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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2005; 51(1): 33-42


The influence of no on the efficiencyof oxygen usage by working skeletalmuscle under its fatigue

A.Y. Boguslavskiy, Dmitrieva A.V., Sagach V.F.

    О.О. Bogomolets Institute of Physiology National Academyof Sciences of Ukraine, Kyiv


Abstract

The influence of NO on the efficiency of oxygen usage by a skeletal muscle under fatigue of dog’s gastrocnemius muscle was investigated. In control experiments was shown, that 10 short-term (30'’) electrical stimulation (8 Hz, 5 ms, 20 V) with 5" interval resulted in significant reduction of the muscle contraction force (more than 40 %) and increased considerably oxygen cost of muscle gastrocnemius work (more than 130 %) compared to the initial parameters. The registered depression of the muscle contraction force testified to development of gastrocnemius muscle fatigue, accompanied by mitochondrial factor (MF) appearance in blood from femoralis vein, which, as shown by us earlier, is a marker of the mPTP opening. Injection of L-NMMA, a NOS inhibitor (2.7 mg/kg, i.а.) resulted in pronounced fall (more than 1.5 times) of the initial force parameters, in comparison with the control experiments. Under these conditions the magnitude of oxygen cost of gas- trocnemius muscle work exceeded control parameters considerably. The development of gastrocnemius muscle fa- tigue under L-NMMA action was accompanied, as well as in the control condition by the mPTP opening. The preliminary injection of sodium nitroprusside, a NO donor (0.2 mg/kg, iv) prevented a fall of muscle contractions force and considerable inhibition of oxygen usage efficiency by gastrocnemius muscle under conditions similar to control. Furthemore, gastrocne- mius muscle fatigue was not developed, and MF concentration in blood from femoralis vein was much lower, than in the control experiments, that testified to absence of the mPTP opening. Apparently, preliminary short-term (30") electrical stimulation (8 Hz, 5 ms, 20 V) with 2' interval, created the precondition effect and raised the level of authentic NO. Un- der these conditions, as well as under preliminary injection of the NO donor, we did not register the marked inhibition of oxygen usage efficiency and development of gastrocnemius muscle fatigue. At the same time, MF in blood from v. femoralis was practically absent, that testify to absence of the mPTP opening. Thus, NO in physiological concentration by inhibi- tion of mPTP opening, can prevent decrease of oxygen usage efficiency and development of the working skeletal muscle fatigue.

References

  1. Агаджанян Н.А., Багиров М.М., Березовский В.А.и др. Словарь-справочник по физиологии ипатофизиологии дыхания. – К: Наук. думка, 1984.–256 с.
  2. Надточій С.М., Богуславський А.Ю., Сагач В.Ф.Вивчення стабільного фактору мітохондріальногопоходження in vivo // Фізіол. журн. – 2003. – 49,№5.– С.25–31.
  3. Сагач В.Ф., Богуславський А.Ю., Дмитрієва А.В.,Надточій С.Н. Роль NO та мітохондріальної пори врегуляції кисневих режимів працюючого скелетногом’яза // Там само. – 2004. – 50, №2. – С.19–26.
  4. Сагач В.Ф., Вавілова Г.Л., Струтинська Н.А.,Акопова О.В. Вплив індукторів та інгібіторівмітохондріальної пори на її утворення та навивільнення неідентифікованого мітохондріальногофактора // Там само. –2003. – 49, №1. – С. 3–12.
  5. Сагач В.Ф., Киндыбалюк А.М. О роли эндотелия вразвитии функциональной гиперемии скелетныхмышц // Бюл. эксперим. биологии и медицины. –1991. – 112, № 11. – С. 453–456.
  6. Сагач В.Ф., Шиманська Т.В., Надточій С.М.Вивчення ролі оксиду азоту у змінах споживаннякисню та кисневої вартості роботи серцевого м’яза// Фізіол. журн. – 2000. – 46, №2. – С.33–38.
  7. Сагач В.Ф., Шиманська Т.В., Надточій С.М. Фактор,який вивільнюється під час реперфузії ішемі-зованого серця, може бути маркером відкриттямітохондріальної пори // Там само. – 2003. – 49,№4. – С.6–12.
  8. Balon T.W., Nadler J.L. Evidence that nitric oxide in-creases glucose transport in skeletal muscle // J. Appl.Physiol.– 1997.– 82.– P.359–363.
  9. 9. Beresewicz A., Maczewski M, Duda M. et al. Effectof classic preconditioning and diazoxide on endothelialfunction and O2– and NO generation in the post-is-chemic guinea–pig heart // Cardiovasc. Res. – 2004 –63, № 1. – Р.118–129.
  10. 10. Brookes P. S., Salinas E. P., Darley-Usmar K. et al.Concentration-dependent effect of nitric oxide on mi-tochondrial permeability transition and cytochrom crelease // J. Biol. Chem. – 2000. – 275, 27. – P.20474–20479
  11. Crompton M., Barksby E., Johnson N., Capano M.Mitochondrial intermembrane junctional complexes andthei involvement in cell death // Biochimie. – 2002, –84. – P.143–152.
  12. Endo T., Imaizumi T., Tagawa T. et al. Role of nitricoxide in exercise-induced vasodilation of the forearm // Circulat. – 1994. – 90. – P. 2886–2890.
  13. Halestrap A., Mcstay G., Clarke S. The permeabilitytransition pore complex: another view // Biochimie. –2002. – 84. – P.153–166.
  14. Hausenloy D.J., Yellon D.M., Duchen M.R. et al. Pre-conditioning protects by inhibiting the mitochondrialpermeability transition // Amer. J. Physiol. HeartCirculat. Physiol. – 2004. – 109. – P.1714–1717.
  15. Koge P., Goldhaber J., Weiss J. Phenylarsine oxide in-duces mitochondrial permeability transition, hyper-contracture, and cardiac cell death // Ibid. – 2001. –280. – P.H2203–H2213.
  16. Loke K.E., Laycock S.K., Mital S. et al. Nitric oxidemodulates mitochondrial respiration in failing humanheart // Circulat. – 1999. – 100. – P. 1291–1297.
  17. Marechal G., Gailly P. Effects of nitric oxide on theof skeletal muscle // Cell. Mol. Life Sci. –1999. – 55(8–9). – P. 1088–1102.
  18. Moncada S., Erusalimsci J. Does nitric oxide modulatemitochondrial energy generation and apoptosis? // Natu-ral. Reviews. Mol. Cell. Biol. – 2002.– 3.– P.214–220.
  19. 19. Stamler J.S., Meissner G. Physiology of nitric oxide inskeletal muscle // Physiol. Rev. – 2001. – 81.– №1.– P. 209–237.
  20. 20. Xie Y., Shen W., Zhao G. Role of endothelium-derivedoxide in the modulation of canine miocardial mi-tochondrial raspiration in vitro. Implications for thedevelopment of heart failure // Circulat. Res. – 1996. –73, № 3. – P.381–387

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