ISSN 2415-3060 (print), ISSN 2522-4972 (online)
JMBS
  • 26 of 59
Up
JMBS 2016, 1(1): 120–125
https://doi.org/10.26693/jmbs01.01.120
Biology

Difference of Structural Reconstructions of Myocardium in Acute and Long-Term Physical Training in Experiment

Bezugla V.V.1, Rozova K.V.2, Vinnychuk Yu.D.1
Abstract

The adaptation of sportsmen to physical training is accompanied by changes in morphofunctional indicators, the mechanisms of metabolism regulation, and the functioning of the blood circulation. The long-term physical training leads to an increase in the power of mechanisms of the functional respiratory system (FRS). The increase in a load on FRS causes the formation of the hypoxia training, which is revealed on all levels of organism. The study of the mechanisms of adaptation under the indicated hypoxia, which are related to the ultrastructure and the functioning of the mitochondrial apparatus of organism’s cells, is of significant importance, since the damage of mitochondria, which are organelles most sensitive to hypoxia, causes violations in the energy supply, antioxidant protection, and stability of membranes. Myocardium is one of the most active consumers of oxygen in organism. Therefore, the detailed research of its functional state is necessary for the detection of signs of the disadaptation to loads and the prevention of the development of an overstrain and pathological states in sportsmen. Therefore, it is actual to study the peculiarities of changes in the mitochondrial apparatus and the capillarization of myocardium tissues at the modeling of acute and long-term physical training in experiment. The studies are executed on rats-males of the Wistar line 220-250 g in mass. Their physical training was modeled by means of the swimming of rats in a warm water. Under the acute physical training, rats were swimming for 30 min with the additional weight equal to 7.0±3.0 % of body’s mass; the long-term physical training was modeled by a daily 30-min swimming with the analogous additional weight for 3 weeks. The degree of hypoxia was determined by РО2, рН of blood, and the level of consumption of oxygen in percents of VO2max. The determination of the rate of consumption of oxygen was carried out by the manometric method. In morphological and morphometric studies, we used specimens of the heart tops of animals. The preparations for the electron-microscopic studies were produced by the commonly accepted method and studied on an electron microscope, by determining the numbers of functioning capillaries and mitochondria. It is shown that an acute physical training induces the following destructive changes in tissues of rats’ myocardium: edema and destruction of the sarcolemma of cardiomyocytes, destruction of the endothelium of capillaries, and loosening and breaking of the transverse striation of myofibrillae. The negative changes occur also in the ultrastructure of cells: the vacuolization, increase in the number of structurally changed mitochondria, and fragmentation of cristae. This indicates the breaking of the integrity and the dysfunction of the cardiac muscle cells mitochondrial apparatus. The long-term physical training is characterized by structural reconstructions of the adaptive character with reliable increase in the number of functioning capillaries of myocardium tissue (21.2±2.1 unitμm-2 as compared with 14.3±1.2 unitμm-2 under acute training); as well as the increase in the number (15.0±1,3 unitμm-2 as compared with 9.0±0,6 unitμm-2 under acute training) and total area of mitochondria in volume of tissue (14.2±1.0 μm2 as compared with 11.0±0.8 μm2 under acute training). Such changes evidence to an increase in the blood circulation intensity in the microcirculation and the energy power of the mitochondrial apparatus of rats’ myocardium cells, which favor a decrease in manifestations of secondary tissue hypoxia.

Keywords: physical training, myocardium, mitochondrial apparatus, capillarization of tissue

