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Cited by 66Mitochondrial Function and PathologyCardiac Ischemia and ReperfusionCardiovascular and exercise physiology

Endurance training reverts heart mitochondrial dysfunction.; permeability transition and apoptotic signaling in long-term severe hyperglycemia

Lumini-Oliveira, José, Magalhães, José, Pereira, Cláudia V., Moreira, Ana C., Oliveira, Paulo J., Ascensão, António·2011·Mitochondrion
DOI 10.1016/j.mito.2010.07.005
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Abstract

The present study analyzed the effects of endurance training against cardiac mitochondrial dysfunction, particularly on the susceptibility to mitochondrial permeability transition pore (MPTP) induction in streptozotocin (STZ)-induced hyperglycemia. Twenty-four young male Wistar rats were randomly assigned into sedentary citrate (SED+CIT), sedentary type I diabetes (SED+STZ; 50mg/kg), T+CIT (14-week treadmill running, 60min/day) and T+STZ (injected 4weeks before training). After 18weeks, isolated heart mitochondria were used for in vitro oxygen consumption and transmembrane potential (∆Ψ) assessment. Cyclosporin-A (CyclA)-sensitive osmotic swelling and Ca(2+) fluxes were measured to study MPTP susceptibility. Voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), cyclophilin D (CypD), transcription factor A (Tfam), Bax, Bcl-2 contents, caspase-3 and -9 activities were determined. In the sedentary group, long-term severe hyperglycemia decreased state 3, CCCP-induced uncoupling and increased oligomycin-inhibited respiration, state 4 and lag phase with glutamate-malate. A decreased state 3 and state 4 with succinate were observed. Moreover, hyperglycemia decreased Ca(2+) uptake and increased CyclA-sensitive Ca(2+) release and Ca(2+)-induced mitochondrial swelling. The oxygen consumption and ∆Ψ parameters impaired by long-term severe hyperglycemia were reverted by endurance training (SED+STZ vs. T+STZ). Training increased mitochondrial Ca(2+) uptake and decreased Ca(2+) release in hyperglycemic groups. Additionally, endurance training reverted the hyperglycemia-induced CypD elevation, attenuating decrease of ANT, VDAC and Tfam. Moreover, training prevented the STZ-induced elevation in Bax, Bax-to-Bcl-2 ratio, caspase-3 and -9 and the increased Bcl-2. Endurance training reestablished heart mitochondrial respiratory dysfunction caused by long-term severe hyperglycemia and reduced the increased susceptibility to MPTP induction probably by modulation of MPTP regulatory proteins.

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Authors
Lumini-Oliveira, J., Magalhães, J., Pereira, C. V., Moreira, A. C., Oliveira, P. J., & Ascensão, A.
Affiliations
  • Universidade do Porto (PT)
  • Centro de Neurociências e Biologia Celular (PT)
Corresponding author
Ascensão, António
ORCID
Venue
Mitochondrion
Publisher
Elsevier BV
Published
2011-01
Volume
11
Issue
1
Pages
54-63
ISSN
1567-7249 (ISSN-L)
DOI
10.1016/j.mito.2010.07.005
OpenAlex
W2079881379
Cited by
66
References
65
Citations by year
2026: 1 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 2 · 2016: 4 · 2015: 10 · 2014: 7 · 2013: 8 · 2012: 9
FWCI
3.12
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Mitochondrion (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
endurance training, cardiac mitochondrial dysfunction, mitochondrial permeability transition, hyperglycemia, type 1 diabetes, streptozotocin-induced diabetes, mitochondrial calcium handling, cyclophilin D, adenine nucleotide translocase, voltage-dependent anion channel, Bax/Bcl-2 ratio, caspase-3, caspase-9, apoptosis, mitochondrial respiration, membrane potential
MeSH terms
Mitochondrial Permeability Transition Pore, Animals, Diabetes Mellitus, Experimental, Energy Metabolism, Gene Expression Regulation, Humans, Hyperglycemia, Male, Membrane Potentials, Mitochondria, Heart, Mitochondrial Swelling, Motor Activity, Physical Endurance, Severity of Illness Index, Signal Transduction, Rats, Wistar, Apoptosis, Cell Respiration, Mitochondrial Membrane Transport Proteins, Rats

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