title: Regular exercise is associated with a protective metabolic phenotype in the rat heart.
abstract: 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 wk, 4 days/wk) female Sprague-Dawley rats submitted to 20 min ischemia and 40 min reperfusion. Training resulted in myocardial hypertrophy (1.65 +/- 0.05 vs. 1.30 +/- 0.03 g heart wet wt, P < 0.001) and improved recovery of function after ischemia by nearly 50% (P < 0.05). Glycolysis was 25-30% lower in T hearts before and after ischemia (P < 0.05), whereas 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, twofold and 25% greater in T hearts (P < 0.05). Palmitate oxidation was 50-65% greater in T than in C before and after ischemia (P < 0.05), whereas 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.
authors.affiliation: James Hogg/iCAPTUR4E Centre for Cardiovascular and Pulmonary Research, Department of Pathology and Laboratory Medicine, University of British Columbia-St. Paul's Hospital, Vancouver, British Columbia V6Z 1Y6, Canada.
authors.forename: Yan
authors.initials: Y
authors.lastname: Burelle
authors.forename: Richard B
authors.initials: RB
authors.lastname: Wambolt
authors.forename: Mark
authors.initials: M
authors.lastname: Grist
authors.forename: Hannah L
authors.initials: HL
authors.lastname: Parsons
authors.forename: Jeffrey C F
authors.initials: JC
authors.lastname: Chow
authors.forename: Christine
authors.initials: C
authors.lastname: Antler
authors.forename: Arend
authors.initials: A
authors.lastname: Bonen
authors.forename: Angelica
authors.initials: A
authors.lastname: Keller
authors.forename: George A
authors.initials: GA
authors.lastname: Dunaway
authors.forename: Kirill M
authors.initials: KM
authors.lastname: Popov
authors.forename: Peter W
authors.initials: PW
authors.lastname: Hochachka
authors.forename: Michael F
authors.initials: MF
authors.lastname: Allard
mesh_terms: D000818:Animals; D004734:Energy Metabolism; D004798:Enzymes / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D066298:In Vitro Techniques; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D010641:Phenotype; D010805:Physical Conditioning, Animal; D011506:Proteins / Q000378:metabolism; D011522:Protons; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function
chemical_list: D004798:Enzymes; D005227:Fatty Acids; D011506:Proteins; D011522:Protons; D005947:Glucose