Meeting Abstract

P2.22  Saturday, Jan. 5  Influence of Acute Exercise and Ethanol on Mitochondrial Biogenesis Pathways ALMEIDA MANSILLA, E*; DYAL, J; LEWIS, JM; BRIM, D; CLYMAN, T; BLANK, JM; California Polytechnic State University; California Polytechnic State University; California Polytechnic State University; California Polytechnic State University; California Polytechnic State University; California Polytechnic State University nerfe_a@hotmail.com

Acute ethanol exposure inhibits muscle protein synthesis, while chronic ethanol exposure causes muscle wasting in humans and laboratory animals. In contrast, resistance exercise increases protein synthesis and endurance exercise stimulates mitochondrial biosynthesis. Few studies have addressed the interaction of ethanol and exercise. To assess this interaction, Sprague-Dawley rats were familiarized on a treadmill for three weeks and then subjected to an exhaustive acute run. Following the acute bout of exercise, each rat was injected with ethanol (75 mmol/kg) or an equivalent volume of saline. Subjects were sacrificed three hours later and tissues harvested, freeze-clamped, and stored at -80oC. Proteomic techniques were used in order to detect proteins whose phosphorylation state changed due to exercise and/or ethanol exposure. Mass spectrometry was used to identify the proteins that vary in their state. Standard western blot procedures were used to measure phosphorylation state of proteins known to be involved in up-regulation of mitochondrial biosynthesis, such as proliferator-activated receptor -γ coactivator-1α (PGC-1α), cAMP response element-binding (CREB), and p38 MAP Kinase (p38MAPK). These techniques were used to test the hypothesis that alcohol reduces the activation of proteins involved in mitochondrial biogenesis. This work was sponsored by the Department of the Navy, Office of Naval Research, under Award #N00014-11-1-0359.