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International Journal of Physiology and Pathophysiology
SJR: 0.106

ISSN Imprimer: 2155-014X
ISSN En ligne: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

International Journal of Physiology and Pathophysiology

DOI: 10.1615/IntJPhysPathophys.v7.i1.20
pages 9-18

Long-term Exercise Training Improves Heart Function in Rats by NO-Dependent Decrease in Mitochondrial Pore Sensitivity to Calcium

Snizhana V. Chorna
Bogomoletz Institute of Physiology, National Academy of Science of Ukraine, Kyiv
Nataliya A. Strutynska
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Olena M. Semenykhina
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Sergiy O. Talanov
Bogomoletz Institute of Physiology of the National Academy of Sciences of Ukraine, Kyiv, Ukraine
Viktor E. Dosenko
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Anatoliy V. Kotsuruba
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Galyna L. Vavilova
Bogomoletz Institute of Physiology, National Academy of Science of Ukraine, Kyiv
Vadim F. Sagach
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

RÉSUMÉ

The effects of long-term exercise training on the functional state of isolated by Langendorff heart were investigated in old rats during ischemia-reperfusion, as well as the sensitivity of calcium-induced mitochondrial permeability transition pore (MPTP) opening, and the role of NO-dependent mechanisms of pore-formation. Myocardial contractile function in reperfusion and oxygen metabolism were less pronounced in old rats adapted to long-term exercise training, indicating positive effect of the latter. It has been revealed that MPTP sensitivity to its inductor (Ca2+ ) in the heart of old trained rats decreases due to an increase in the threshold ion concentration 1.5 − 2 times, compared with untrained animals, leading to swelling of organelles. In the heart mitochondria of trained adult rats, the activity of constitutive NO-synthase (cNOS) increases almost twice compared with the control value (6.02 ± 008 versus (3.64 ± 0.27) pmol / min mg protein, P ≤ 0.05), and the activity of inducible NO-synthase (iNOS) slightly increases. Pore-formation in old trained animals is regulated through the significant decrease in iNOS activity compared with the control old rats (9.25 ± 1.24 versus (12.29 ± 3.11) pmol/min·mg protein, P ≤ 0.05) on the background of a slight increase in cNOS activity. We suggest that a decrease in MPTP sensitivity to opening results from enhanced NO production, pointing to its role as an inhibitor of pore-formation during exercise training. In trained animals of all ages, MPTP sensitivity to Ca2+ increases when NO production in the heart is reduced by injection of NO synthase inhibitor N (omega)-nitro-L-arginine methyl ester (L-NAME) in a dose of 10 mg/kg. In addition, by the method of real-time polymerase chain reaction, we have shown that expression of eNOS mRNA in the heart is significantly greater compared to nNOS mRNA and iNOS mRNA expression. In particular, in the heart of adult trained rats, expression of nNOS mRNA increased 5 times, iNOS mRNA expression increased 24 times (P < 0.05), and expression of eNOS mRNA decreased 3.5 times compared with untrained rats. In contrast, in the heart of old trained rats, expression of nNOS mRNA decreased 4 times (P < 0.05), and iNOS mRNA decreased 2 times, compared with the old untrained animals. In the heart of old rats, training promoted the restitution of eNOS mRNA expression to the values observed in control adult animals. Taken together, the data obtained suggest that long-term exercise training improves the functional state of the heart during aging, including its contractile function. Moreover, exercise training increases body resistance to oxidative stress under reperfusion injury due to reduced MPTP sensitivity to calcium ions in the heart against the background of increased activity of mitochondrial cNOS and restitution of eNOS mRNA expression, which ensures nitric oxide synthesis as an endogenous inhibitor of pore-formation.


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