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Respiratory muscle dysfunction in chronic obstructive pulmonary disease (COPD)
Dysfunction of the respiratory muscles, especially the diaphragm, is known to occur in patients with severe chronic obstructive pulmonary disease (COPD).1-3 Weakness of the diaphragm is part of a generalised process involving all (respiratory and peripheral) skeletal muscles. Causative factors for respiratory muscle dysfunction in COPD include disturbances in electrolytes,4hypercapnia,5 forward failure,6 and prolonged use of oral corticosteroids.7 In addition, the altered geometry of the thorax in severe emphysema compromises the ventilatory pump function of the diaphragm.8 Malnutrition, which frequently occurs in moderate to severe COPD,9 could also play a part in respiratory muscle dysfunction. Recent studies have indicated that wasting of fat free mass in COPD is associated with peripheral skeletal muscle weakness.10 However, few data are available regarding the effects of malnutrition on respiratory muscle strength. Maximal inspiratory pressure (Pimax) in nutritionally depleted patients with COPD (forced expiratory volume in one second (FEV1) 45.5 (15.1)% predicted) was lower than in non-depleted patients, but this did not reach statistical significance.9
Little is known about the underlying mechanisms of muscle dysfunction and the structural alterations that occur in the diaphragm with COPD. Levine et al 11 have shown that the diaphragm in patients with severe COPD (FEV1 33 (4)% predicted) has a higher proportion of type I (slow) fibres and a lower proportion of type II (fast) fibres than in those without COPD. It has recently been shown that a strong correlation exists between pulmonary functional residual capacity and the proportion of slow myosin heavy chain fibres in the diaphragm.12 This fast to slow fibre transition in the diaphragm can be regarded as an advantageous adaptation since it will attenuate fatiguability of the diaphragm.13 However, eventually most patients with COPD die from respiratory muscle …