From muscle disuse to myopathy in COPD: potential contribution of oxidative stress

Abstract

Evidence has been accumulating that chronic inactivity leading to muscle disuse is unlikely to be the only explanation for the peripheral muscle dysfunction of chronic obstructive pulmonary disease (COPD) patients. Although a new concept of myopathy was recently proposed, the question of disuse and/or a form of myopathy is still being debated. This review proposes definitions for the terms used in this debate, discusses the relevant studies and concludes that the evidence points to a myopathy associated with muscle disuse in COPD. COPD myopathy implies pharmacological and/or pathophysiological mechanisms that need to be identified in order to optimally orient therapeutic strategies. The literature indicates that corticosteroids, inflammation, hypoxaemia and oxidative stress are among the factors contributing to COPD muscle dysfunction, but their relative contributions have not been fully elucidated. This review presents the advances in understanding each of these mechanisms, especially the data showing that muscle oxidative stress occurs and contributes to muscle dysfunction in chronic obstructive pulmonary disease. The current review also reports the studies that have elucidated the molecular mechanisms underlying this stress in chronic obstructive pulmonary disease by demonstrating alterations in oxidant and/or antioxidant systems. Finally, the review considers how inflammation and hypoxaemia may trigger oxidative stress in chronic obstructive pulmonary disease muscles and presents the therapeutic modalities that should be proposed to prevent it.