Abstract

We investigated the hypothesis that very long chain acyl CoA dehydrogenase (VLCAD) deficiency would alter recovery of skeletal muscle from high and low intensity exercise. The groups were non-VLCAD deficient, not exercised (NN); non-VLCAD deficient, high intensity exercised (NI); non-VLCAD deficient, low intensity exercised (NE); VLCAD deficient, not exercised (DN); VLCAD deficient, high intensity exercised (DI); and VLCAD deficient, low intensity exercised (DE). High intensity exercised mice were matched by weight with low intensity exercisers. High intensity mice initially ran at a speed of 16 m· min−1 and 0% grade. The speed and grade were increased at 6 min intervals to 24 m· min−1 at 0% grade, 30 m· min−1 at 2% grade, 35.5 m· min−1 at 4% grade, 41 m· min−1 at 6% grade, and 47 m· min−1 at 8% grade. Low intensity mice ran at 24 m· min−1. The duration of low intensity exercise was determined by the performance of the matched high intensity exerciser and was sufficient to equate the amount of work done by both mice. Twenty-four hours following exercise, skeletal muscle function of the gastrocnemius was determined. Measures included peak twitch tension (p t), the force-frequency response at 40, 60, 80, 100, 120, and 140 Hz, maximum tetanic tension (p o), and the fatigue index (FI). Data were analyzed using ANOVA of data in a 2×3 factorial design. Exercise had no adverse effects on skeletal muscle function after 24 hours of rest in non-enzyme deficient mice. DN mice generated significantly higher absolute pt (p < 0.05), po (p < 0.05), and force-frequency response at 40, 60, 80, 100, 120, and 140 Hz (p < 0.05) than DE mice. Similar non-significant responses were observed for the DI mice except at 100, 120, and 140 Hz, the differences were significant (p < 0.05). The FI was not effected by exercise. These data indicate that acute exercise in VLCAD deficient mice causes a decline in skeletal muscle function in muscle of mixed fiber type regardless of the type of exercise performed.

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