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Department of Exercise and Sport Sciences and Physiology and the Center for Exercise Science, University of Florida, Gainesville, Florida 32611
These experiments
examined the independent effects of short-term exercise and heat stress
on myocardial responses during in vivo ischemia-reperfusion
(I/R). Female Sprague-Dawley rats (4 mo old) were randomly
assigned to one of four experimental groups: 1) control,
2) 3 consecutive days of treadmill exercise [60 min/day at
60-70% maximal O2 uptake
(
O2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60-70%
O2 max), and 4) whole body
heat stress (15 min at 42°C). Twenty-four hours after heat stress or
exercise, animals were anesthetized and mechanically ventilated, and
the chest was opened by thoracotomy. Coronary occlusion was maintained
for 30-min followed by a 30-min period of reperfusion. Compared with
control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher (P < 0.05) left ventricular
developed pressure (LVDP), maximum rate of left venticular pressure
development (+dP/dt), and maximum rate of left ventricular
pressure decline (
dP/dt) at all measurement periods during
both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/dt,
and dP/dt at any time during ischemia or
reperfusion. Both heat stress and exercise resulted in an increase
(P < 0.05) in the relative levels of left ventricular
heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days)
increased (P < 0.05) myocardial glutathione levels and
manganese superoxide dismutase activity. These data indicate that
3-5 consecutive days of exercise improves myocardial contractile
performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.
endurance exercise; heart; reactive oxygen species; heat shock proteins; lipid peroxidation; antioxidant enzymes
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