Beta adrenergic agonists such as clenbuterol, salbutamol, and albuterol are sympathomimetic substances capable of activating beta receptors in vivo. One important function of these substances is to produce effects resembling those of the impulses transmitted by postganglionic fibers of the central nervous system, thereby mimicking normal innervation control in tissues such as skeletal muscle. A dietary administration of these beta adrenoceptor agonists in rat produce growth-promoting protein anabolic effects in skeletal muscle [1,15,21,23,28]. The chronic administration of these agonists causes a hypertrophy of skeletal muscle in mice [17] and in the diaphragm of hamster [31]. The stimulation of the growth of skeletal muscle as a result of an application of beta adrenergic agonists is believed to be largely because of an accelerated protein turnover rate [10] coupled with a decrease degradation rate [27], or a combination of both these processes.The growth-promoting effects of beta adrenergic agonists are not only restricted to normal innervated muscle, but also have been equally confirmed under conditions characterized by the atrophy of constituent muscle fibers such as aging, denervation atrophy, and/or dystrophic conditions. An administration of these agonists to denervated rats not only limited, but also even reversed the process of denervation atrophy [13,19,20,35]. Similarly, an examination of the effects of clenbuterol on dystrophic mice has established that the drug could serve as a valuable adjunct Key words: beta adrenergic agonists, isoproterenol, clenbuterol, gastrocnemius muscle, denervation atrophy, 3-methylhistidine, myofibrillar degeneration. Abstract:The effects of beta adrenergic agonists, clenbuterol (2 mg/kg body weight/d) and isoproterenol (12 mg/kg body weight/d), in normal innervated and denervated rat gastrocnemius muscle were investigated. The daily administration of beta adrenergic agonists to normal innervated rats for a short period (7 d) resulted in the hypertrophy of gastrocnemius as confirmed from the measurement of total tissue protein contents. The development of denervation atrophy witnessed a stimulation in the expression of acid and alkaline phosphatases, pointing to an enhanced myofibrillar degeneration. An administration of beta adrenergic agonists inhibited the expression of raised levels of these enzymes in denervated muscle. A measurement of 3-methylhistidine in muscle revealed a loss of amino acid with the progress in the development of denervation atrophy. Serum and urine samples from denervated rats showed a progressive accumulation of 3-methylhistidine. Clenbuterol and isoproterenol treatment to these rats resulted in an inhibition of 3-methylhistidine accumulation. When 3-methylhistidine was used as a marker of myofibrillar degeneration, the results seemed to suggest that the degeneration of cyto-contractile apparatus accompanying denervation atrophy is attenuated in the presence of beta adrenergic agonists, implying that these sympathomimetic drugs are capable of re...