Increasing lean yield, i.e., muscle mass, while also increasing feed efficiency would greatly benefit the beef cattle industry. One unique physiological characteristic of skeletal muscle tissue compared to other tissues is that the number of multinucleated cellular units, muscle fibers, is fixed at birth. This obviates hyperplastic growth as a means of increasing muscle mass, so increasing muscle hypotrophy has been a primary focus of research scientists at universities, government agencies, and pharmaceutical companies. Post-mitotic growth of muscle is achieved through either DNA accumulation or through increasing the ratio of protein to DNA in muscle fibers. Whereas steroidal implants tend to increase muscle mass by increasing the accumulation of DNA in muscle, beta-adrenergic agonists (?-AA) increase muscle mass by increasing the ratio of protein to DNA (Walker et al., 2010), similar to effects seen with the administration of somatotropin to beef cattle (Vann et al., 1998). Steroidal implants and ?-adrenergic receptors (?-AR), commonly used in the North and South American cattle industries, have similar physiological responses of muscle hypertrophy, appear to have different mechanisms of action to achieve muscle growth, but the mode of action of ?-AA in beef cattle is still not fully understood. Even less is known about the mechanisms by which ?-AA depress adipose accretion in livestock species. This review will focus primarily on the biology of ?-AA as it relates to lipid metabolism in adipose tissue and protein metabolism in skeletal muscle of livestock species.