Relevance. Early diagnosis of chronic overstress among athletes remains an important problem for coaches and specialists in the field of sports physiology and medicine. The goal is to study in an animal model the dynamics of autoimmune response to physical activity of different duration and intensity and to establish the prospects of the method of determining autoantibodies to cardiomyocyte proteins as an indicator of the morphofunctional state of the heart in the conditions of adaptation to muscle loads. Materials and Methods. The study was conducted in male white rats. Animals were subjected to 9 weeks of training simulated with treadban. The intensity of the load changed the angle of inclination and the speed of the tape. The amount of cardiospecific autoantibodies (auto-AB) to troponin I, to alpha-actin 1, to the human cardiac beta-myosin heavy chain MYH7 was determined in the blood by enzyme immunoassay. The relative heart mass was measured. Histomorphological assessment of cardiomyocyte condition was carried out. Statistical processing was carried out using the Student and Mann-Whitney criteria. Results and Discussion. Animal training was accompanied by moderate cardiac hypertrophy of pathological changes in cardiomyocytes. Heart weight increased by 6.9 %; 10.6 %; 12.9 % in the dynamics of 6-8-9 weeks of training. Concentrations of auto-AB to troponin I and to alpha-actin 1 were characterized by cyclicity, manifested by an increase in week 2 and a decrease by the 8th and 9th weeks of training. In the dynamics of 0-2-8-9 weeks of the experiment, the amount of auto-AB to troponin I was: 3.10.3; 4.20.9; 2.10.2; 2.00.04 ng/ml. For auto-AB to actin: 26.71.2; 31.31.4; 13.71.8; 12.11.6 ng/ml, respectively. The level of auto-AB to beta-myosin was manifested by a decrease in the dynamics of 0-6-9 weeks of training and amounted to: 16.30.9; 10.91.5; 8.20.8; 9.6 0.9 ng/ml. Conclusion. The results of determining cardiospecific auto-AB demonstrate a clear response of the immune system to the processes taking place in cardiomyocytes, which makes it possible to recommend further study of the method of determining auto-AB to cardiomyocyte proteins as a diagnostic test of the functional state of the heart muscle during the period of adaptation to physical activity.

Relevance. In conditions of ever-increasing volume of training loads, the frequency of cases of chronic physical overstrain (CPO) among athletes is increasing. It determines the importance of early diagnosis of the formed pathology of the cardiovascular system in order to prevent its further development. The aim of the study was to study the dynamics of autoantibodies to cardiomyocyte proteins using an experimental model of CPO and to determine the prospects of a laboratory method for the determination of autoantibodies for early diagnosis of pathomorphological changes in the heart. Materials and Methods. The study was conducted on male white rats. A treadmill was used to model CPO. In animals, the heart rate was measured, electrical phenomena in the heart were recorded. The content of hemoglobin and erythrocytes was determined in the blood. The level of cardiospecific autoantibodies (auto-AB) to troponin I, to alpha-actin 1, and to the heavy chain of beta-myosin 7B was measured. Heart mass was measured and histomorphological assessment of the state of cardiomyocytes was carried out. Results and Discussion. While modeling CPO, a decrease in body weight of the animals, the development of anemia, and cardiac hypertrophy were recorded. A decrease in body weight by more than 30 % was recorded from days 25 to 35 of the modeled CPO. A decrease in the number of erythrocytes in the blood was noted on day 25 with a peak fall on days 30-35. The mass of heart of animals in the dynamics of 0-15-35 days was 0.39±0.003; 0.41±0.001; 0.44±0.005 g/100 g, respectively. On day 25, sinus tachycardia was recorded in 2 % of the animals. On days 30 and 35, in 10 % of the studied rats, a violation of the processes of repolarization of the left ventricle by the type of subepicardial ischemia was recorded. On the 25th day, fibrosis of the perivascular region was visualized, passing into the interstitial field between the myofibrils. Reticulate structures of connective tissue fibers between cardiomyocytes were found. The period of 30-35 days was characterized by even greater severity of pathomorphological changes: myocardial hypertrophy, moderate myocardial dystrophy, interstitial and perivascular fibrosis. An increase in the number of detectable auto-ABs to cardiomyocyte proteins was noted on the 10th day of the experiment. A multiple increase in autoantibodies to cardiomyocyte proteins was recorded earlier than functional disorders in the heart and morphological changes in cardiomyocytes were detected. Conclusion. The laboratory method for determining auto-ABs to myocardial proteins can be the earliest of the complex methods for diagnosing disorders that are formed in the body in conditions of adaptation to intense and prolonged physical exertion.

