Syndromes of exercise-induced muscle damage and delayed onset of muscle soreness are considered one of the main causes of the development of fatigue and subsequent overstrain in athletes. Therefore, in modern scientific literature the number of publications on this topic is growing steadily. They describe and examine various physiological and pathophysiological aspects of this problem; mechanisms of the fatigue development in athletes using loads of various intensity and duration practicing different kinds of sports, qualifications, age and gender. The authors of numerous publications in chaotic conjugation describe multidirectional changes in numerous biochemical, immunological and endocrine parameters of homeostasis, which may reflect the presence and severity of both syndromes. These works compare the changes in the studied laboratory parameters with the parameters of physical performance, the characteristics of the visual analogue scale for assessing pain. Since the development of fatigue and overtraining in athletes largely depends on the intensity of energy supply processes, the researchers pay attention to the enzymes of energy metabolism (lactate dehydrogenase, aldolase) and contractile proteins of skeletal muscles (actin, myosin), where most of the stored energy is used. The well-known and widely used indicator of the serum lactate content is also used in scientific works concerning this problem. The recent research has started to trace the dependence of changes in laboratory parameters of the severity of the studied syndromes on a single pathophysiological factor. A certain systematic search led to the idea that oxidative stress could be such a factor. Oxidative stress is formed during physical activity of both a cyclic and non-cyclic nature, among highly qualified athletes specializing in various sports. The authors of scientific works described various parameters of lipoperoxidation (malondialdehyde, reactive oxygen species), and antioxidant factors of enzymatic (catalase, superoxide dismutase, glutathione peroxidase) and non-enzymatic (ceruloplasmin, reduced glutathione) nature. It was a step forward in building laboratory control of exercise-induced muscle damage and delayed onset of muscle soreness syndromes. At the end of 2019 beginning of 2020, there appeared works examining factors which were more specific to the aseptic inflammatory process, which further created delayed muscle soreness that limited the athletes' functional capabilities and developed exercise-induced muscle damage syndrome. Thus, the determination of β-hydroxy-β-methylbutyrate in blood serum, acute phase proteins (gelsolin (pGSN) and orosomcoid) and N-terminal fragment of titin protein in urine proved to be highly informative. Conclusion. Based on the analysis and synthesis of literature data and our own results, we formed an algorithm for diagnosing the severity of exercise-induced muscle damage syndrome and delayed onset of muscle soreness syndromes. The algorithm includes five consecutive steps, four of which are mandatory and one optional, since the equipment for determining new specific parameters is far from being available in all sports research laboratories. We believe that this stage will also become mandatory after some time, which will completely form the algorithm.
Keywords: exercise-induced muscle damage syndrome, delayed onset of muscle soreness syndrome, sports, overtraining, laboratory diagnostics
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