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Pathogenetic Mechanisms of Undue Fatigue and Main Directions of its Pharmacological Correction



E.B. Shustov
V.S. Novikov
S.V. Okovitiy
shustov-msk@mail.ru
raen.vsn@mail.ru
sergey.okovity@pharminnotech.com
Chief Researcher, the Institute of Toxicology of Federal Medical Biological Agency of Russia, professor, the Department of Pharmacology and Clinical Pharmacology, St. Petersburg Chemical and Pharmaceutical University of the Ministry of Health of the Russian Federation, member of the Russian Academy of Natural Sciences, Winner of the State Prize of the Russian Federation in Science and Technology, Doctor of Medicine, professor
vice-president of the Russian Academy of Natural Sciences, chairperson of the section of interdisciplinary problems of science and education of the Russian Academy of Natural Sciences, a recipient of the State Prize in Science and Engineering, Honored Science Worker, member of the Russian Academy of Natural Sciences, Doctor of Medicine, professor
head of the Department of Pharmacology and Clinical Pharmacology, St. Petersburg State Chemical Pharmaceutical Academy, Doctor of Medicine, professor
St. Petersburg
St. Petersburg
St. Petersburg

Keywords:

  • adaptation
  • asthenia
  • recovery
  • deadaptation
  • preventive use
  • productivity
  • stress
  • fatigue
  • pharmacological correction
  • We look at the factors significantly affecting the mechanisms of developing undue fatigue – concurrent conditions, working conditions, individual characteristics of the body (immunity, reactivity of vegetative and endocrine regulation, resistance to psychoemotional stress, adaptive capability, fitness, resistance to a wide range of adverse effects, capacity of mitochondrial oxidation and antioxidant protection systems, provision of energy and plastic substrates, vitamins and microelements, etc.). The development of asthenia significantly increases the fatigue. We demonstrate that the level of fatigue reflects the balance between energy consumption and emergency recovery mainly characterized by the intensity of mitochondrial reactions of ATP synthesis, lactate and ammonia utilization, gluconeogenesis, support of adaptive protein synthesis and stabilization of cytoplasmic and subcellular membranes. These processes determine the directions of pharmacological correction of undue fatigue, the prevention of rapid consumption of functional, regulatory and substrate body reserves during prolonged or intensive activity.