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 degrees C room (3WK, 6WK, and 9WK, respectively)
or in a 4-8 degrees C environment with wetted fur (3WKC, 6WKC, and 9WKC, r
espectively). The colder room prevented elevations in core temperature. Dur
ing weeks 3-9 the animals ran 5 days/wk up a 6% grade at 20 m/min for 60 mi
n. 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 runn
ers. Compared with SED rats, <alpha>B-crystallin was 90% higher in 9WKC ani
mals, 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 in
creased and mitochondrial SOD decreased (P < 0.05) in 3WK and 6WK rats comp
ared 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 peroxida
se. 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 prote
ins over time which are influenced by core temperature. In addition, cardio
protection resulting from chronic exercise appears to be due to increased H
SP 70.