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Abstract
Two studies were conducted to determine the relationship of endogenous muscle proteinase systems and muscle growth. Due to the enhanced muscling in $\beta$-adrenergic agonist (BAA)-fed animals, this system was used to investigate the temporal responses of these proteinase systems in BAA-treated animals. In the first study, BAA administration increased muscle growth in lambs within two weeks of treatment. This was accompanied by decreased proteolytic capacity, increased protein synthetic capacity, and decreased tenderness of the BAA-treated muscle. The decreased proteolytic capacity appeared related to a 73% increase in calpastatin activity and a 23% decrease in $\mu$-calpain activity during the first two weeks of BAA administration. Muscle RNA concentrations and RNA:DNA ratios increased during the first two weeks of treatment. Although these variables generally remained higher in the treated lambs than in the controls, the BAA response attenuated over the treatment period. In the second study, rabbits were used to investigate the short-term changes in muscle growth caused by BAA administration. Muscle growth did not increase in the treated rabbits compared to controls until after 16 days of treatment. Contrary to the first study, there did not appear to be any relationship between the calpain-calpastatin system and BAA-induced muscle growth in rabbits. This was also true for hepatic and cardiac tissues. Similar changes in the protein synthetic capacity of muscle (increased RNA concentrations and RNA:DNA ratios) occurred in both studies, with an initial rise and subsequent attenuation. However, rabbit muscle weight did not increase until after the response in protein synthetic capacity had peaked and begun to drop. These results indicate that the response to BAA administration is species dependent. There appears to be a strong positive relationship between calpastatin activity and muscle growth in BAA-treated lambs. However, increased muscle growth in BAA-treated rabbits seems more closely related to an increase in the protein synthetic capacity of the muscle.