Relevance. Early diagnosis of chronic overstress among athletes remains an important problem for coaches and specialists in the field of sports physiology and medicine. The goal is to study in an animal model the dynamics of autoimmune response to physical activity of different duration and intensity and to establish the prospects of the method of determining autoantibodies to cardiomyocyte proteins as an indicator of the morphofunctional state of the heart in the conditions of adaptation to muscle loads. Materials and Methods. The study was conducted in male white rats. Animals were subjected to 9 weeks of training simulated with treadban. The intensity of the load changed the angle of inclination and the speed of the tape. The amount of cardiospecific autoantibodies (auto-AB) to troponin I, to alpha-actin 1, to the human cardiac beta-myosin heavy chain MYH7 was determined in the blood by enzyme immunoassay. The relative heart mass was measured. Histomorphological assessment of cardiomyocyte condition was carried out. Statistical processing was carried out using the Student and Mann-Whitney criteria. Results and Discussion. Animal training was accompanied by moderate cardiac hypertrophy of pathological changes in cardiomyocytes. Heart weight increased by 6.9 %; 10.6 %; 12.9 % in the dynamics of 6-8-9 weeks of training. Concentrations of auto-AB to troponin I and to alpha-actin 1 were characterized by cyclicity, manifested by an increase in week 2 and a decrease by the 8th and 9th weeks of training. In the dynamics of 0-2-8-9 weeks of the experiment, the amount of auto-AB to troponin I was: 3.10.3; 4.20.9; 2.10.2; 2.00.04 ng/ml. For auto-AB to actin: 26.71.2; 31.31.4; 13.71.8; 12.11.6 ng/ml, respectively. The level of auto-AB to beta-myosin was manifested by a decrease in the dynamics of 0-6-9 weeks of training and amounted to: 16.30.9; 10.91.5; 8.20.8; 9.6 0.9 ng/ml. Conclusion. The results of determining cardiospecific auto-AB demonstrate a clear response of the immune system to the processes taking place in cardiomyocytes, which makes it possible to recommend further study of the method of determining auto-AB to cardiomyocyte proteins as a diagnostic test of the functional state of the heart muscle during the period of adaptation to physical activity.

Relevance . Despite the large list of biological markers of cardiovascular diseases, not all have evidence-b ased effectiveness and independent prognostic value. Laboratory diagnostics of serum cardiospecific auto-antibodies for the diagnosis of myocyte cell damage has several potential advantages compared to the evaluation of traditional methods. These include the analysis of natural globulins to troponin I (cTnI), to alpha-a ctin 1 (ACTC1), to the heavy chain of beta-myosin 7B (MUN7B), which are based on a self-sustaining immune response to the myocardium’s own auto-antigens, which leads to damage to the cells expressing them. Purpose: To determine the diagnostic and practical value of quantitative indicators for the autoantibody complex to cardiomyocyte proteins to troponin I, to alpha-a ctin 1 and to the heavy chain of beta-myosin 7B in patients with cardiac pathology. Materials and Methods. The study of auto-antibodies to cTnI, ACTC1 and MUN7B in blood serum using laboratory enzyme immunoassay was carried out in patients with cardiac pathology undergoing inpatient treatment at the Regional Clinical Cardiology Dispensary in Stavropol. Additionally, an instrumental and laboratory examination was carried out in accordance with the clinical recommendations developed by the Association of Cardiovascular Surgeons, the Cardiological Society of Russia and approved by the Scientific and Practical Council of the Ministry of Health of the Russian Federation. The work was examined and approved by the Ethics Committee of the North Caucasus Federal University. Results and Discussion . Changes in the level of autoantibodies to cTnI, ACTC1 and MUN7B proteins in blood serum were statistically significant (p 0.01 v. s. p 0.01). A persistent increase in the level of auto-antibodies to cTnI by 2.36 ng/ml (694.11 %), to ACTC1 by 3.6 ng/ml (141.73 %) and to MUN7B by 1.74 ng/ml (119.17 %) was found in individuals with confirmed cardiac pathology, when other criteria for laboratory analysis were within acceptable values, which determine their diagnostic and evidentiary effectiveness. Conclusion . The results of the study showed the relationship of changes in the activity of cardiospecific auto-A T to cardiomyocyte proteins (Anti-cTnI, Anti ACTC1, Anti-M YH7B) in patients with cardiac pathologies, indicating not only systemic membrane disorders (membranopathies), but also serve as convincing evidence of direct chemical changes in cardiomyocytes. A correlation has also been established between cardiomarkers of necrosis and ischemia and autoimmune globulins Anti-cTnI, Anti ACTC1, Anti-MYH7B, that confirms diagnostic and practical value of this laboratory analysis.