Angelov, A.

Ganchev, T.

Popdimitrov, I.

Tzekov, Tz.

English

Varna Medical University Press: Journals

1 M O R P H O L O G I C A L C H A N G E S I N T H E M Y O C A R D I U M A N D S K E L E T A L M U S C U L A T U R E W I T H E X T R E M E P H Y S I C A L L O A D I N G S U N D E R E X P E R I M E N T A L C O N D I T I O N S A. Angelov, I . Popdimitrov, T z . Tzekov, T. Ganchev Key-words: myocardium — skeletal musculature — morphology — physical loading — protein metabolism Recent ly , the interest in functional and morphological myocardia l alte­rations result ing from long-lasting and exhausting physical loading increases signif icantly (7—9). There are also single, predominantly functional, bioche­mica l and ultrastructural investigations of the striated musculature of the lower l imbs in Marathon runners (fO, 11). However, parallel morphological studies of both myocardium and skeletal str iated musculature under condit ions of long-lasting exhausting physical loading are s t i l l absent. The purpose of the present work is to study the morphological a l te ra t ions in the myocardium and striated musculature wi th extreme physical loading and the influence of some substances improving protein metabolism. Material and methods A total of 66 white rats of both sexes wi th mean body weight at the beginning of the t r i a l of 150— 160 g were morphologically studied. A l l the animals were phys ica l ly loaded by means of swimming in cold water (at 10°C) after the method of A v a k y a n and Sh i ryan in (1977). P r e l im ina ry testing of untra ined an imals showed an average endurance of 28 m i n . Exper imenta l animals of a l l the groups underwent t r a in ing for 15 or 20 days twice daily at every 5 hours w i t h g radua l ly increasing t ra in ing duration from 10 up to 40 m i n . A n i m a l s were divided into three groups. E a c h group consisted of three subgroups as fol lowed: F i r s t group (19 animals) wi th 20 t ra in ing days inc luding: I s t a) subgroup (5 rats) — they were given perorally a preparation based on protein hydroly-sate «Hydropro t» — «0—80—G» at a dofee of 60ц g/100 g b. w. I s t b) subgroup (6 rats) — they were given perorally Bionabol at a dose of 30 ^tg/lOOg b. w. I s t c) subgroup (8 rats) — they were given placebo. Second group (23 animals) w i t h 15 t r a in ing days including: I I n d a) subgroup (8 rats) — treatment w i t h «0—90—G» at a dose of Щ g/100 g b. w. I I n d b) subgroup (7 rats) — treatment w i th Bionabol at a dose of 30pi g/.lOO g b. w. I I n d c) subgroup (8 rats) — given placebo. T h i r d group (24 animals) with 20 training days including: I I I r d a) subgroup — the same as I I n d a) subgroup Morphological changes in the. I I r d b) subgroup (8 rats) — the same as I I n d b) subgroup I I r d c) subgroup — the same as I F d c) subgroup. Animals from the first and second groups continued to swim after the end f the experiment unt i l complete exhaustion and death (for 5 -— 11 hours i n arious groups). Animals from the th i rd group were put in hypobaric chamber ith a pressure of 0.8 atmospheres (corresponding to 13 873 m altitude) u n t i l eath (for 9 — 1 5 min) . Mater ia l for histologic examinat ion from visceral organs and skeletal usculature of shoulder girdle was taken immediately after death. Paraf f in ections were stained wi th H E , Azan after K r u c h a j , toluidine b lau at p H 2 and 4, P A S , P T A H and after Lee for fuxinophil ic necroses. Myocardial pieces ere f ixed in glut&r aldehyde and osmium acid and embedded in D u r c o p a n о be electron microscopically examined. esults and discussion The morphological investigation of the myocardium and skeletal museu-ature reveals one-type morphological alterations wi th certain quanti tat ive ifferences between single groups. Myocyte hypertrophy (thickness up to 20 r i m) and ischemic changes can be established in the myocardium. Ischemia is manifested by myofibr i l lar undu-ations and dispersed fuxinophilic necroses mainly in subendocardial zones fig. 1). Besides in 12 animals ( in 18 per cent of them) microinfarctions of d i ­fferent duration are found out. Some of these infarctions undergo an organiza­t ion process. Ul t ras t ruc tura l ly , an outlined mitochondrial hyperplasia and hypertro-phia in the myocardium comes to the fore. Mitochondrial arrangement in re la­tion to myofibrils is destroyed. The count of mitochondrial