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.

At present time, the rational search for a protection of cardiovascular system of athletes and the assessment of such protection efficiency are the very important problems in sports pharmacology and sports cardiology. It is worth noting that athletic training pharmacology, aimed at the stimulation of physical workability in the majority of sports events, can become, together with overloads, the principal reason for a deterioration of health and life’s quality as well as for the sudden death of athletes without a proper cardioprotection. The problem of protection is significantly complicated under modern conditions due to the permanent hardening of anti-doping sanctions (e.g., the recent ban on the use of trimetazidine and meldonium) that essentially limit the possibilities for sports cardiologists. Therefore, the most grounded exit, from the current position, is the use of metabolitotropic medications, in particular, those on the basis of L-carnitine (gamma-butyrobetaine). The wide spectrum of physiologic and biochemical influence of this substance on organism gives possibility to moderately affect the physical and mental workability of athletes even under the conditions of long-term intense physical loads. The complex action of pharmacological agents on the basis of L-carnitine on organism allows one to use it on all stages of the preparation with high efficiency of the cardioprotective and ergogenic effects. Despite the bans of WADA, sports cardiologist possesses a sufficient pool of pharmacological agents that can ensure the protection of myocardium under conditions of training process and competition and can preserve athlete’s health as well as his/her physical workability.

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.