SKELETAL-MUSCLE PROTEIN-METABOLISM AND SERUM GROWTH-HORMONE, INSULIN, AND CORTISOL CONCENTRATIONS IN GROWING STEERS IMPLANTED WITH ESTRADIOL-17-BETA, TRENBOLONE ACETATE, OR ESTRADIOL-17-BETA PLUS TRENBOLONE ACETATE

Skeletal muscle protein degradation, measured by urinary N(tau)-methylhistidine excretion, and circulating concentrations of growth hormone [GH], insulin [INS], and cortisol [CT] were monitored in steers before and after implantation with estradiol-17-beta [E2; 24 mg] and trenbolone acetate [TBA; 300 mg]. Yearling crossbred steers [n = 43] were randomly assigned to four treatment groups in a 2 x 2 factorial arrangement: nonimplanted controls [C]; TBA; E2; and TBA plus E2 [TBA + E2]. A subgroup [Block 1] of 16 steers was bled on d -12, 31, and 72 after implanting. Deposition of skeletal muscle protein was markedly increased [P < .001] by E2 and TBA + E2 treatment. This response occurred mainly within the first 40 d after implantation and declined [P < .001] in concert with decreasing [P < .01] concentration of serum E2. Anabolic steroid treatment did not affect the rate of skeletal muscle protein breakdown. There was no apparent relationship between reduced serum CT concentration [linear effect; P < .01] in TBA-treated steers and skeletal muscle protein degradation rate. Blood concentration and pulse activity of INS were not affected by anabolic steroid administration. Both TBA- and TBA + E2-implanted steers displayed a linear decrease [P < .05] in serum GH concentration over time, which was similar to C. Lowered mean GH concentration resulted from a reduction [TBA main effect; P < .05] in pulse amplitude of GH. Unlike TBA, TBA + E2, and C, only E2 maintained serum GH concentrations over time. Although increased muscle protein deposition was evident in TBA + E2-treated steers, an obvious causal relationship between this response and circulating GH, INS, and CT was not revealed. These results do not support the concept that combined androgenic agent and estrogen administration effectively reduce bovine muscle protein degradation by static modulation of circulating endogenous anabolic and antianabolic hormones.