© 2003 BMJ Publishing Group & British Thoracic Society
EDITORIAL
Peripheral muscle weakness in COPD
Peripheral muscle weakness in COPD: where does it come from?
Department of Respiratory Medicine, Royal Brompton Hospital and National Heart & Lung Institute, London SW3 6NP, UK; m.polkey@rbh.nthames.nhs.uk
Do patients with frequent exacerbations of COPD have a more rapid rate of decline in quadriceps strength than those with stable disease?
| The first 150 words of the full text of this article appear below. |
Exertional dyspnoea is usually the main complaint of a patient with chronic obstructive pulmonary disease (COPD). Although this is partly a result of impaired pulmonary mechanics, exercise performance remains substantially reduced even if both lungs are replaced,1 which suggests that the lungs alone cannot explain exertional dyspnoea. Quadriceps myopathy is a feature of COPD. Histological examination of quadriceps biopsy tissues shows a switch towards fatiguable type II fibres2 and reduced oxidative enzymes. This in turn leads to anaerobic metabolism at lower work rates than in normal subjects.3 Lactic acid, generated as a byproduct of anaerobic metabolism, is buffered by bicarbonate with the generation of carbon dioxide. Patients with severe COPD cannot clear carbon dioxide by increasing their ventilation and thus treadmill walking may result in transient hypercapnia and acidosis.4 It is perhaps not surprising therefore that quadriceps weakness is demonstrably related to the utilisation of
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