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Cardiac Metabolism Laboratory, Department of Kinesiology, University of Texas, Austin, Texas 78712
This study determined the role of body temperature
during chronic exercise on myocardial stress proteins and antioxidant
enzymes as well as functional recovery after an ischemic
insult. Male Sprague-Dawley rats were exercised for 3, 6, or 9 wk in a
23°C room (3WK, 6WK, and 9WK, respectively) or in a 4-8°C
environment with wetted fur (3WKC, 6WKC, and 9WKC, respectively). The
colder room prevented elevations in core temperature. During
weeks 3-9 the animals ran 5 days/wk up a 6% grade at
20 m/min for 60 min. Myocardial heat shock protein 70 (HSP 70)
increased 12.3-fold (P < 0.05) in 9WK versus sedentary
(SED) rats but was unchanged in the cold-room runners. Compared with
SED rats, 
B-crystallin was 90% higher in 9WKC animals, HSP 90 was
50% higher in 3WKC and 6WKC animals, and catalase was 23% higher in
3WK animals (P < 0.05 for all). Cytosolic superoxide
dismutase increased and mitochondrial SOD decreased (P < 0.05) in 3WK and 6WK rats compared with 3WKC and 6WKC rats. Antioxidant
enzymes returned to SED values in all runners by 9 wk. No differences
were observed among any of the groups for glucose-regulated protein 75, heme oxygenase-1, or glutathione peroxidase. Mechanical recovery of
isolated working hearts after 22.5 min of global ischemia was
enhanced in 9WK (P < 0.05) but not in 9WKC rats. We
conclude that exercise training results in dynamic changes in
cardioprotective proteins over time which are influenced by core
temperature. In addition, cardioprotection resulting from chronic
exercise appears to be due to increased HSP 70.
ischemia-reperfusion; rat; perfused heart; stress proteins; antioxidants
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