Related Experiment Videos
Elevated muscle vitamin E does not attenuate eccentric exercise-induced muscle injury.
J A Warren1, R R Jenkins, L Packer
1Exercise Biochemistry Laboratory, University of Georgia, Athens 30602.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 1, 1992
Summary
High vitamin E diets did not protect rats against skeletal muscle damage from eccentric exercise. Muscle injury markers remained unchanged, suggesting free radicals may not initiate exercise-induced muscle damage.
Area of Science:
- Exercise Physiology
- Muscle Biology
- Nutritional Biochemistry
Background:
- Eccentric exercise can cause skeletal muscle damage.
- Oxidative stress is implicated in exercise-induced muscle injury.
- Vitamin E is an antioxidant that may protect against muscle damage.
Purpose of the Study:
- To investigate the effect of elevated muscle vitamin E on skeletal muscle damage after eccentric exercise.
- To determine if increased vitamin E content in muscle attenuates exercise-induced injury.
Main Methods:
- Sixty Sprague-Dawley rats were fed either a normal or vitamin E-supplemented diet for 5 weeks.
- Eccentric exercise was induced via a downhill walking protocol.
- Muscle damage was assessed by measuring maximal tetanic force, intact fiber count, glucose 6-phosphate dehydrogenase activity, and plasma creatine kinase activity.
Main Results:
- Muscle vitamin E levels were 3- to 4-fold higher in supplemented rats.
- Vitamin E supplementation did not reduce skeletal muscle damage markers.
- Maximal tetanic force, intact fiber count, glucose 6-phosphate dehydrogenase activity, and plasma creatine kinase activity showed similar changes in both groups post-exercise.
Conclusions:
- Elevated muscle vitamin E content does not protect against skeletal muscle damage from eccentric exercise.
- These findings do not support a major role for free radical damage in the initiation of eccentric exercise-induced muscle injury.
- Further research is needed to fully elucidate the role of free radicals in muscle damage etiology.