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This Article Full Text Full Text (PDF) All Versions of this Article: 290/4/H1549    most recent 00913.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Marcil, M. Articles by Burelle, Y. Search for Related Content PubMed PubMed Citation Articles by Marcil, M. Articles by Burelle, Y.

Exercise training induces respiratory substrate-specific decrease in Ca²⁺-induced permeability transition pore opening in heart mitochondria

Département de Kinésiologie, Université de Montréal, Montreal, Quebec, Canada

Submitted 24 August 2005 ; accepted in final form 9 November 2005

The purpose of this study was to determine whether regular exercise (treadmill running, 10 wk) alters the susceptibility of rat isolated heart mitochondria to Ca²⁺-induced permeability transition pore (PTP) opening and whether this could be associated with changes in the modulation of PTP opening by selected physiological effectors. Basal leak-driven and ADP-stimulated respiration in the presence of substrates for complex I, II, and IV were not affected by training. Fluorimetric studies revealed that in the control and exercise-trained groups, the amount of Ca²⁺ required to trigger PTP opening was greater in the presence of complex II vs. I substrates (230 ± 12 vs. 134 ± 7 nmol Ca²⁺/mg protein, P < 0.01; pooled average of control and trained groups). In addition, with a substrate feeding the complex II, training increased by 45% (P < 0.01) the amount of Ca²⁺ required to trigger PTP opening both in the presence and absence of the PTP inhibitor cyclosporin A. However, membrane potential, reactive oxygen species production, NAD(P)H ratio, and Ca²⁺ uptake kinetics were not different in mitochondria from both groups. Together, these results suggest the existence of a substrate-specific regulation of the PTP in heart mitochondria and suggest that regular exercise results in a reduced sensitivity to Ca²⁺-induced PTP opening in presence of complex II substrates.

mitochondrial function; calcium stress

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