Sceletal muscle characteristics and physical activity patterns in COPD

University dissertation from Örebro : Örebro universitet

Abstract: Chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality worldwide. Besides abnormities within the respiratory system COPD is also associated with effects outside the lungs, so called systemic effects. One systemic effect that has been highlighted is skeletal muscle dysfunction which has also been associated with reduced exercise capacity. Apart from changes in muscle morphology, low levels of physical activity have also been suggested as a plausible mediator of reduced exercise capacity in COPD. The aim of this thesis was to study muscle morphology and physical activity patterns in patients with different degrees of COPD and to examine the associations between muscle morphology, physical activity and exercise capacity in these patients. Skeletal muscle morphology was found to shift towards a more glycolytic muscle profile in COPD patients and changes in muscle morphology were found to be correlated to disease severity and to exercise capacity. Muscle capillarization was also found to be lower in COPD compared with healthy subjects and to be correlated to disease severity and exercise capacity. When studying signalling pathways involved in muscle capillarization, an overexpression of VHL was found in patients with mild and moderate COPD compared with healthy subjects. Furthermore, COPD patients were found to be less physically active compared with healthy subjects and the level of physical activity was associated with exercise capacity.In conclusion, changes in skeletal muscle morphology and low levels of physical activity are present in COPD patients and may partly explain the lower exercise capacity observed in these patients. The more glycolytic muscle profile in COPD is suggested to be mediated by hypoxia and low levels of physical activity in this patient group. Furthermore, increased levels of VHL may lead to impaired transduction of the hypoxic signalling pathway, which may contribute to the decreased muscle capillarization observed in COPD.

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