| 研究概要 |
In 2013, we reported that p38 mitogen-activated protein kinase(MAPK) and Akt pathways play a functional role in the adaptation to β2-agonist, clenbuterol(CLE) treatment and exercise, particularly in slow-twitch muscle. Although CLE induces muscle hypertrophy by stimulating protein synthesis, the precise mechanism by which CLE increases muscle power and muscle mass is unknown. Further, CLE selectively causes muscle hypertrophy in fast-twitch muscles, but it is not clear whether its repressive effects on atrophy differ according to skeletal muscle fiber types.
In 2014, therefore, we studied histochemically whether daily administration of CLE(1mg/kg BW/day) prevents casted-immobilization(IMM)-induced atrophy of skeletal muscle fibers. Adult male Sprague-Dawley rats were divided into control, CLE, IMM, and IMM+CLE groups, and were maintained for 9 days. The extensor digitorum longus(EDL) and soleus muscles were isolated and analyzed histochemically after ATPase staining. EDL and soleus muscle weights in the IMM group were lower than those in the control group. Analysis of cross-sectional areas revealed that EDL muscle atrophy was limited to type II fibers; soleus muscle atrophy involved type I and type II fibers. In the IMM+CLE group, IMM-induced muscle atrophy was attenuated in the EDL, but not in the soleus muscle. Moreover, the attenuating effect of CLE was observed in type II fibers. These results suggest that CLE attenuated IMM-induced atrophy of type II fibers in the fast-twitch EDL muscle but not in the slow-twitch soleus muscle.
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