Document Detail

Cellular and molecular basis of age-related sarcopenia.
MedLine Citation:
PMID:  11880689     Owner:  NLM     Status:  MEDLINE    
Sarcopenia, the decline in muscle bulk and performance associated with normal aging, is an important component of frailty in the elderly. The gradual loss of both motor nerves and muscle fibers during senescence appears to be the major problem. Atrophy (especially in fast-twitch fibers) and impaired function of the surviving cells also contribute to sarcopenia. Although skeletal muscle has the capacity to regenerate itself, this process is not activated by the gradual age-related loss of muscle fibers. The endocrine, autocrine, and paracrine environment in old muscle is less supportive of protein synthesis, reinnervation of muscle fibers, and satellite cell activation, proliferation, and differentiation. Lifelong exposure of DNA to free radical damage results in accumulation of somatic mutations in nerves and muscle fibers. Reduced protein synthesis leads to atrophy, and slower fractional protein turnover contributes to longer retention of proteins that may have been damaged by free radicals. Many genes are differentially expressed in young and old muscle, but additional research is needed to determine which of these genes have a significant role in the pathogenesis or adaptation to sarcopenia.
Stephen Welle
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Canadian journal of applied physiology = Revue canadienne de physiologie appliquée     Volume:  27     ISSN:  1066-7814     ISO Abbreviation:  Can J Appl Physiol     Publication Date:  2002 Feb 
Date Detail:
Created Date:  2002-03-06     Completed Date:  2002-04-17     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9306274     Medline TA:  Can J Appl Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  19-41     Citation Subset:  IM    
Department of Medicine, University of Rochester, Rochester, New York 14642, USA.
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MeSH Terms
Aging / physiology*
Cytokines / physiology
Gene Expression
Hormones / physiology
Motor Neurons / physiology
Muscle Fibers, Fast-Twitch / physiology
Muscle, Skeletal / physiology*
Muscular Atrophy / genetics,  physiopathology*
Grant Support
Reg. No./Substance:
0/Cytokines; 0/Hormones

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