Submission Date

7-20-2018

Document Type

Paper- Restricted to Campus Access

Department

Health & Exercise Physiology

Faculty Mentor

Stephen Kolwicz

Student Contributor

Ian Dysinger

Comments

Presented during the 20th Annual Summer Fellows Symposium, July 20, 2018 at Ursinus College.

Project Description

Acetyl CoA carboxylase 2 (ACC2) produces Malonyl CoA, which inhibits fatty acid oxidation in the mitochondria. The deletion of ACC2 has been proposed to decrease exercise performance due to mitochondrial defects. Previous studies on mice with a full body deletion of ACC2 (ACC2-null) have shown no decrease in heart mitochondrial function, despite those mice having impaired performance on endurance exercise tests when compared to control mice. Additionally, this impairment in ACC2-null mice can be corrected through the use of chronic exercise training over the course of several weeks. The purpose of our study is to develop a procedure for the isolation and analysis of skeletal mitochondria to better understand why this impairment occurs and why chronic exercise training corrects it.

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