Current status of research on muscle wasting associated with chronic obstructive pulmonary disease

Abstract Due to persistent airflow limitation, COPD patients frequently develop sarcopenia, creating a bidirectional worsening cycle: Diagnosis involves pulmonary function tests for COPD and consensus criteria (e.g., EWGSOP2) for sarcopenia. COPD promotes sarcopenia through chronic inflammation, protein metabolic imbalance, oxidative stress, and hypoxia, while sarcopenia impairs immune and respiratory muscle function, accelerating pulmonary decline. Pathogenesis is complex, involving signaling pathways that regulate inflammation, protein balance, muscle fiber transformation, and mitochondrial function. Contributing factors include sarcopenic obesity, malnutrition, hormonal disorders, corticosteroid use, and inactivity. Treatment focuses on smoking cessation, pharmacotherapy, nutritional support, and resistance exercise, with acupuncture showing potential. Current research is preliminary, with mechanisms unclear and no specific therapies available. Early diagnosis and personalized multidisciplinary interventions are crucial to disrupt the COPD-sarcopenia cycle, delay disease progression, and enhance physical function and quality of life. Therefore, this review summarizes how skeletal muscle metabolism participates in the pathophysiological processes of COPD and potential therapeutic agents for sarcopenia, aiming to provide beneficial recommendations for the clinical prevention and treatment of sarcopenia in COPD patients from a complex mechanistic perspective.