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.
Highlights
The contemporary exercise training process does not consist in repetitive exercise but encompasses regular regeneration as an integral part of a successful training program
Oxidative muscle fibres contain a large number of myonuclei and satellite cells (Sc) compared with glycolytic fibres [20, 21]
Increased mitochondrial biogenesis via AMP-activated AMPK is accompanied by suppression of the myofibrillar protein synthesis through pathways mediated by mitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-kB)
Summary
The contemporary exercise training process does not consist in repetitive exercise but encompasses regular regeneration as an integral part of a successful training program. Exerciseinduced skeletal muscle damage mainly follows unaccustomed and sustained metabolically demanding training processes [1]. Muscle fibres regenerate via the activation of quiescent muscle precursor cells (Figure 1) and proceed with the formation of proliferating progenitors that fuse to generate differentiated myofibres [9]. These satellite cells (Sc) activated by muscle injury give rise to intermediate progenitor cells expressing the MyoD and myogenic transcription factor Pax, which are asymmetrically divided and differentiated into Pax, Myf-5 and desmin myoblasts [10]. Regeneration in exhausted skeletal muscle, caused by both endurance and strength training, is slow as the lack of insulin-like growth factor-I (IGF-I). Morpho-functional characteristics of injured muscle and the role of Sc and different myogenic factors in the repair of myofibres after damage are discussed
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