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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.v3.i4.10
pages 299-308

Changes in Arginase-Nitric Oxide Synthase System at Adaptation to Prolonged Exercise Training by Swimming in Adult and Aged Rat Hearts

Anatoliy V. Kotsuruba
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Yulia P. Korkach
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
Olga V. Bazilyuk
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Lyubov G. Stepanenko
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Vadim F. Sagach
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

RÉSUMÉ

We studied the contractile activity of isolated hearts from adult rats adapted to prolonged exercise training by swimming. It has been shown that stimulation of NO production in the mitochondrial compartment of the heart from trained adult rats resulted in the left ventricular force increase, the myocardial stiffness decrease, and both systolic and diastolic heart function improvement. In the heart mitochondria of adult rats trained by swimming, an activation of all examined enzymes of nitric oxide synthesis, namely, inducible, constitutive NO-synthase (de novo synthesis) and nitrate reductase (nonoxidative salvage synthesis) has been established, whereas in old animals, only oxidative enzymes of de novo pathways were stimulated. Exercise training significantly reduced the mitochondrial pools of nitrate anion in adult rats, while in old ones the contents of urea, nitrite anion pools did not change in that situation. Mitochondrial H2O2 pools after training in adult rats increased, while in the old animals those pools, conversely, decreased. Exercise training resulted in a significant increase in oxygenation index in the mitochondria of adult rats and a decrease in the activity of mitochondrial arginase II. The results give reason to believe that swimming as a physical training stimulates N0 production in the mitochondria of adult and old rats, and therefore, it can be considered effective non-pharmacological correction of the age-specific dysfunction of the heart.


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