Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease.
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.
Jagoe
R T
RT
Pulmonary and Rehabilitation Research Group, Dept of Medicine, Clinical Sciences Centre, University Hospital Aintree, Liverpool, UK. tjagoe@liverpool.ac.uk
Engelen
M P K J
MP
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D015992:Body Mass Index; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D009124:Muscle Proteins / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D009133:Muscular Atrophy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
D000596:Amino Acids; D018836:Inflammation Mediators; D009124:Muscle Proteins