The article notes that the development of oxidative stress and the violation of cellular energy balance is the primary link of the vast majority of systemically-forming homeostatic shifts in the athlete’s body and changes the vital structure and function of cellular and subcellular proteins membrane. Changes in the quantitative and qualitative composition of lipid components of membranes, inhibition of the activity of key glycolysis enzymes, as well as the deterioration of bioenergy mechanisms, result from the accumulation of free radicals due to activation of lipid peroxidation. The protection of the organelles responsible for energy supply from oxidative effects is provided by mitochondrial disconnecting proteins that exist in the myocardium. The development of metabolic ischemia due to the imbalance between the delivery of oxygen to cardiomyocytes and their need for myocardium is accompanied firstly by the inhibition of the process of oxidation of glucose and an increase in the use of fatty acids, and then the accumulation of lactate with the development of acidosis of the intracellular environment and the impairment of the ability of myocytes and cardiomyocytes to relaxtion and contraction. It has been established that strenuous muscle activity leads to the formation of a hypoxic state with its characteristic redistribution and increase of energy, metabolic, structural resources of the body in the interests of the tissue where adaptive adjustments are taking place. The insufficiency of energy generation due to the development of this state leads to the dysfunction of the mitochondrial apparatus, which subsequently causes the violation of the energy supply, antioxidant protection, membrane stability due to intensification of lipid peroxidation and leads to cell apoptosis. This forms a background for the occurrence of fatigue and tension, followed by reduction of physical performance of athletes. The detection of the above changes makes it possible to prevent and correct in a timely manner the negative effects of oxidative stress associated with ultra-intensive physical loads.

Straipsnyje apžvelgiama natūralių antioksidantų metabolizmą skatinanti veikla sportuojant oksidacinio streso sąlygomis. Nustatyta, kad oksidacinį stresą, vieną pagrindinių veiksnių, trukdančių pasiekti gerų sportinių rezultatų, galima valdyti parenkant tinkamus fizinius krūvius. Nurodyti natūralių antioksidantų – ceruloplazmino, omega‑3 polinesočiųjų riebalų rūgščių ir probiotinių produktų, fizinės veiklos skatinimo komponentų, veiklos mechanizmai. Paaiškėjo, kad be tiesioginio antioksidacinio efekto, ergogeninis veiksmas pasižymi membraną tausojančiomis, detoksinėmis, imuninę ir širdies kraujagyslių sistemą apsaugančiomis savybėmis. Buvo nustatyta, kad pateikti veiksniai, dalyvaujantys metabolinių procesų susidaryme fizinės veiklos metu ir turintys antioksidacinį poveikį organizmui, gali būti susiję su daugybe kitų homeostazės pokyčių organizme, pradedant ATF išeikvojimu ląstelėse bei katecholaminų kaupimu ir baigiant mitochondrijų biogenezė. [...]

Both specific and nonspecific metabolic transformations, occurring in the body of athlete under intensive and prolonged physical loads, have been characterized in the review paper. It has been emphasized that oxidative stress, which belongs to general pathogenic factors of further myocardium pathology formation, and load induced hypoxia, which is later associated with tissue hypoxia of metabolic origin, represent the initial link of subsequent homeostatic balance changes. Changes in the activity of creatine phosphokinase-MB fraction, content of cardiac troponins I and T as well as terminal natriuretic peptides are referred to specific markers of myocardium strain. Wider range of myocardium strain nonspecific markers includes both alterations of lipid metabolism and numerous, oxidative stress mediated, metabolic changes at the level of cellular and subcellular membranes of cardiomyocytes, followed by changes in the activity of membrane-bound enzymes and lysosomal proteinase ejection first into extracellular matrix and then – into circulatory bed as well as erythrocyte membranes and their ATP content that are accompanied by deterioration of blood oxygen transport function. The above mentioned negatively influences myocardial contractility and leads to the development of hypertrophic cardiomyopathy. Identification of the markers of athlete heart strain allows timely to be corrected by pharmacological means, aimed at normalization of metabolic disorders and prevention of myocardial hypertrophy, which is the major cause of sudden coronary death among athletes.