cristae increases. However, in some places cr is tolysis and matr ix l ightening can be established. Besides there is a subsareolemmal oedema, appearance of single m y e l i n figures and l ip id inclusions as wel l as endoplasmic ret iculum di latat ion (fig. 2) . G l y ­cogen grhnulae in myocyte cytoplasm are strongly reduced and even absent. Nuclei possess deep invaginations of the nuclear membrane and marg ina l ly located chromatin. There are severe destructive shanges including also a complete necrosis in single myocytes. Capi l la ry endothelial cells show an increased pinocytotic ac t iv i ty , vacuo­l iza t ion and formation of luminal protrusions sometimes completely remoted from endothelial cel ls . Sludge and thrombocyte aggregations are observed as manifestation of Theological disturbances. Severe morphological alterations are sound out in the striated musculature of the shoulder girdle . I t is the musculature wi th the most intensive loading in the experiment carr ied out. Myofibri ls are hypertrophic and their thickness reaches here and there up to 45(t m. Manifested ischemic changes are also ob­served — contracture changes, disappearing of striatedness, fuxinophil ic ne­croses and even almost complete myocyte destruction in single regions (f ig. 3 ) -Comparisdn between single groups demonstrates that myocardia l infarc­tions ( i . e. microinfarctions) develop more often in animals given placebo (e. g-> there are 4 myocardial infarctions in the'subgroup 1-е ( including a total of 8 rats) than in animals given «0—80—G» ( in the subgroup I -a (one rat out of F i g . 2. Aiyelin-like body formation in the cytoplasm of myocardial myocytes. Electronogram. Magn. x 40000. ' 7 6 iMorphofojfcal changes in the . . . has a microinfarction) and in rats given Bionabol (in t h i subgroup I-b (no farctions are found). There are certain differences between anitnals from various groups when aximal endurance is concerned. Endurance is the strongest one in animals m the first g ro in and given Bionabol (for 11. 16 hours) or placebo (for и) ig. 3. Contracture alterations, disappearance of striatedness and fuxinophilic "necroses in I skeletal musculature. Stain after Lee. Magn. 10 x 16. ours) during a 20-day training. Differences are smaller in the second group wi th a 15-day training). Animals given Bionabol show the strongest endurance, oo (7.26 hours long). These results obtained show that extreme physical loading for many hours duces severe irreversible structural damages not only in the myocardium but lso in the skeletal musculature of trained rats. I t is known that sudden death can set in in Marathon runners. E c h o -ardiographically, data about depression of left ventr icular contracti le fun-tion combined wi th a sharp serum creatinine-kinase level increase in such thletes has been established. I t is accepted that creatinine-kinase increase is ue to the damage of skeletal musculature mainly (8) . On the other hand, some xperimental investigations on untrained rats (7, 8) immediately after exhau-ting swimming (about 3 hours long at watet temperature of *32°C) indica te hat in myocardium interst i t ial oedema, swelling and oedema of mi tochondr ia ncl contracture changes in sarcomeres without necroses set in . I n the present study we found out that despite prel iminary t r a i n i n g exha­usting and long-lasting (for 5—11 hours) swimming in cold water (at .0°C) caused considerably more severe alterations including even dispersed fuxiono-h i l i c necrosses in the myocardium and striated musculature. Undoubtedly, some of the changes observed such as mitochondrial hyper-lasia and well-outlined microinfarctions some of which are already at the stage of organization have set in during the intensive t ra ining process. 