Clenbuterol treatment affects myosin heavy chain isoforms and MyoD content similarly in intact and regenerated soleus muscles

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Abstract
Pharmacological treatment with the beta2-adrenoceptor agonist clenbuterol is known to induce a slow-to-fast fibre type and myosin heavy chain (MHC) isoform transition in intact muscle. This study examined the sensitivity of regenerated soleus muscle to 4 weeks of clenbuterol treatment (2 mg kg-1 day-1). Female Wistar rats were divided into two groups: vehicle treated (n = 8) and clenbuterol treated (n = 8). The clenbuterol effects on MHC and MyoD expression were examined in soleus muscles either intact, or previously degenerated by venom of the Notechis scutatus scutatus snake. Post-treatment body weights and skeletal muscle weights were not affected by clenbuterol treatment. Muscle protein concentration was higher, and body fat lower in clenbuterol-treated rats than in vehicle-treated animals (P < 0.05). Polyacrylamide gel electrophoresis of soleus myofibrillar protein indicated a clenbuterol-induced decrease in the relative percentage of type I MHC with a concomitant increase in type IIa MHC (31%, P < 0.001). No degeneration effect was observed after 28 days of recovery on the MHC isoform content, and regenerated soleus muscles exhibited the same phenotypical profile as intact soleus muscles, whether or not they were treated with clenbuterol. In intact and in regenerated soleus muscles, MyoD protein levels were significantly increased by clenbuterol treatment (90 and 77%, respectively, P < 0.001). These results show that regenerated soleus muscles, comprising a homogeneous population of fibres deriving from satellite cells, have a similar response to clenbuterol as intact muscle arising from at least two discrete populations of myotubes; it is suggested that the activity of signalling pathways involved in the effects of clenbuterol on MHC transitions is not related to the developmental history of myofibres.