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The developmental origins of sarcopenia: from epidemiological evidence to underlying mechanisms

Published online by Cambridge University Press:  05 March 2010

A. A. Sayer*
Affiliation:
Ageing and Health, MRC Epidemiology Resource Centre, MRC Epidemiology Resource Centre, University of Southampton, Southampton, UK
C. Stewart
Affiliation:
Molecular and Cell Biology, Institute for Biomedical Research into Human Movement and Health, Manchester Metropolitan University, Manchester, UK
H. Patel
Affiliation:
Ageing and Health, MRC Epidemiology Resource Centre, MRC Epidemiology Resource Centre, University of Southampton, Southampton, UK
C. Cooper
Affiliation:
Ageing and Health, MRC Epidemiology Resource Centre, MRC Epidemiology Resource Centre, University of Southampton, Southampton, UK
*
Address for correspondence: A. A. Sayer, MRC Epidemiology Resource Centre, University of Southampton, Southampton, SO16 6YD, UK. (Email aas@mrc.soton.ac.uk)

Abstract

Sarcopenia is defined as the loss of skeletal muscle mass and strength with age. There is increasing recognition of the serious health consequences in terms of disability, morbidity and mortality as well as major healthcare costs. Adult determinants of sarcopenia including age, gender, size, levels of physical activity and heritability have been well described. Nevertheless, there remains considerable unexplained variation in muscle mass and strength between older adults that may reflect not only the current rate of loss but the peak attained earlier in life. To date most epidemiological studies of sarcopenia have focused on factors modifying decline in later life; however, a life course approach to understanding sarcopenia, additionally, focuses on factors operating earlier in life including developmental influences. The epidemiological evidence linking low birth weight with lower muscle mass and strength is strong and consistent with replication in a number of different groups including children, young and older adults. However, most of the evidence for the cellular, hormonal, metabolic and molecular mechanisms underlying these associations comes from animal models. The next stage is to translate the understanding of mechanisms from animal muscle to human muscle enabling progress to be made not only in earlier identification of individuals at risk of sarcopenia but also in the development of beneficial interventions across the life course.

Type
Reviews
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

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