Some aspects of heat stress on the plasticity of skeletal muscle cells

抄録

Hypertrophic stimuli, such as strength training and exercise, induce the up-regulation of heat shock proteins (HSPs), called stress proteins, in skeletal muscles. However, the physiological roles for induction of HSPs in skeletal muscles are still not fully understood. Heat stress also up-regulates the expression of HSPs, which are considered to function as molecular chaperones in eukaryotic cells, via heat shock transcription factor (HSF)-mediated stress response. Intracellular protein synthesis mediated by Akt/p70 S6 kinase (p70S6K) and/or calcineurin signaling pathways might be directly activated by heat stress. The number of muscle satellite cells, which play a key role in postnatal growth and regeneration of skeletal muscle cells, are increased by heat stress. Heat stress facilitates the regenerative process of injured skeletal muscle. Absence of heat shock transcription factor 1 (HSF1) partially depresses the regrowth of unloading-associated muscle atrophy. Therefore, heat stress could in part induce muscle hypertrophy via HSF1-mediated stress response. Heat stress-associated skeletal muscle hypertrophy has been confirmed in experimental animals as well as healthy human subjects. Application of heat stress on skeletal muscle may be a useful tool for gaining muscle mass and force generation not only in healthy subjects but also in patients during rehabilitation. Heat stress could also be a useful countermeasure for prevention of muscle atrophy during bed rest inactivity and/or space flight.