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1 School of Clinical Sciences, University of Liverpool, United Kingdom
2 School of clinical Sciences, University of Liverpool, United Kingdom
3 Medicine, University of Liverpool, University of Liverpool, Liverpool, L69 3GA, United Kingdom; School of Clinical Sciences, University of Liverpool, Liverpool, United Kingdom
* To whom correspondence should be addressed. E-mail: mdcr02{at}liverpool.ac.uk.
Skeletal muscle atrophy and weakness are major causes of frailty in the elderly. Functional deficits in muscles of old humans and rodents are associated with an attenuated production of heat shock proteins (HSPs) following exercise and transgenic overexpression of HSP70 reversed this functional decline. We hypothesised that training would increase HSP70 content of muscle in adult and old wild-type mice and that this would protect against the development of age-related functional deficits. A 10 week treadmill training protocol at 15m/min, for 15 minutes, 3 days per week resulted in a significant increase in HSP70 content of muscles of adult mice. Muscles of old untrained mice demonstrated a significant increase in HSP70 protein content and a reduction in HSP70 mRNA content compared with adult untrained mice. Training for 12 months from 12 - 14 months old, or for 10 weeks from 24 months old, resulted in modification of HSP70 protein and mRNA content to levels of adult mice. Training did not change force generation of EDL muscles of old mice or improve recovery following damaging contractions. The 2 fold increase in HSP70 content in muscles of adult mice following training may have not been sufficient to provide protection in this instance.
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