Full text: PDF (Ukr) 171K

References
  1. Emelyanov NA. Izmerenie vyideleniya ili pogloscheniya gazov volyumetricheskim metodom s pomoschyu apparata Varburga. Ukrainskiy biohimicheskiy zhurnal. 1971; 43 (3): 390-2.
  2. Zagoruyko GE. Zkaonomernosti strukturnoy perestroyki stromyi miokarda pri adaptatsii k tkanevoy gipoksii i kraniotserebralnoy gipotermii. Kriobiologiya. 1990; 2: 3-10.
  3. Kaladze NN, Zagorulko AK, Kutozova LA, Novikov NYu. Morfogenez strukturyi kletok i sosudov miokarda u eksperimentalnyih zhivotnyih s modelirovannyim URA. Tavricheskiy mediko-biologicheskiy vestnik. 2010; 13 (2): 4-7.
  4. Karpman VL. Serdtse i sport: ocherki sportivnoy kardiologii. M: Meditsina; 1968. 254 s.
  5. Karupu VYa. Elektronnaya mikroskopiya. K: Vischa shkola; 1984. 208 s.
  6. Kirichek LT, Scherban NG. Metabolitnyie i metabolitotropnyie preparatyi v sisteme stressoprotektsii. Mezhdunarodnyiy meditsinskiy zhurnal. 2012; 2: 103-8.
  7. Kolchinskaya AZ, Tsyiganova TN, Ostapenko LA. Normobaricheskaya intervalnaya gipoksicheskaya trenirovka v meditsine i sporte. M: Meditsina; 2003. 407 s.
  8. Kudrya ON, Belova LE, Kapelevich LV. Adaptatsiya serdechno-sosudistoy sistemyi sportsmenov k nagruzkam raznoy napravlennosti. Byulleten sibirskoy meditsinyi. 2012; 3: 48-53.
  9. Lukyanova LD. Molekulyarnyie mehanizmyi tkanevoy gipoksii i adaptatsiya organizma. Fiziol zhurn. 2003; 49 (3): 17-35.
  10. Lukyanova LD, Dudchenko AM, Tsyibina TA, Germanova EL. Regulyatornaya rol mitohondrialnoy disfunktsii pri gipoksii i ee vzaimodeystvie s transkriptsionnoy aktivnostyu. Vestnik RAMN. 2007; 2: 3-13.
  11. Nevzorova OF, Taraban IA, Nevzorov VP. Submikroskopicheskaya otsenka patogeneza poliorgannoy nedostatochnosti. Harkivska hirurgichna shkola. 2010; 4 (42): 54-62.
  12. Osipov VP, Lukyanova EM, Antipkin YuG, i dr. Metodika statisticheskoy obrabotki meditsinskoy informatsii v nauchnyih issledovaniyah. K: Planeta lyudey; 2002. 200 s.
  13. Pokotilo PB. Ultramikrosklpichne doslidzhennya mitohondrialnogo aparatu kardiomiotsitiv intaktnih schuriv. Svit meditsina ta biologiyi. 2014; 2 (44): 148-51.
  14. Rozova EV, Tavolzhanova TI. Vliyanie morfofunktsionalnogo sostoyaniya tkaney legkih i serdtsa na osnovne parametryi vneshnego dyihaniya, krovoobrascheniya i gazoobmena pri gipoksicheskih sostoyaniyah razlichnogo tipa. Zagalna patologiya ta patologichna fiziologiya. 2010; 5 (3): 109-13.
  15. Ryamova KA, Rozenfeld AS. Osobennosti dyihaniya mitohondriy pri gipoksii i atsidoze. Vestnik Yuzhno-Uralskogo gosudarstvennogo universiteta. Seriya: Obrazovanie, zdravoohranenie, fizicheskaya kultura. 2008; 16: 31-5.
  16. Smulskiy VL, Zemtsova II, Sutkovoy DA. Povyishenie ustoychivosti organizma k napryazhennoy myishechnoy deyatelnosti putem korrektsii sostoyaniya ego antioksidantnoy sistemyi. Nauka v olimpiyskom sporte. 1999; Spets vip: 87-93.
  17. Tashke K. Vvedenie v kolichestvennuyu tsitogistologicheskuyu morfologiyu. Buharest: Izd-vo Akademii SRR; 1980. 192 s.
  18. Uilmor D. Kostill D. Fiziologiya sporta i dvigatelnoy aktivnosti. K: Olimpiyskaya literatura; 1997. 432 s.
  19. Filippov MM. Protsess massoperenosa respiratornyih gazov pri myishechnoy deyatelnosti. Stepeni gipoksii zagruzki. Vtorichnaya tkanevaya gipoksiya. Pod red. AZ Kolchinskoy. K: Naukova dumka; 1983. s. 197-216.
