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Skeletal muscle dysfunction in chronic obstructive pulmonary disease

It has become increasingly recognized that skeletal muscle dysfunction is common in patients with chronic obstructive pulmonary disease (COPD). Muscle strength and endurance are decreased, whereas muscle fatigability is increased. There is a reduced proportion of type I fibers and an increase in typ...

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Detalles Bibliográficos
Autores principales: Jeffery Mador, M, Bozkanat, Erkan
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2001
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC59579/
https://www.ncbi.nlm.nih.gov/pubmed/11686887
http://dx.doi.org/10.1186/rr60
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author Jeffery Mador, M
Bozkanat, Erkan
author_facet Jeffery Mador, M
Bozkanat, Erkan
author_sort Jeffery Mador, M
collection PubMed
description It has become increasingly recognized that skeletal muscle dysfunction is common in patients with chronic obstructive pulmonary disease (COPD). Muscle strength and endurance are decreased, whereas muscle fatigability is increased. There is a reduced proportion of type I fibers and an increase in type II fibers. Muscle atrophy occurs with a reduction in fiber cross-sectional area. Oxidative enzyme activity is decreased, and measurement of muscle bioenergetics during exercise reveals a reduced aerobic capacity. Deconditioning is probably very important mechanistically. Other mechanisms that may be of varying importance in individual patients include chronic hypercapnia and/or hypoxia, nutritional depletion, steroid usage, and oxidative stress. Potential therapies include exercise training, oxygen supplementation, nutritional repletion, and administration of anabolic hormones.
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spelling pubmed-595792001-11-06 Skeletal muscle dysfunction in chronic obstructive pulmonary disease Jeffery Mador, M Bozkanat, Erkan Respir Res Review It has become increasingly recognized that skeletal muscle dysfunction is common in patients with chronic obstructive pulmonary disease (COPD). Muscle strength and endurance are decreased, whereas muscle fatigability is increased. There is a reduced proportion of type I fibers and an increase in type II fibers. Muscle atrophy occurs with a reduction in fiber cross-sectional area. Oxidative enzyme activity is decreased, and measurement of muscle bioenergetics during exercise reveals a reduced aerobic capacity. Deconditioning is probably very important mechanistically. Other mechanisms that may be of varying importance in individual patients include chronic hypercapnia and/or hypoxia, nutritional depletion, steroid usage, and oxidative stress. Potential therapies include exercise training, oxygen supplementation, nutritional repletion, and administration of anabolic hormones. BioMed Central 2001 2001-05-02 /pmc/articles/PMC59579/ /pubmed/11686887 http://dx.doi.org/10.1186/rr60 Text en Copyright © 2001 BioMed Central Ltd
spellingShingle Review
Jeffery Mador, M
Bozkanat, Erkan
Skeletal muscle dysfunction in chronic obstructive pulmonary disease
title Skeletal muscle dysfunction in chronic obstructive pulmonary disease
title_full Skeletal muscle dysfunction in chronic obstructive pulmonary disease
title_fullStr Skeletal muscle dysfunction in chronic obstructive pulmonary disease
title_full_unstemmed Skeletal muscle dysfunction in chronic obstructive pulmonary disease
title_short Skeletal muscle dysfunction in chronic obstructive pulmonary disease
title_sort skeletal muscle dysfunction in chronic obstructive pulmonary disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC59579/
https://www.ncbi.nlm.nih.gov/pubmed/11686887
http://dx.doi.org/10.1186/rr60
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