Heat stress-induced deficits in growth, metabolic efficiency, and cardiovascular function coincided with chronic systemic inflammation and hypercatecholaminemia in ractopamine-supplemented feedlot lambs

Abstract

Heat stress hinders growth and well-being in livestock, an effect that is perhaps exacerbated by the β1 agonist ractopamine. Heat stress deficits are mediated in part by reduced feed intake, but other mechanisms involved are less understood. Our objective was to determine the direct impact of heat stress on growth and well-being in ractopamine-supplemented feedlot lambs. Commercial wethers were fed under heat stress (40 °C) for 30 d, and controls (18 °C) were pair-fed. In a 2 × 2 factorial, lambs were also given a daily gavage of 0 or 60 mg ractopamine. Growth, metabolic, cardiovascular, and stress indicators were assessed throughout the study. At necropsy, 9th to 12th rib sections (four-rib), internal organs, and feet were assessed, and sartorius muscles were collected for ex vivo glucose metabolic studies. Heat stress increased (P < 0.05) rectal temperatures and respiration rates throughout the study and reduced (P < 0.05) weight gain and feed efficiency over the first week, ultrasonic loin-eye area and loin depth near the end of the study, and four-rib weight at necropsy. Fat content of the four-rib and loin were also reduced (P < 0.05) by heat stress. Ractopamine increased (P < 0.05) loin weight and fat content and partially moderated the impact of heat stress on rectal temperature and four-rib weight. Heat stress reduced (P < 0.05) spleen weight, increased (P < 0.05) adrenal and lung weights, and was associated with hoof wall overgrowth but not organ lesions. Ractopamine did not affect any measured indicators of well-being. Heat stress reduced (P < 0.05) blood urea nitrogen and increased (P < 0.05) circulating monocytes, granulocytes, and total white blood cells as well as epinephrine, TNFα, cholesterol, and triglycerides. Cortisol and insulin were not affected. Heat stress reduced (P < 0.05) blood pressure and heart rates in all lambs and increased (P < 0.05) left ventricular wall thickness in unsupplemented but not ractopamine-supplemented lambs. No cardiac arrhythmias were observed. Muscle glucose uptake did not differ among groups, but insulin-stimulated glucose oxidation was reduced (P < 0.05) in muscle from heat-stressed lambs. These findings demonstrate that heat stress impairs growth, metabolism, and well-being even when the impact of feed intake is eliminated by pair-feeding and that systemic inflammation and hypercatecholaminemia likely contribute to these deficits. Moreover, ractopamine improved muscle growth indicators without worsening the effects of heat stress.

256 Heat stress and β-adrenergic agonists alter the adipose transcriptome and fatty acid mobilization in ruminant livestock

“…Several loci implicated (Wagner and Efrel, 2005). Additional data from this study demonstrated an inflammatory response due to HS that was moderated by RH (Swanson et al, 2020). Heat stress alone altered expression of two loci in adipose.…”

Heat stress and β-adrenergic agonists alter the adipose transcriptome and fatty acid mobilization in ruminant livestock1

“…Others such as FOS and FOSB are associated with inflammation ( Wagner and Efrel, 2005 ). Additional data from this study demonstrated an inflammatory response due to HS that was moderated by RH ( Swanson et al, 2020 ). Heat stress alone altered expression of two loci in adipose.…”

“…Decreased FFA mobilization due to HS was possibly an effect of chronic exposure. In study 1, HS caused increased circulating epinephrine ( Swanson et al, 2020 ). If steers in study 2 responded likewise, it is reasonable to speculate that their βAR became desensitized and less responsive to epinephrine.…”

“…ATXN7L1 is associated with neurological disorders ( Carlson et al, 2009 ), but Komolka et al (2016) reported it is downregulated in the longissimus dorsi of cattle with greater intramuscular fat. Increased ATXN7L1 expression in HS lambs could therefore contribute to the observed decrease in fat ( Swanson et al, 2020 ). Pathway analyses predicted adipogenesis to be dysregulated due to HS.…”

Heat Stress-Mediated Activation of Immune–Inflammatory Pathways

“…Sheep exposed to heat stress exhibit increased concentrations of plasma TNF-α, a key mediator of inflammation, and increased total white blood cell, monocyte, and granulocyte counts (40 °C for 12 h followed by 30 °C for 12 h for 30 days) [ 55 ]. Expression of proteins associated with the innate immune response, such as haptoglobin, heat shock protein 90-α (HSP90AA1), and the endoplasmic precursor (HSP90B1), is induced in heat-stressed pigs (constant 30 °C for 21 days) [ 56 ].…”