New Insights into the Mechanisms of Skeletal Muscle Atrophy in COPD

Background: In 2020, it was estimated that there were over 480 million cases of chronic obstructive pulmonary disease (COPD) worldwide. Up to 40% of COPD patients suffer from certain degrees of muscle atrophy. The severity of this muscle atrophy is normally correlated with an increased mortality rate among these patients. The goal of this study is to underline the causes of muscle atrophy/dysfunction in the COPD population and to investigate treatment options. Methods: We conducted an extensive literature review using the PubMed database, mainly focusing on publications from 2013 to 2024. Our objective was to identify the biological mechanisms underlying muscle atrophy and dysfunction in COPD patients. Our further aim was to realize possible management and treatment strategies that could be put into practice for better patient outcomes. This review afforded us an opportunity to put together what is currently known on the subject and highlight new approaches becoming available in offsetting the muscle atrophy effects in COPD patients. Results: Through our review of the body of research, we were able to find that muscle atrophy in COPD patients is a multifactorial issue. The muscle atrophy that occurs is not only a result of COPD pathophysiology itself, but also because of treatments, limitations brought about by COPD, and by comorbidities that frequently appear in COPD patients. Through our review of the scientific literature, we saw that as many as 98% of COPD patients have at least one comorbidity. This makes studying COPD in isolation difficult in the general population because of the prevalence of comorbidities. Using animal models, researchers can induce COPD to study the effects that it has without confounding factors. We were able to find that there are multiple biological mechanisms that cause muscle dysfunction/atrophy in COPD patients. We also looked at the possible interventions for the treatment of muscle atrophy. Interventions have been proposed with regard to strength-training, structured eating, anabolic steroids to address muscle wasting, and several others that will disrupt the metabolic pathways leading to muscle atrophy in COPD. Conclusion: Muscle wasting in COPD is partly caused by metabolic pathways activated in response to the hypoxia induced by COPD. A certain number of studies have concentrated on particular pathways that lead to muscle atrophy in order to develop potential treatments to address this problem. Most of the research has shown that these treatments are expected to lessen or reverse muscle atrophy in COPD as well as reduce the burden of the disease.