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1 Department of Pathology and Laboratory Medicine, University of British Columbia - St Paul's Hospital, Vancouver, BC, Canada; Department of Zoology and Radiology and the Division of Sports Medicine, University of British Columbia, Vancouver, BC, Canada
2 Department of Pathology and Laboratory Medicine, University of British Columbia - St Paul's Hospital, Vancouver, BC, Canada
3 Department of Human Biology & Nutritional Sciences, University of Guelph, Guelph, ON, Canada
4 Faculte des Sciences, Universite de Paris XII, Paris, France
5 Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL, USA
6 Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL, USA
7 Department of Zoology and Radiology and the Division of Sports Medicine, University of British Columbia, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: mallard{at}mrl.ubc.ca.
Adaptation of myocardial energy substrate utilization may contribute to the cardioprotective effects of regular exercise, a possibility supported by evidence showing that pharmacological metabolic modulation is beneficial to ischemic hearts during reperfusion. Thus, we tested the hypothesis that the beneficial effect of regular physical exercise on recovery from ischemia-reperfusion is associated with a protective metabolic phenotype. Function, glycolysis and oxidation of glucose, lactate, and palmitate were measured in isolated working hearts from sedentary control (C) and treadmill-trained (T: 10 wks, 4d/wk) female Sprague-Dawley rats submitted to 20min ischemia and 40min reperfusion. Training resulted in myocardial hypertrophy (1.65±0.05 vs. 1.30±0.03 g wet heart wt, P<0.001) and improved recovery of function after ischemia by nearly 50% (p<0.05). Glycolysis was 25 to 30% lower in T hearts before and after ischemia (P < 0.05), while rates of glucose oxidation were 45% higher before ischemia (P<0.01). As a result, the fraction of glucose oxidized before and after ischemia was, respectively, two-fold and 25% greater in T hearts (p<0.05). Palmitate oxidation was 50 to 65% greater in T than in C before and after ischemia (P<0.05), while lactate oxidation did not differ between groups. Alteration in content of selected enzymes and proteins, as assessed by immunoblot analysis, could not account for the reduction in glycolysis or increase in glucose and palmitate oxidation observed. Combined with the studies on the beneficial effect of pharmacological modulation of energy metabolism, the present results provide support for a role of metabolic adaptations in protecting the trained heart against ischemia-reperfusion injury.
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