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Copyright ©ERS Journals Ltd 2002
Skeletal muscle fibre-type shifting and metabolic profile in patients with chronic obstructive pulmonary disease
1 Dept of Pulmonology, 2 Dept of Anatomy and Embryology and 3 Dept of Physiology, University of Maastricht, Maastricht, the Netherlands
CORRESPONDENCE: H.R. Gosker, Dept of Pulmonology Maastricht University, P.O. Box 616, 6200 MD, Maastricht, The Netherlands. Fax: 31 433875051. E-mail: H.Gosker@pul.unimaas.nl
Keywords: chronic obstructive, histochemistry, myosin heavy chain isoforms, oxidative capacity, pulmonary disease, skeletal muscle
Received: June 7, 2001
Accepted October 30, 2001
This study was supported by a grant from the Netherlands Asthma Foundation (project number 96.16).
The aim of this study was to examine the nature of fibre-type redistribution in relation to fibre metabolic profile in the vastus lateralis in chronic obstructive pulmonary disease (COPD) and COPD subtypes.
Fifteen COPD patients (eight with emphysema stratified by high-resolution computed tomography) and 15 healthy control subjects were studied. A combination of myofibrillar adenosine triphosphatase staining and immunohistochemistry was used to identify pure, as well as hybrid fibre types. For oxidative capacity, fibres were stained for cytochrome c oxidase and succinate dehydrogenase activities, and glycogen phosphorylase for glycolytic capacity.
The proportion of type-I fibres in COPD patients was markedly lower (16% versus 42%), especially in emphysema, and the proportion of hybrid fibres was higher (29% versus 16%) compared to controls. The proportion of fibres staining positive for oxidative enzymes was lower in COPD patients, which correlated with the proportion of type-I fibres. In COPD oxidative capacity was lower within IIA fibres.
The authors conclude that fibre-type transitions are involved in the fibre-type redistribution in chronic obstructive pulmonary disease. Low oxidative capacity is closely related to the proportion of type-I fibres, but an additional reduction of oxidative enzyme activity is present within IIA fibres. Fibre-type abnormalities may be aggravated in emphysema.
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