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1 Kinesiology, The University of Western Ontario, London, Canada
2 London, Canada; Kinesiology, The University of Western Ontario, London, Canada
3 Kinesiology, The University of Western Ontario, London, Canada; Lawson Health Research Institute, London, Canada
* To whom correspondence should be addressed. E-mail: enoble{at}uwo.ca.
An issue central to understanding the biological benefits associated with regular exercise training is to elucidate intracellular mechanisms governing exercise-conferred cardioprotection. Heat Shock Proteins (HSPs), most notably the inducible 70-kDa HSP family member, Hsp70, are believed to participate in the protection of the myocardium during cardiovascular stress. Following acute exercise, activation of Protein Kinase A (PKA) mediates suppression of an intermediary protein kinase, Extracellular Regulated Protein Kinase (ERK1/2), that phosphorylates and suppresses the activation of the Heat Shock transcription Factor 1 (HSF1). However, following exercise training, ERK1/2 has been reported to regulate the transcriptional activation of several genes involved in cell growth and proliferation and has been shown to be associated with training-mediated myocardial hypertrophy. The current project examined the transcriptional activation of hsp70 gene expression in acutely-exercised (60 min at 30 m/min) naive sedentary and aerobically trained (8 week: low intensity) male Sprague-Dawley rats. Following acute exercise stress no significant differences were demonstrated in expression of myocardial hsp70 mRNA and activation of PKA between sedentary and trained animals. However, trained animals elicited expression of the hsp70 gene (p < 0.05) in the presence of elevated ERK1/2 activation. Given the association of ERK1/2 and the suppression of hsp70 gene expression following acute exercise in naive sedentary rats, these results suggest that training results in adaptations which allow for the simultaneous initiation of both proliferative and protective responses. While it is unclear what factors are associated with this training-related shift, increases in HSF1 DNA-binding affinity (p < 0.05) are suggested.
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