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Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease

¹ Pulmonary and Rehabilitation Research Group, Dept of Medicine, Clinical Sciences Centre, University Hospital Aintree, Liverpool, UK, ² Dept of Respiratory Medicine, University Hospital Maastricht, Maastricht, The Netherlands

CORRESPONDENCE: R.T. Jagoe, Pulmonary and Rehabilitation Research Group, Dept of Medicine, Clinical Sciences Centre, University Hospital Aintree, Longmoor Lane, Liverpool, L9 7AL, UK. Fax: 44 1515295888. E-mail: tjagoe@liverpool.ac.uk

Keywords: amino acids, chronic obstructive pulmonary disease, muscle wasting, protein degradation, protein synthesis

Received: June 30, 2003
Accepted June 30, 2003

Loss of skeletal muscle mass is now recognised as an important feature of chronic obstructive pulmonary disease (COPD) which contributes to symptoms and influences prognosis. The changes in skeletal muscle remain poorly understood, largely because only a few studies have been performed to define the adaptations in whole body and muscle protein metabolism in COPD.

The first sections of this review summarise background information about skeletal muscle wasting in COPD, and focuses on the studies concerned with amino acid profiles and protein synthesis and degradation rates. To aid interpretation some discussion of the techniques commonly used is included.

A variety of different catabolic factors may determine whether chronic obstructive pulmonary disease patients become cachectic. The precise role for each one of these factors as well as the intracellular pathways activated in muscle as a result of chronic obstructive pulmonary disease are unknown and remain to be defined. Details of the actions of a range of different catabolic factors and potential mechanisms will be discussed.

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