38 A. Angelov, I . Popdimitrov, T z . Tzekov, T. Ganchev Morphological myocardial alterations do not s ignif icantly differ from le­sions occurred after severe hypoxia , shock, and under hypobaric conditions (2—4,6). Severe hypoxia presents probably a common pathogenetic factor i n a l l these states. Long-lasting exhausting physical loading combined wi th an increase of the requirements of oxygen in myocardium and striated musculature on the background of severe metabolic changes, acidosis and hypercateehola-minaemia (6) makes these organs par t icular ly vulnerable. Cold water acting as a stress factor and contributing to an increased liberation of endogenous ca­techolamines plays a certain role, too. Severe microcirculatory dis tyrbances in visceral organs resulting in formation of microthrombi wi th different lo­cal izat ion in 38 per cent of the animals (unpublished data) thus arguing for development of intravascular coagulation are undoubtedly important, too (5) . A l l that enables us to accept that severe ischemic changes in myocardium and striated musculature have a complex genesis. Both microcircula tory and meta­bolic disorders combined wi th hypercatecholaminaemia intensify hypoxia which appears during long-lasting physical loading and present the most important factors in this genesis. Our results demonstrate also that dur ing extreme long-lasting p h y s i c a l loading means improving protein metabolism do not influence essent ia l ly upon the degree of lesions, i . e. their protective effect is reduced to a m i n i m a l l e v e l . These morphological alteration i n myocardium and skeletal musculature are irrevocable and, therefore, i t cannot be expected that they can be influenced by means which improve protein metabolism. R E F E R E N C E S 1. А в а к я н, О. М., Г . А. Ш и р я н и н. Бюлл. эксперим. виол, и мед., 1977, № 9, 375—377. — 2. Г о р д е л а д з е , Д . Г. Морфология сердца при разных механизмах смерти. Тбилиси, Мецниерба, 1976. - З . С е м е н о в а , Л . А., Ю. Г. Ц е л л а р и у с. Ультра структур а мышечных клеток сердца при очаговых метаболических повреждениях. Новосибирск, Наука , Сибирское отделение, J978. —4. Ц е л л а р и у с, Ю. Г., Л . А. С е м е н о в а . Гистопатология очаговых метаболических повреждений миокарда. Ново­сибирск, Наука , Сибирское отделение, 1972. — 5. Н а г d a w а у, R . М. Лтег. J. Car­diol., 20, 1967, 161 —173.— 6. Н е с h t, A . Einfuhrung in experimentelle Grundlagen der modernen Herzmuskelpathologie. Jena, G . Fischer Verlag, 1970, 502 p. — 7. L u с е n a,, M. C , R . P a n i a g u a . Acta Cardiol., 39, 1984, No 1, 41—54. — 8. L u с е n a, M. C . R . P a n i a g u a . Acta Cardiol., 39, 1984, 463—477. — 9. N i е m е 1 а, К- О., I . J . P a l a t s i , M. J l I k a h e i m o , J . . T . T a k k u n e n , J . J . V u o r i . Circulation 70, 1984, No 3, 350—356. — 10. S с h m i d t, S. A . , K- — S. P i е p е r, D . A p p е 1 t' H . В u h 1. Wiss. Z. Friedrich-Schiller-Univ. Jena, Math. — Naturwiss, R.4 32, 1983,» No 4—5, 609—615. — 11. W a r h o 1, M. J . , A . J . S i e g e l , W. J . E v e n s , L . М. S i l v e r m a n . Amer. J. Pathol., 118, 1985, No 2, 331—339. Morphological changes in the. МОРФОЛОГИЧЕСКИЕ ИЗМЕНЕНИЯ МИОКАРДА И ПОПЕРЕЧНО-ПОЛОСАТОЙ МУСКУЛАТУРЫ ПРИ ЭКСТРЕМАЛЬНЫХ ФИЗИЧЕСКИХ НАГРУЗКАХ В ЭКСПЕРИМЕНТАЛЬНЫХ УСЛОВИЯХ ^тАнгглов, И. Поп) ими трое, Ц. Цеков, Т. Ганчев ИРзю М Е Ир*' - : - ' ' Li 4 * -и;- нимЛ*1Э Морфологически исследовано 66 белых крыс, тренированных предварительно плавать В течение 15—20 дней. Животные были распределны в три основные группы: получавшие препшат ни блзе а) белкового гидролизата («0—80—Г»), б) бионабола, в) плацебо. После Ько 14 ш и я тренировочного процесса они оставлялись плавать до ' полного истощения и смерти, или же помещались в гипобзрическую камеру до наступления смерти вследствие асфикеи и. В сердечной мышце животных всех групп обнаруживаются значительные ультраструк-jrypHbie изменения, включающие в себя гиперплазию митохондрией, дилатацию саркоплаз-матического ретикулума, появление липидных вакуол и миелоноподобных фигур. Методом светового микроскопнрования устанавливаются фуксинофильные некрозы, а у некоторых животных и микроинфаркты различной давности. Б поперечно-полосатой скелетной муску­латуре также наблюдается фуксинофильные некрозы и тяжелые контрактурные изменения.-/7°«лученные результаты показывают, что при продолжительной экстремальной физи­ческо/'/ на рузке в миокарде и скелетной мускулатуре наступают необратимые морфологи­ческие увреждения, которые невозможно предупредить средствами, способствующими улуч-ению белкового обмена организма. 

MORPHOLOGICAL CHANGES IN THE MYOCARDIUM AND SKELETAL MUSCULATURE WITH EXTREME PHYSICAL LOADINGS UNDER EXPERIMENTAL CONDITIONS

https://journals.mu-varna.bg/index.php/ssm/article/download/3747/3229

MORPHOLOGICAL CHANGES IN THE MYOCARDIUM AND SKELETAL MUSCULATURE WITH EXTREME PHYSICAL LOADINGS UNDER EXPERIMENTAL CONDITIONS

Abstract

Similar works

Full text

Available Versions

Varna Medical University Press: Journals