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© 2006 the European Respiratory Society
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Impacting patient-centred outcomes in COPD: deconditioning
CORRESPONDENCE: R. Casaburi, Rehabilitation Clinical Trials Center, Division of Respiratory and Critical Care Physiology and Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 West Carson Street Torrance California CA90502 USA. Fax: 1 3102228249. E-mail: casaburi{at}ucla.edu
Patients with chronic obstructive pulmonary disease (COPD) frequently suffer from exercise intolerance, leading to a reduced ability to participate in activities of daily life and, therefore, to a reduced health-related quality of life (HRQoL). An important determinant of exercise intolerance is the loss of muscle mass.
Although the mechanism for loss of muscle function is multi-factorial, deconditioning appears to play a primary role in many patients. COPD patients often have decreased fat-free mass compared with healthy counterparts and reduced muscle cross-sectional area. It seems, then, that a cycle of decline often characterises COPD, in which inactivity results in muscle weakness, which in turn acts as a further deterrent to exercise. Such deconditioning can be reversed by pulmonary rehabilitation, leading to significant improvements in exercise tolerance and HRQoL.
Recent research suggests that the effectiveness of pulmonary rehabilitation can be amplified with concomitant administration of tiotropium (a long-acting bronchodilator) or supplemental oxygen. This suggests that facilitating higher training work-rates can enhance the anabolic effects of training.
Patients should be encouraged to maintain activity levels in the follow-up period after training, in order to retain the benefits of rehabilitation.
KEYWORDS: Chronic obstructive pulmonary disease, deconditioning, exercise tolerance, muscle dysfunction, pulmonary rehabilitation, tiotropium
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