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Bodine, S.C., Stitt, T.N., Gonzalez, M., Kline, W.O., Stover, G.L., Bauerlein, R., Zlotchenko, E., Scrimgeour, A., Lawrence, J.C., Glass, D.J. and Yancopoulos, G.D. (2001) Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nature Cell Biology, 3, 1014-1019.

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• TITLE: Muscle damage and regeneration: Response to exercise training

  AUTHORS: Teet Seene, Priit Kaasik

  KEYWORDS: Skeletal Muscle; Regeneration Capacity; Resistance; Endurance and Overtraining

  JOURNAL NAME: Health, Vol.5 No.6B, June 27, 2013

  ABSTRACT: Exercise training influences the function of skeletal muscle, modifying fibre structure, metabolism and promoting the release of growth factors and other signalling molecules. The number of satellite cells under the basal lamina of type I and type IIA muscle fibres increases during endurance training and under the basal lamina of both type II fibres during resistance training. An increase in satellite cells is related to several factors expressing different genes and type II muscle fibre hypertrophy. Insulin-like growth factor-I has a role in the hypertrophy of muscle fibres through the stimulation of the differentiation of satellite cells. The increased mitochondrial biogenesis via adenosine myophosphate-activated protein kinase is accompanied by the suppression of myofibrillar protein synthesis through pathways mediated by mitogen-activated protein kinases and the nuclear factor kappa B. Insulin-like growth factor-I expression is higher in type I fibres. Myostatin, the expression inhibitor of muscle hypertrophy, is higher in type II fibres. The proteasome-, lysosome- and Ca2+-mediated protein degradation is more intensive in fibres with higher oxidative capacity. Both, oxidative capacity and satellite cells number in muscle fibres play important roles in skeletal muscle regeneration. In this review, we explore the regeneration capacity changes in different types of skeletal muscle fibres in response to resistance, endurance and overtraining.