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The article investigates how heat stress and beta-adrenergic agonists independently and interactively affect adipose tissue in ractopamine hydrochloride (RH)-supplemented lambs and zilpaterol hydrochloride (ZH)-supplemented cattle. Topics discussed include adipose's lipolytic activity, fatty acid mobilization, and adipogenesis and lipolysis in sheep.

The article presents a study examining the role of ractopamine HCl that improved cardiac hypertrophy but not poor growth, metabolic inefficiency, or greater white blood cells associated with heat stress in concentrate-fed lambs. It discusses that Heat stress decreases livestock performance and well-being, causes metabolic dysfunction that decreases growth efficiency, and alters cardiovascular function.

The article presents a study on body composition estimation by bioelectrical impedance analyses is diminished by prenatal stress in neonatal lambs and by heat stress in feedlot wethers. Topics discussed include use of body composition correlates to carcass value in livestock; use of bioelectrical impedance analysis (BIA) to predict changes to body composition in live neonatal lambs; and causes of intrauterine growth restriction (IUGR).

Feedlot performance is reduced by heat stress and improved by β adrenergic agonists (βAA). However, the physiological mechanisms underlying these outcomes are not well characterized, and anecdotal reports suggest that βAA may confound the effects of heat stress on wellbeing. Thus, we sought to determine how heat stress and βAA affect growth, metabolic efficiency, and health indicators in lambs on a feedlot diet. Wethers (38.6 ± 1.9 kg) were housed under thermoneutral (controls; n = 25) or heat stress (n = 24) conditions for 21 d. In a 2 × 3 factorial, their diets contained no supplement (unsupplemented), ractopamine (β1AA), or zilpaterol (β2AA). Blood was collected on days −3, 3, 9, and 21. On day 22, lambs were harvested and ex vivo skeletal muscle glucose oxidation was determined to gauge metabolic efficiency. Feet and organ tissue damage was assessed by veterinary pathologists. Heat stress reduced (P < 0.05) feed intake by 21%, final bodyweight (BW) by 2.6 kg, and flexor digitorum superficialis (FDS) muscle mass by 5%. β2AA increased (P < 0.05) FDS mass/BW by 9% and average muscle fiber area by 13% compared with unsupplemented lambs. Blood lymphocytes and monocytes were greater (P < 0.05) in heat-stressed lambs, consistent with systemic inflammation. Plasma insulin was 22% greater (P < 0.05) and glucose/insulin was 16% less (P < 0.05) in heat-stressed lambs than controls. Blood plasma urea nitrogen was increased (P < 0.05) by heat stress on day 3 but reduced (P < 0.05) on days 9 and 21. Plasma lipase and lactate dehydrogenase were reduced (P < 0.05) by heat stress. Glucose oxidation was 17% less (P < 0.05) in muscle from heat-stressed lambs compared with controls and 15% greater (P < 0.05) for β2AA-supplemented compared with unsupplemented lambs. Environment and supplement interacted (P < 0.05) for rectal temperature, which was increased (P < 0.05) by heat stress on all days but more so (P < 0.05) in β2AA-supplemented lambs on days 4, 9, and 16. Heat stress increased (P < 0.05) the frequency of hoof wall overgrowth, but βAA did not produce any pathologies. We conclude that reduced performance in heat-stressed lambs was mediated by reduced feed intake, muscle growth, and metabolic efficiency. β2AA increased muscle growth and improved metabolic efficiency by increasing muscle glucose oxidation, but no such effects were observed with ractopamine. Finally, βAA supplementation was not detrimental to health indicators in this study, nor did it worsen the effects of heat stress. [ABSTRACT FROM AUTHOR]