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Fatty acids (FAs) are an important energy source for long duration endurance exercise. Mitochondrial uptake of (FAs) is inhibited by malonyl CoA, which is produced via the enzyme acetyl CoA carboxylase 2 (ACC2). In the present study, we generated mice with a systemic deletion of ACC2 (ACC2-null) to increase fatty acid oxidation (FAO) and promote endurance exercise capacity. Using metabolic chambers, the respiratory quotient during the initial hours of the dark cycle was lower in male ACC2-null mice, suggesting increased FAO. Body weight, as well as heart, skeletal muscle, liver, and adipose tissue mass in untrained ACC2-null mice were similar to control (CON). No differences in cage activity and food intake were noted between CON and ACC2-null mice. When subjected to an endurance exercise capacity (EEC) test on a motorized treadmill, ACC2-null mice showed a 25% decrease in EEC, which was associated with a ~20% reduction of citrate synthase (CS) activity in the soleus but not in liver and heart. Electron microscopy analysis suggested lower mitochondria density and abnormal size distribution in ACC2-null soleus muscle. However, 10 weeks of exercise training normalized the decreased EEC in ACC2-null mice and corrected the deficit in skeletal muscle CS activity. Systemic deletion of ACC2 impairs EEC in untrained mice, due to a negative effect on skeletal muscle mitochondria size and function. However, exercise training corrects this defect. The present data suggests that increasing mitochondrial FA transport, via ACC2 deletion, is not effective for improving exercise capacity and may negatively affect skeletal muscle mitochondria.
Kurzinsky, Katherine, "Exercise Training Rescues Impaired Exercise Capacity in Mice With Systemic Deletion of Acetyl CoA carboxylase 2 (ACC2)" (2020). Health and Exercise Physiology Presentations. 9.
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