Contraction-induced injury to the extensor digitorum longus muscles of rats: the role of vitamin E.

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Abstract
Three days after a protocol of 225 pliometric (lengthening) contractions was administered to in situ extensor digitorum longus muscles of rats, the force deficit was 64 +/- 7% and the percentage of damaged muscle fibers was 38 +/- 5% of the control values. We then tested the hypothesis that at 3 h and 3 days after the protocol an elevation in the muscle vitamin E content would decrease the force deficit, the percentage of damaged muscle fibers, and the serum activities of creatine kinase and pyruvate kinase. The 5-8 days of intravenous injections of alpha-tocopherol increased muscle vitamin E content threefold compared with vehicle (ethanol)-treated rats. Despite the difference in vitamin E content, the force deficit and number of damaged fibers were not different. After the contraction protocol, the serum creatine kinase and pyruvate kinase activities of the vehicle-treated rats increased fourfold at 3 h and twofold at 3 days, whereas the vitamin E-treated rats showed no change. We conclude that vitamin E treatment did not ameliorate either the induction of the injury or the more severe secondary injury at 3 days. Despite the absence of evidence for an antioxidant function, the lack of any increase in serum enzyme activities for vitamin E-treated rats at 3 h and 3 days supported a role for vitamin E in the prevention of enzyme loss after muscle damage.