title: Short term training attenuates opening of the mitochondrial permeability transition pore without affecting myocardial function following ischemia-reperfusion.
abstract: Opening of the mitochondrial permeability transition pore (PTP) is known to occur during reperfusion of the ischemic heart and to cause dysfunction and injury. The purpose of the present study was to determine whether short-term training (treadmill dunning for 5 days, 30 m.min(-1), 0%) in male Sprague Dawley rats reduces the occurrence of PTP opening in the ischemic-reperfused heart. Hearts from control (C) and trained (T) rats perfused in the Langendorff mode were submitted to ischemia-reperfusion (I-R: 30 and 40 min respectively). In situ PTP opening was quantified using the mitochondrial 2-deoxy [(3)H]glucose ([(3)H]DOG) entrapment method. Following I-R, the recovery of intact mitochondria upon isolation was significantly greater in T vs C hearts (11.7 +/- 0.5 vs 9.1 +/- 0.4 mU citrate synthase.g(-1) wet ventricles, p < or = 0.01). Training also reduced the entrapment of mitochondrial [(3)H]DOG normalized for the loss of intact mitochondria (14.4 +/- 1.4 vs 9.6 +/- 0.8 [(3)H]DOG ratio units, p < or = 0.01). However, under the experimental conditions used the recovery of contractile function, coronary flow and release of LDH in the coronary effluent were similar in both experimental groups. Taken together, these results suggest that short-term training can confer mitochondrial protection and reduce PTP opening.
authors.affiliation: Département de kinésiologie, Université de Montréal, Succursale Centre-Ville, C.P. 6128, Montréal, Québec, Canada, H3C 3J7.
authors.forename: Marc
authors.initials: M
authors.lastname: Ciminelli
authors.forename: Alexis
authors.initials: A
authors.lastname: Ascah
authors.forename: Karine
authors.initials: K
authors.lastname: Bourduas
authors.forename: Yan
authors.initials: Y
authors.lastname: Burelle
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000201:enzymology; D003847:Deoxyglucose / Q000378:metabolism; D006321:Heart / Q000503:physiopathology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D009119:Muscle Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D010477:Perfusion; D010805:Physical Conditioning, Animal; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014316:Tritium
chemical_list: D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D014316:Tritium; D003847:Deoxyglucose; D007770:L-Lactate Dehydrogenase