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Vitamin E and ExerciseAngela Mastaloudis
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| For my masters
thesis project I studied the role of vitamin E in exercise induced oxidative
stress. There are many well-known health benefits of exercise, including
cardiovascular fitness, maintenance of muscle and healthy body weight, reducing
abdominal fat, and improving insulin sensitivity. Exercise also exerts positive
effects on the blood lipid profile. However, there is evidence suggesting
that aerobic or endurance exercise (1 hour or more) causes oxidative stress.
Oxidative stress results from damage to tissues caused by free radicals.
Even when we are physically inactive, our bodies produce small amounts of
reactive oxygen species (ROS), including free radicals. Our antioxidant
defenses, including the antioxidant vitamins E and C, dispose of these low
levels of ROS. In contrast, during endurance exercise when we are using
100 to 200 times more oxygen in our active skeletal muscle, it’s likely
that we produce much higher levels of ROS. Such exercise could result in
the production of ROS at rates that exceed the body's antioxidant defense
mechanisms, which could ultimately damage our cells and tissues. Since vitamin
E (alpha-tocopherol) is the major fat-soluble antioxidant responsible for
protecting our cells from oxidative damage, an increase in oxidative stress
caused by exercise could deplete our vitamin E stores. Similarly, vitamin
C, the major water-soluble antioxidant, could also be depleted as a result
of oxidative stress during strenuous exercise.
In order to investigate this issue, we studied 11 runners (3 women and 8 men) with an average age of 45 years on two different occasions. For the first half of the study, the subjects ate a controlled diet for five days, and on the fourth day of the diet they ran a 50 kilometer (32 mile) ultramarathon. The race is an annual event that takes place in Corvallis, Oregon, in the OSU McDonald Research Forest. This rigorous race consists of a trail run over rugged terrain, with a total gain and loss in elevation of more than 12,000 feet. For the second half of the study (one month later) subjects consumed an identical diet for five days, but on the fourth day of the trial, rather than running an ultramarathon, the subjects remained inactive for the day. Subjects consumed a capsule of alpha-tocopherol labeled with deuterium with dinner on the night before either the race or the period of inactivity. All 11 subjects completed the 50 km race with an average run time of 6.5 hours, ranging from about 5 hours to about 8 hours. Average energy expenditure during the race was about 3,400 kilocalories, and energy expenditure for men was about 1.5 times that of women due to their larger size. The average running pace was relatively fast for an event of this duration at nearly 13 minutes per mile. Vitamin E utilization was determined by tracking the disappearance of labeled vitamin E from blood collected during the race. Labeled vitamin E disappeared faster during exercise compared to the sedentary period, indicating that it was being used up at a faster rate. This suggests that vitamin E was being used to protect against oxidative stress generated during the endurance run. In order to assess any oxidative damage resulting from the strenuous exercise, we measured compounds in the blood known as F2-isoprostanes, which are formed when free radicals attack our cell membranes. The presence of F2-isoprostanes in the blood is a good indicator of oxidative stress. During the run, blood levels of F2-isoprostanes nearly doubled, but they did not change at all during the sedentary trial, supporting the idea that the exercise increased oxidative stress. Considering the duration and intensity of this exercise, it is not surprising that a 57% increase in F2-isoprostanes was observed immediately after the race. The most important result of our study was that the rate of vitamin E utilization increased during endurance exercise compared to the sedentary period. This is the first time that exercise has been reported to increase the rate of vitamin E utilization, a discovery that indicates increased oxidative stress during exercise. The increase in F2-isoprostane levels observed during the ultramarathon further supports our hypothesis that the runners experienced increased oxidative stress. Oxidative stress is a feature of many diseases, including diabetes and cardiovascular disease. In these diseases, markers of oxidative stress like F2-isoprostanes are chronically elevated. We found that F2-isoprostanes increased transiently during exercise and then diminished after exercise. Therefore, oxidative stress generated during exercise may not cause much damage because it lasts only briefly. In fact, the brief increase in oxidative stress during exercise may actually boost the body's antioxidant defense system. This concept is supported by observations that antioxidant enzymes are chronically elevated in the blood of individuals who exercise regularly. It also appears that oxidative stress helps us break down our muscles and build them up even stronger during training. The results of our study show that strenuous exercise generates oxidative stress and suggest that the increase of crucial antioxidants like vitamin E, vitamin C, and uric acid in the blood during exercise may reflect enhanced antioxidant defenses in response to the oxidative stress of exercise. To investigate this more thoroughly, we are currently carrying out a placebo-controlled double-blind study examining the effects of taking supplemental vitamin E and vitamin C or placebos for six weeks prior to running an identical ultramarathon. We hope to determine whether antioxidant supplementation can alleviate oxidative stress generated during exercise and if such supplementation can improve the recovery from post-marathon fatigue. For additional information on vitamin E, see the Linus Pauling Institute's Micronutrient Information Center. Last
updated May, 2002 | ||
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Honoring a
Scientific Giant with Nutritional Research
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