Skeletal muscle dysfunction in chronic obstructive pulmonary disease.

Abstract

During the last decade evidence has been accumulated on the role of skeletal muscle dysfunction in reducing exercise capacity and affecting the quality of life of patients with chronic obstructive pulmonary disease (COPD). An appreciable body of research has helped to identify morphological and biochemical alterations, physiological consequences, and possible therapeutic interventions. There are, however, still many areas of uncertainty. For example it is not clear how much of the alterations are within the muscle itself or the consequence of the altered environment in which the muscle works. Similarly it is not clear how much of the impairment is simply due to aging and chronic inactivity. Another key issue is the possible additive effect of drugs often used in COPD patients, such as steroids, beta 2-agonist and cyclosporin. A specific additional layer of complexity comes from nutritional considerations and in particular loss of muscle mass which not infrequently accompanies severe disease and even greater exercise intolerance. Studies on the effects of training or other therapeutic interventions have shown that muscle dysfunction is partially reversible. There is, however, a clear need for studies based on cellular and molecular methods aimed to clarify the role of factors such as oxidative stress, inflammation and nutritional deficiencies on skeletal muscle structure and function. The focus of this review is to highlight the current knowledge on skeletal muscle dysfunction in COPD and briefly summarize the possible therapeutic implications.