary disease (COPD). Mitochondrial dysfunction is one of the core factors that damage structure and function in COPD skeletal muscle and is closely related to smoke exposure, hypoxia, and insufficient physical activity. The currently known phenotypes of mitochondrial dysfunction are reduced mitochondrial content and biogenesis, impaired activity of mitochondrial respiratory chain complexes, and increased mitochondrial reactive oxygen species production. Significant progress has been made in research on physical therapy (PT), which has broad prospects for treating the abovementioned potential mitochondrial-function changes in COPD skeletal muscle. In terms of specific types of PT, exercise therapy can directly act on mitochondria and improve COPD SMD by increasing mitochondrial density, regulating mitochondrial biogenesis, upregulating mitochondrial respiratory function, and reducing oxidative stress. However, improvements in mitochondrial-dysfunction phenotype in COPD skeletal muscle due to different exercise strategies are not entirely consistent. Therefore, based on the elucidation of this phenotype, in this study, we analyzed the effect of exercise on mitochondrial dysfunction in COPD skeletal muscle and the regulatory mechanism thereof. We also provided a theoretical basis for exercise programs to rehabilitate this condition.
Keywords: chronic obstructive pulmonary disease; exercise; mechanisms; mitochondrial dysfunction; skeletal muscle dysfunction.
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