Abstract
Postnatal skeletal muscle growth is a result of hypertrophy of existing skeletal muscle fibers in food producing animals. Accumulation of additional nuclei, as a source of DNA, to the multinucleated skeletal muscle fiber aids in the process of fiber hypertrophy during periods of rapid skeletal muscle growth. Muscle satellite cells are recognized as the source of nuclei to support muscle hypertrophy, and this accumulation has been considered the rate limiting step of postnatal skeletal muscle growth. Exogenous growth-enhancing compounds have been used to modulate growth rate and efficiency in meat animals for nearly 70 years. In cattle, these compounds enhance efficiency of growth by preferentially stimulating skeletal muscle growth compared to adipose tissue. There are two main classes of compounds approved for use in cattle in the United States, anabolic steroids and β-adrenergic agonists (β-AA). Administration of both trenbolone acetate (TBA) and estradiol-17β (E2), as implants, increased carcass protein accumulation 8 to 10% in yearling steers. Muscle satellite cells isolated from steers implanted with TBA/E2 had a shorter lag phase in culture compared to satellite cells isolated from control steers. Collectively, these data indicate that activation, increased proliferation, and subsequent fusion of satellite cells in muscles of implanted cattle may be an important mechanism by which anabolic steroids enhance muscle hypertrophy. Oral administration of β-AA to ruminants does not alter DNA accumulation in skeletal muscle over a typical feeding period (28 to 42 d). Enhanced muscle hypertrophy observed due to β-AA feeding occurs by direct, receptor-mediated changes in protein synthesis and degradation rates of skeletal muscle tissue. Proper timing of anabolic steroid administration when coupled with β-AA feeding could result in a synergistic response in skeletal muscle growth due to the effects of anabolic steroids at increasing satellite cell activity, which then can support the rapid hypertrophic changes of the muscle fiber when exposed to β-AA. At the same time each of these classes of compounds are stimulating lean tissue deposition, they appear to decrease adipogenesis in meat animals. The use of these exogenous compounds can lead to very low but, yet, detectable residues of the parent compounds in edible tissues of meat animals. Research studying the mode of action of exogenous growth-enhancing compounds in meat animals has increased our understanding of underlying mechanisms of postnatal skeletal muscle growth.