Skeletal muscle myosin heavy chain isoforms and energy metabolism after clenbuterol treatment in the rat

Prolonged treatment with the β₂-adrenoceptor agonist clenbuterol (1-2 mg·kg body mass^-1·day ^-1) is known to induce the hypertrophy of fast-contracting fibers and the conversion of slow- to fast-contracting fibers. We investigated the effects of administering a lower dose of clenbuterol (250 μg·kg body mass^-1·day ^-1) on skeletal muscle myosin heavy chain (MyHC) protein isoform content and adenine nucleotide (ATP, ADP, and AMP) concentrations. Male Wistar rats were administered clenbuterol (n = 8) or saline (n = 6) subcutaneously for 8 wk, after which the extensor digitorum longus (EDL) and soleus muscles were removed. We demonstrated an increase of type IIa MyHC protein content in the soleus from ~0.5% in controls to ~18% after clenbuterol treatment (P < 0.05), which was accompanied by an increase in the total adenine nucleotide pool (TAN; ~19%, P < 0.05) and energy charge [E-C = (ATP + 0.5 ADP)/(ATP + ADP + AMP); ~4%; P < 0.05]. In the EDL, a reduction in the content of the less prevalent type I MyHC protein from ~3% in controls to 0% after clenbuterol treatment (P < 0.05) occurred without any alterations in TAN and E-C. These findings demonstrate that the phenotypic changes previously observed in slow muscle after clenbuterol administration at 1-2 mg·kg body mass^-1·day^-1 are also observed at a substantially lower dose and are paralleled by concomitant changes in cellular energy metabolism.