Abstract
Abstract Our 1st study evaluated the effects of □-adrenergic agonist (ractopamine) supplementation on growth, health, and wellbeing in heat-stressed feedlot wethers. Chronic heat stress impaired growth, metabolism, and wellbeing even when the impact of reduced feed intake was eliminated by pair-feeding. We observed systemic inflammation and hypercatecholaminemia that were likely mediators of these deficits. Moreover, ractopamine did not diminish any wellbeing indicators and improved muscle growth without worsening the effects of heat stress. Our 2nd study assessed the effects of pubertal cyclicity (weaning to 1st breeding) in cows on myoblast-mediated muscle growth, metabolism, and growth efficiency of their offspring. Maternal fertility and postnatal growth efficiency of offspring are imperative to successful beef cattle production. A maternal condition was previously identified in which cows exhibited irregular cyclicity patterns or were non-cyclic between weaning and 1st breeding. This condition is thought to be associated with high concentrations of androstenedione in their follicular fluid, which causes cows to be sub-fertile but also wean heavier calves when they do become pregnant. We hypothesized that calves from cows exhibiting irregular pubertal cyclicity would have enhanced growth efficiency compared to calves from cows with normal pubertal cyclicity. To test this hypothesis, we evaluated myoblast function, growth, and metabolism pre-weaning, as well as growth efficiency in the feedlot and carcass characteristics at harvest in calves from cows that were previously identified as having typical, start-stop, or non-cycling pubertal cyclicity patterns. Calves from irregular cycling cows had reductions in insulin sensitivity, plasma proteins and lipids paired with increased myoblast function and reduced myoblast glycolytic capacity. Data independently and combined suggest calves from cows with irregular cyclicity from weaning to 1st breeding have chronic inflammation. While the specific mechanism of inflammation is unknown, further research may allow mediators of abnormal cyclicity and offspring inflammation-induced dysfunction to be elucidated.
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