Effects of zilpaterol hydrochloride on methane production, total body oxygen consumption, and blood metabolites in finishing beef steers

An indirect calorimetry experiment was conducted to determine the effects of feeding zilpaterol hydrochloride (ZH) for 20 d on total body oxygen consumption, respiratory quotient, methane production, and blood metabolites in finishing beef steers. Sixteen Angus steers (initial BW = 555 ± 12.7 kg) were individually fed at ad libitum intake and used in a completely randomized design. The model included the fixed effects of dietary treatment, day, and treatment × day. Dry matter intake did not differ between the treatments (P = 0.89), but was greater on d 0 than any other day (P < 0.01). Oxygen consumption was not different between treatments (P = 0.79), but was different across day (P < 0.01) on d 7, 14, 21, and 28. Respiratory quotient was less for cattle fed ZH than control (P < 0.01), and also different across day (P < 0.01), being greater on d 7, 21, and 28 than d 3 or 21. Methane production (L/kg of DMI) was greater for steers fed the control vs. the ZH diet (P < 0.01), and it also differed by day (P < 0.01), being greater on d 21 and 28 than d 0, 3, 7, and 14. Nonesterified fatty acids were not different across treatments (P = 0.82), and there was no effect of treatment on β-hydroxybutyrate concentration (P = 0.45). Whole blood glucose concentrations were not affected by feeding ZH in this experiment (P = 0.76); however, lactate concentrations were reduced by feeding ZH (P = 0.03). Additionally, there was no treatment effect on ɑ-amino-N, blood glutamate, or glutamine (P ≥ 0.16). Plasma NH₃ was not affected by ZH (P = 0.07), but plasma urea nitrogen was reduced by ZH (P < 0.01). Urinary creatinine was increased by steers receiving ZH (P = 0.01), and urine 3-methylhistidine (3-MH) concentrations were normalized to creatinine, the 3-MH:creatinine ratio decreased from d 0 to d 3 in steers fed ZH, and remained less than control steers until d 28. These data provide insight into how β-agonists alter nutrient partitioning and improve the efficiency of tissue accretion, mainly through decreased muscle protein turnover and altering the catabolic fuel for peripheral tissues.