Mitochondrial Mechanisms of Resistance Exercise in COPD-Related Skeletal Muscle Dysfunction: A Narrative Review

Chronic obstructive pulmonary disease (COPD) is a heterogeneous pulmonary disorder characterized by airway or alveolar abnormalities. Beyond pulmonary impairment, COPD frequently leads to skeletal muscle dysfunction, manifesting as muscle atrophy, myofibrillar type switching, and reduced muscle strength and endurance, which severely impair exercise capacity and quality of life. Mitochondrial dysfunction, including reduced mitochondrial density, altered respiratory function, and increased oxidative stress, is recognized as a key contributor to skeletal muscle impairment in COPD. Resistance exercise (RE), an effective exercise therapy, has been shown to improve lower-limb muscle function and quality in COPD patients, and it appears feasible even for those with severe airflow obstruction and significant dyspnea. Mechanistically, RE may enhance mitochondrial respiratory capacity and promote mitochondrial biogenesis, and might also counteract mitochondrial dysfunction induced by secondhand smoke. In this narrative review, we analyze the effects of RE on skeletal muscle dysfunction in COPD and summarize the underlying mitochondrial mechanisms.