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1 Royal Brompton Hospital & National Heart Lung Institute, Respiratory Muscle Laboratory, London, United Kingdom
2 Royal Brompton Hospital & National Heart Lung Institute, Respiratory Muscle Laboratory, London, United Kingdom; Imperial College, Biomedical Sciences Division, London, United Kingdom
3 Royal Brompton Hospital, Department of Thoracic Surgery, London, United Kingdom
4 Medicale Hopital Saint Louis, Departement de Biostatistique et Informatique, Paris, France
5 King's College London School of Medicine, Respiratory Muscle Laboratory, London, United Kingdom
6 Imperial College, Biomedical Sciences Division, London, United Kingdom
* To whom correspondence should be addressed. E-mail: a.moore{at}ic.ac.uk.
Structural adaptations that occur in the diaphragm muscle of patients with chronic obstructive pulmonary disease (COPD), namely an increase in Type I fibres and a decrease in Type II fibres, have been explored in terms of the active contractile properties of the diaphragm. The aim of this study was to test the passive properties of the diaphragm by measuring the force response of relaxed diaphragm muscle fibres to stretching, in order to determine the effect of COPD on these properties. Costal diaphragm biopsies were taken from patients with COPD, and from controls with normal pulmonary function. From these biopsies, titin expression was assessed in diaphragm homogenates by gel electrophoresis, and the restoring force measured by incremental stretching of single fibres in the relaxed state and measuring the force response to stretching. A quadratic model was used to illustrate the relationship between restoring force and muscle fibre length, and revealed that COPD fibres generate significantly lower restoring forces than control fibres as judged by the area under the force-length curve. Furthermore, this finding applies to both Type I and Type II fibres. Gel electrophoresis revealed different titin isoforms in COPD and controls, consistent with the conclusion that COPD results not only in a change in muscle fibre type distribution, but in a structural change in the titin molecule in all muscle fibre types within the diaphragm. This may assist the muscle with the energetic changes in the length of the diaphragm required during breathing in COPD.
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