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1 Department of Kinesiology, University of Western Ontario, London, Ontario, Canada N6A 3K7; and 2 Department of Kinesiology and Applied Physiology, University of Colorado, Boulder, Colorado 80309
High-intensity treadmill exercise increases the
expression of a cardioprotective, inducible 72-kDa stress protein
(SP72) in cardiac muscle. This investigation examined whether voluntary free wheel exercise training would be sufficient to confer a similar response. Male Sprague-Dawley rats were randomly assigned to either treadmill (TM-Tr) or free wheel (FW-Tr) training groups. By the end of
the 8-wk training period, TM-Tr animals ran 1 h/day, 5 days/wk up a
10% grade, covering a distance of 8,282 m/wk. FW-Tr rats ran, on
average, 5,300 m/wk, with one-third of the animals covering distances
similar to those for the TM-Tr group. At the time of death, hearts of
trained and caged sedentary control (Sed) animals were divided into
left (LV) and right (RV) ventricles. Citrate synthase activity and the
relative immunoblot contents of SP72, SP73 (the constitutive isoform of
the SP70 family), and a 75-kDa mitochondrial chaperone (SP75) were
subsequently determined. LV and RV did not differ on any measure, and
SP73, SP75, and citrate synthase were not affected by training. Cardiac
SP72 levels were elevated over fourfold in both ventricles of TM-Tr
compared with RV of FW-Sed rats. Despite the animals having run a
similar total distance, cardiac SP72 content in FW-Tr rats was not
different from that in Sed animals. These data indicate that voluntary
exercise training is insufficient to elicit an elevation of SP72 in rat heart and suggest that exercise intensity may be a critical factor in
evoking the cardioprotective SP72 response.
exercise training; heat shock proteins; glucose-regulated protein 75; heat shock protein 72; heat shock protein 73
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