  20. Breen E, Tang K, M. Olfert, Amy Knapp, and Peter Wagner. Skeletal muscle capillarity during hypoxia: VEGF and its activation. High Alt Med Biol. 2008; 9 (6): 158-66. https://doi.org/10.1089/ham.2008.1010
  21. Delavar H, Nogueira L, Wagner P, Michael C. Hogan, Daniel Metzger, Ellen C. Breen. Skeletal myofiber VEGF is essential for the exercise training response in adult mice. Am J Physiol Regul Integr Comp Physiol. 2014; 306 (6): R586-95. https://doi.org/10.1152/ajpregu.00522.2013
  22. Hoppler H, Vogt M. Muscle tissue adaptation to hypoxia. J Experim Biol. 2001; 204 (18): 3133-9. https://www.ncbi.nlm.nih.gov/pubmed/11581327
  23. Hoppler H, Fluck M. Plasticity of skeletal muscle mitochondria: structure and function. Med Sci Exerc. 2003; 35 (1): 95-104. https://doi.org/10.1249/01.MSS.0000043292.99104.12
  24. Kay L, Nicolay K, Wieringa B, et al. Direct evidence for the control of mitochondrial respiration by mitochondrial creatine kinase in oxidative muscle cells in situ. J Biol Chem. 2000; 275 (10): 6937-44. https://doi.org/10.1074/jbc.275.10.6937
  25. Kraus RM, Stallings HW 3rd, Yeager RC, Gavin TP. Circulating plasma VEGF response to exercise in sedentary and endurance-trained men. J Appl Physiol. 2004; 96 (4): 1445-50. https://doi.org/10.1152/japplphysiol.01031.2003
  26. Lesnefsky E, Moghaddas S, Tandler B, Kerner J, Hoppel CL. Mitochondrial disfunction in cardiac disease: ischemia-reperfusion, aging, and heart failure. J Mol Cell Cardiol. 2001; 33 (1): 102-12. https://doi.org/10.1006/jmcc.2001.1378
  27. Magalhães J, Gonçalves I, Lumini-Oliveira J, et al. Modulation of cardiac mitochondrial permeability transition and apoptotic signaling by endurance training and intermittent hypobaric hypoxia. Int J Cardiol. 2014; 173 (1): 40-5. https://doi.org/10.1016/j.ijcard.2014.02.011
  28. Park SY, Gifford JR, Andtbacka RH, Joel D. Trinity, John R. Hyngstrom, Ryan S. Garten, Nikolaos A. Diakos, Stephen J. Ives, Flemming Dela, Steen Larsen, Stavros Drakos, Russell S. Cardiac, skeletal, and smooth muscle mitochondrial respiration: are all mitochondria created? Am J Physiol Heart Circ Physiol. 2014; 307 (3): H346-352. https://doi.org/10.1152/ajpheart.00227.2014
  29. Shey-Shing S, Dirksen R, Pugh E Jr. The 65th Symposium of the Society for General Physiologists: Energizing research in mitochondrial physiology and medicine. J Gen Physiol. 2011; 138 (6): 563-7. https://doi.org/10.1085/jgp.201110739
  30. Siegel AJ, Lewandrowski KB, Strauss HW, Fischman AJ, Yasuda T. Normal post-race antimyosin myocardial scintigraphy in asymptomatic marathon runners with elevated serum creatine kinase MB isoenzyme and troponin T levels. Evidence against silent myocardial cell necrosis. Cardiology. 1995; 86 (6): 451-6. https://doi.org/10.1159/000176922
  31. Wagner PD. The critical role of VEGF in skeletal muscle angiogenesis and blood flow. Biochem Soc Trans. 2011; 39 (6): 1556-9. https://doi.org/10.1042/BST20110646
  32. Zhao YC. Effects of exercise training on myocardial mitochondrial miR-499-CaN-Drp-1 apoptotic pathway in mice. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2015; 31 (3): 259-63. https://www.ncbi.nlm.nih.gov/pubmed/26387191