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

Prolonged treatment with the beta(2)-adrenoceptor agonist clenbuterol (1-2 mg . kg body mass(-1).day(-1)) is known to induce the hypertrophy of fast-c ontracting fibers and the conversion of slow- to fast-contracting fibers. W e investigated the effects of administering a lower dose of clenbuterol (25 0 mu g.kg body mass(-1).day(-1))on skeletal muscle myosin heavy chain (MyHC ) protein isoform content and adenine nucleotide (ATP, ADP, and AMP) concen trations. 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 similar to 0.5% in controls to similar to 18% after clenbuterol treatment (P< 0.05), which was accompanied by an increase in the total adenine nucleotide pool (TAN; similar to 19%, P< 0.05) and energy charge [E- C = (ATP + 0.5 ADP)/(ATP + ADP + AMP); simil ar to 4%; P< 0.05]. In the EDL, a reduction in the content of the less prev alent type I MyHC protein from similar to 3% in controls to 0% after clenbu terol 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.