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Regeneration in heat- and mechanically-stressed skeletal muscles in rats. K. Goto1, S. Morioka1, A. Kojima1, T. Akema1, T. Sugiura2, Y. Ohira3 and T. Yoshioka1,4. 1Dept. of Physiol., St. Marianna Univ. Sch. of Med., Kawasaki; 2Yamaguchi Univ., Yamaguchi; 3Graduate Sch. of Med., Osaka Univ., Toyonaka; 4Hirosaki Gakuin Univ., Hirosaki, Japan.

   It has been considered that muscle satellite cells are responsible for the postnatal growth, regeneration, and regrowth of skeletal muscle and that the maintaining of muscle mass might be regulated by a similar mechanism as that for the regeneration.  Mechanical-stress as well as heat-stress facilitate the proliferation and differentiation of muscle satellite cells, and induce muscle hypertrophy.  If the application of cellular stress could activate muscle satellite cells, the application of cellular-stress may facilitate the regeneration.  The purpose of this study was　performed to investigate the effects of heat- and mechanically-stressed on the regeneration of injured skeletal muscles.  In the heat-stressed experiment, male Wistar rats were divided into normal control, heat-stressed, and non-heated groups.  To activate a necrosis-regeneration cycle, cardiotoxin (CTX) was injected into the tibialis anterior muscles of experimental groups with or without heating, except for the normal control group. Rats in the heat-stressed group were exposed to environmental heat stress (41°C for 60 min) in a heat chamber 24 hours before or immediately after CTX injection without anesthesia.  In the mechanically-stressed experiment, male C57BL/6J mouse were divided into control and overloaded groups.  CTX was injected into soleus muscles to activate a necrosis-regeneration cycle.  In overloaded group, soleus muscle overload was induced by tenotomy.  The muscle protein contents in the both heat- and mechanically-stressed groups were significantly higher than the non-heated group 28 days after CTX injection (p<0.05).  The CTX-injection-related increment of satellite cells in stressed groups was greater than that in non-stressed groups.  Evidences suggest that cellular stress could activate satellite cells and facilitate the regeneration of muscle.