Department of Animal Science

 

Date of this Version

2020

Citation

Transl. Anim. Sci. 2020.4:S94–S97

doi: 10.1093/tas/txaa112

Comments

© The Author(s) 2020. Published by Oxford University Press on behalf of the American Society of Animal Science. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License

Abstract

Beta-adrenergic agonists (βAA), Ractopamine HCl (RH) and Zilpaterol HCl (ZH), are FDAapproved supplements utilized in pigs and cattle to improve growth performance, carcass weight, and longissimus muscle area (Arp et al., 2014; Lean et al., 2014). Previous studies within our group have focused on understanding molecular changes in skeletal muscle due to βAA supplementation. This work has shown that βAA supplementation increases glucose oxidation in muscle from thermoneutral and heat-stressed lambs (Barnes et al., 2019) and in rat skeletal muscle stimulated with ZH (Cadaret et al., 2017). Skeletal muscle transcriptomics of lambs supplemented ZH revealed upregulation of genes associated with the callipyge phenotype of sheep (Yu et al., 2018) as well as the upregulation of mitochondrial solute carrier SLC25A25 (Kubik et al., 2018). SLC25A25 is a Ca2+ sensitive ATP-Mg2+/Pi inner mitochondrial membrane solute transporter. Due to the role of the mitochondria in metabolism and the results of prior transcriptomics studies, the objective of this study was to understand how βAA affect mitochondrial function of bovine skeletal muscle stem (i.e., satellite) cells. We hypothesized that βAA would improve efficiency and ATP production capacity of muscle stem cells by modifying mitochondrial function.

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