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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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