Cited by 71Mitochondrial Function and PathologyCardiac Ischemia and ReperfusionCardiovascular and exercise physiology

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

Marcil, Mariannick, Bourduas, Karine, Ascah, Alexis, Burelle, Yan·2006·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

The purpose of this study was to determine whether regular exercise (treadmill running, 10 wk) alters the susceptibility of rat isolated heart mitochondria to Ca(2+)-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 Ca(2+) required to trigger PTP opening was greater in the presence of complex II vs. I substrates (230 +/- 12 vs. 134 +/- 7 nmol Ca(2+)/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 Ca(2+) 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 Ca(2+) 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 Ca(2+)-induced PTP opening in presence of complex II substrates.

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Crossref · 10.1152/ajpheart.00913.2005

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Authors
Marcil, M., Bourduas, K., Ascah, A., & Burelle, Y.
Affiliations
Université de Montréal (CA)
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2006-04
Volume
290
Issue
4
Pages
H1549-H1557
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2045877099
Cited by
71
References
64
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 1 · 2017: 7 · 2015: 4 · 2014: 5 · 2013: 2 · 2012: 5
FWCI
1.25
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Keywords
exercise training, mitochondrial permeability transition pore, heart mitochondria, respiratory substrates, cyclosporine, mitochondrial respiration, mitochondrial calcium uptake, cardioprotection
MeSH terms
Mitochondrial Permeability Transition Pore, Animals, Calcium, Cells, Cultured, Dose-Response Relationship, Drug, Female, Ion Channels, Mitochondria, Heart, Oxygen, Physical Conditioning, Animal, Physical Fitness, Ion Channel Gating, Rats, Sprague-Dawley, Cell Respiration, Mitochondrial Membrane Transport Proteins, Rats

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