Β-Adrenergic Agonist Mediated Changes in Muscle Energy Metabolism in AMPKγ3 R200Q Pigs

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ObjectivesThe β-adrenergic agonist Ractopamine (RAC) repartitions nutrients from adipose to skeletal muscle and enhances muscle accretion in a fast-fiber type specific manner. In contrast, muscles from pigs with a mutation in the key energy sensor, AMP-activated protein kinase (AMPK), exhibit a slower, more oxidative phenotype and elevated glycogen. Our objective was to utilize RAC and AMPK-mutated pigs to investigate the cellular signaling pathways regulating energy metabolism. Materials and MethodsAt approximately 90 kg, wild-type and AMPKγ3ᴿ²⁰⁰Q barrows (n = 29) were assigned to control diet or diet supplemented with RAC (9 ppm; Elanco Animal Health) for 28 d. Pigs were harvested and muscle was collected from the longissimus lumborum (LL) immediately after exsanguination (t = 0 min) and deep (red) and superficial (white) portions of the semitendinosus (RST and WST respectively) were collected at 15 min. Glycogen content and parameters of glycogen metabolism were analyzed, and muscle metabolic phenotype was assessed by measuring glycolytic and oxidative enzyme activities. ResultsRegardless of RAC or muscle, AMPKγ3ᴿ²⁰⁰Q increased glycogen (P < 0.001) and glycolytic potential (P < 0.001) compared to wild-type. In the LL, RAC decreased glycolytic potential in AMPK but not wild-type (genotype × diet, P < 0.05). Dietary RAC decreased glucose in RST and LL (P < 0.05) and WST (P = 0.08). The glycolytic capacity, indicated by lactate dehydrogenase activity, was differentially influenced by RAC and genotype in WST (genotype × diet, P < 0.02), whereas in the LL, lactate dehydrogenase was increased by RAC (P = 0.05). In contrast, oxidative capacity, assessed by citrate synthase activity, was increased (P < 0.001) in AMPK regardless of RAC in both LL and STW. ConclusionWhile AMPKγ3ᴿ²⁰⁰Q is associated with altered glycogen storage and a more oxidative metabolism, RAC administration affects muscle metabolic characteristics and alters metabolites toward glycolytic usage in a muscle specific manner. These results indicate that AMPK and RAC influence glycogen storage and energy metabolism, which may ultimately impact capacity for muscle growth.