Zumbro, Emily L.Gordon, R.A.Guerin, G.D.Duplanty, Anthony A.2019-04-232019-04-232019https://hdl.handle.net/11274/11226Creative Arts and Research SymposiumSkeletal muscle (SKM) is a prime regulator of metabolism. Exercise greatly enhances this regulation by increasing SKM metabolism and growth. PURPOSE: The purpose of this study was to explore the effects of an exercise mimetic, Formoterol (FORM), on the expression of genes related to SKM mitochondrial biogenesis and metabolism In Vitro. METHODS: Human SKM myofibers were treated with FORM or DMSO starting at 24hrs post differentiation, which continued until day 6 of differentiation. Total RNA was extracted on one day (D1), four days (D4), and six days (D6) post differentiation. Gene expression for TFAM, ERRα, NRF‐1, Nrf2, and ATG5 was analyzed by qPCR. RESULTS: FORM preserved genetic expression for TFAM, ERRα, NRF‐1, Nrf2 and ATG5 at D4 compared to D1. CONCLUSION: Formoterol preserved mitochondrial biogenesis and reduced autophagy signaling at D4. (Faculty Sponsor: Dr. Anthony Duplanty)en-USIn vitro FORMSKM cell treatmentMitochondrial biogenesisBeta oxidationFormoterol treatment in vitro preserves expression of genes related to mitochondrial biogenesis, metabolism, and cell survival during skeletal muscle myogenesisPresentation