Purpose of review
The purpose of this review is to identify new advances in our understanding of skeletal muscle dysfunction in patients with chronic obstructive pulmonary disease (COPD).
Recent studies have confirmed the relevance of muscle dysfunction as an independent prognosis factor in COPD. Animal studies have shed light on the molecular mechanisms governing skeletal muscle hypertrophy/atrophy. Recent evidence in patients with COPD highlighted the contribution of protein breakdown and mitochondrial dysfunction as pathogenic mechanisms leading to muscle dysfunction in these patients.
COPD is a debilitating disease impacting negatively on health status and the functional capacity of patients. COPD goes beyond the lungs and incurs significant systemic effects among which muscle dysfunction/wasting is one of the most important. Muscle dysfunction is a prominent contributor to exercise limitation, healthcare utilization and an independent predictor of morbidity and mortality. Gaining more insight into the molecular mechanisms leading to muscle dysfunction/wasting is key for the development of new and tailored therapeutic strategies to tackle skeletal muscle dysfunction/wasting in COPD patients.