Abstract
Although it has been well characterized that COPD muscle dysfunction is the result of the complex interaction between systemic and local factors, the etiology of muscle dysfunction remains to be fully identified. Interestingly, while hyperinflation and an increased work of breathing appear to be the main contributing events to respiratory muscle dysfunction, deconditioning seems to play a major role in the dysfunction of peripheral muscles in COPD. Other factors such as cigarette smoke, nutritional abnormalities, exacerbations, drugs, hypoxia, hypercapnia, comorbidities, and physical activity also influence muscle mass and function in COPD patients (1-3; 5; 9; 15). Besides, derangements of key molecular and cellular processes such as redox imbalance, mitochondrial dysfunction, enhanced protein catabolism and reduced protein anabolism, structural alterations, and systemic inflammation also modify muscle phenotype and function in COPD patients.
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