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Health & Exercise Physiology
Stephen C. Kolwicz, Jr.
Second Student Contributor
Fatty acids are an important energy source in long duration endurance exercise. From the blood, fatty acids enter cells in the skeletal muscle and enter the mitochondria to participate in metabolic pathways to regenerate adenosine triphosphate (ATP). Mitochondrial uptake of fatty acids can be inhibited by malonyl-CoA, which is produced by the enzyme acetyl CoA carboxylase 2 (ACC2). Therefore, ACC2 could be a target to promote fatty acid metabolism and enhance exercise performance. Mice with a systemic deletion of ACC2 (ACC-TKO) and control mice were confirmed by genotyping before the study began. Male and female mice were randomly assigned to voluntary wheel running or sedentary groups. Mice in the voluntary wheel running group were provided unlimited access to a running wheel in the home cage for a total of six weeks. A data acquisition system connected to the running wheel monitored daily activity. Running activity was assessed every hour for twenty-four hours over the course of the six weeks. At the end of six weeks, the mice were weighed and organs (heart, quadriceps, spleen, adipose) were harvested and weighed. Weights were compared to sedentary mice to determine the effects of physical activity. Blood glucose and ketone bodies were measured in blood from all mice. Results from the study will show whether the deletion of ACC2 has a positive effect on exercise performance.
Ponzo, Paige, "The Effects of ACC2 Deletion in Voluntary Wheel Running" (2023). Health and Exercise Physiology Summer Fellows. 26.
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