Endurance and Interval Training and Palmitoyl L-Carnitine Oxidation by Mitochondria from VLCAD Deficient Mice

Abstract

2258 Very-long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is a fatty acid oxidation disorder that limits oxidation of fatty acids sixteen carbons and longer. However, even in VLCAD deficiency, some residual enzyme activity toward palmitate remains because of the overlap of specificity with LCAD. PURPOSE: This project examined the hypothesis that exercise training would enhance gastrocnemius subsarcolemmal (SS) and intermyoflbrillar (IMF) mitochondrial oxidation of palmitoyl l-carnitine plus malate and that high-intensity interval training would have a greater effect than endurance training. METHODS: The groups were sedentary control mice (C), endurance trained mice (E), and interval trained mice (I). Both groups of training mice exercised 5 dfiwk−1. During the first four weeks of training the durations and intensity of exercise were progressively increased. At the end of the four weeks, endurance training mice were running on the motor driven treadmill at a speed of 24 m fimin−1 for 60 min. Interval training mice ran for 2 min at 24 m fimin−1 followed by 2 min at 41 m. min−1. The intervals were then alternated for a total of 46 min. day−1. Beginning at the end of the 8th week, the gastrocnemius muscle was removed and the oxidation of palmitoyl-carnitine plus malate determined polarographically. RESULTS: Oxidation was significantly (p <0.05) depressed in IMF mitochondria from VLCAD deficient mice but not subsarcolemmal mitochondria. High-intensity interval training caused large increases in palmitoyl l-carnitine oxidation by both subsarcolemmal (p < 0.05) and intermyofibrillar mitochondria. Endurance training did not cause a significant increase in either subsarcolemmal or intermyofibrillar oxidation rates. CONCLUSIONS: Unlike previous observations in mice, these results show that high intensity, interval training is more effective than endurance training in improving fatty acid oxidation, at least in subsarcolemmal mitochondria. Further, the results show that mitochondrial oxidation of palmitoyl l-carnitine is reduced in VLCAD deficient mice relative to non-deficient mice.