University of Arkansas, Fayetteville


Disorders of fatty acid metabolism pose a variety of problems including hypoglycemia, muscle weakness, muscle cramping, rhabdomyolysis, and, in the most severe cases, death. Individuals with a deficiency of very-long-chain acyl-CoA dehydrogenase (VLCAD ), the enzyme initiating the oxidation of very-long-chain fatty acids, are particularly prone to exercised-induced declines in muscle function because oft he importance of very-long-chain fatty acids to energy metabolism in exercise. The purpose of this project was to study muscle glycogen resynthesis in the recovery from high intensity exercise in VLCAD deficient mice. Recovery of skeletal muscle function (gastrocnemius) following exercise is not as rapid in VLCAD deficient mice as recovery in non-deficient mice. Based upon previous reports, recovery of muscle from exercise is, at least in part, related to glycogen resynthesis. It was hypothesized that muscle glycogen levels as well as liver glycogen levels would be significantly depressed 24 hours after exercise in VLCAD deficient exercised mice compared to non-exercised VLCAD deficient and exercised and non-exercised non-deficient mice. Twenty VLCAD deficient mice (knockout mice) and 20 non-deficient 129 Sv/C57BL6 mice were used in this project. Ten from each group exercised on a motor-driven treadmill to exhaustion using high intensity interval exercise while an additional] 0 animals from each group served as non-exercised controls. The exercised mice were allowed to recover for 24 hours and then anesthetized using sodium pentobarbital (80 mg ·Kg -1). The right and left gastrocnemius muscles, the vastus lateralis muscle, the heart, and the liver were removed and frozen and the glycogen content subsequently determined. The resynthesis of glycogen was only significantly (p < 0.05) effected in the vastus lateralis muscle and the liver. Resynthesis was significantly reduced in the vastus muscle of VLCAD deficient mice and enhanced in the vastus muscle of non-deficient mice. It was concluded that VLCAD deficiency does delay recovery of muscle glycogen after exercise and that the delay may be affected by muscle fiber type or patterns of recruitment.