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Essential processes in the regeneration of an injured muscle include proliferation of satellite cells and vascularization. Myogenesis and angiogenesis are prerequisites for the subsequent morphological and functional healing of the injured muscle, leading to the reconstruction of the damaged myocytes and vessels, restoration of the blood fl ow and restoration of the oxygen supply to the tissue. Nitric oxide (NO) plays a key role in satellite cells activation. It acts as a signal molecule and vasodilator, promotes expression genes for many growth factors being extracellular signals regulating the functions of the muscular, vascular and nervous systems. NO is produced by three isoenzymes, called nitric oxide synthases (NOS), present in skeletal muscle. The disturbance equilibrium between eNOS and iNOS activities results in pro-apoptotic NO activity and muscle atrophy. A recent study has shown a relationship between NO generation and delayed onset muscle soreness in response to intense resistance exercise. NO generation can be modulated by physical activity, systemic hypoxia (altitude training) or NO precursors such as L-arginine. The present review provides a current overview of NO effects on skeletal muscles and nutritional strategies based on L-arginine intake to aid muscle regeneration.
According to cytokine overtraining theory, skeletal muscle injuries are related to systemic inflammatory reaction. In response to inflammation, cells rapidly produce a series of proteins known as heat shock proteins (HSPs).These are considered to be molecular chaperones which play a universal role in maintaining cellular homeostasis. Among the subset of stress-responsive proteins, HSP27 and HSP70 are considered to be a new approach to monitoring exercise training and adaptive mechanisms. The study was designed to demonstrate the effect of sport training on changes in pro-inflammatory cytokines and HSPs, and their relation with muscle damage and body composition. Six elite canoeists (19.8 ±2.9 yr) were observed during preparatory training period (March) at the 1st, the 4th and after 7 days of the conditioning camp, and then after 3 days of recovery. The canoeing training did not induce muscle damage, decreased in IL-1 ß and HSP27, increased in TNFa and HSP70 concentrations. The highest changes in TNFa and HSP70 were observed 3 days after conditioning camp (during recovery) compared to initial level (the 1st day of conditioning camp). TNFa correlated with HSP27 (r = —0.563; P < 0.01) and HSP70 (r = 0.651; P < 0.001). Any significant changes in body composition were not observed. In conclusion, we could say that typical canoeing training improves cytokines and HSPs release, however, the changes are not related to muscle damage.
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