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1 Institute of Gerontology, University of Michigan, Ann Arbor, Michigan 48109-2007; and 2 Muscle Research Centre, Department of Medicine, University of Liverpool, Liverpool L69 3BX, United Kingdom
Received 4 March 1996; accepted in final form 6 May 1997.
Van der Meulen, Jack H., Anne McArdle, Malcolm J. Jackson,
and John A. Faulkner. Contraction-induced injury to the extensor
digitorum longus muscles of rats: the role of vitamin E. J. Appl. Physiol. 83(3): 817-823, 1997.
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
-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.
pliometric contractions; muscle damage; serum creatine kinase activity; serum pyruvate kinase activity; eccentric exercise
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