The effect of short-term colostrum supplementation on serum malondialdehyde levels and total antioxidant capacity due to acute resistance in healthy men
During intense exercise reactive species produce oxygen that results in cell damage. It seems that the use of antioxidant supplements reduces the oxidative stress caused by such exercises. Therefore the purpose of this study was to investigate the effect of short-term colostrum supplementation on serum malondialdehyde levels and total antioxidant capacity induced by acute resistance in healthy men.
The statistical population of this study was all healthy students of Birjand University with age range of 20 to 24 years old. Ten of them were randomly selected as the statistical sample. The present study was carried out in a semi experimental and applied cross-sectional design with an experimental group (n=10) to control individual differences. Subjects of this research were resistance movement protocol, consisting of six movements in 10 replications with 80% 1Rm, one minute rest between the turns and two minutes of rest between the movements. The subjects were taken from the arterial vein before the beginning of the exercise program at each stage and immediately after the exercise program followed by a 12-hour fasting of 8 ml of blood. After 14 days of supplementation, resting was performed again after 5 minutes, and blood samples were taken from the subjects. From the day the protocol was administered to the subject for a period of two weeks, one day, using the powdered colostrum supplement in a dose of 20 grams that was taken with 200 ml of water. The bleeding process was repeated after two weeks of supplementation.
The concentration of malondialdehyde decreased significantly after colostrum supplementation after two weeks(p=0.001), Also serum total antioxidant capacity increased after colostrum supplementation after two weeks(p=0.007).
Due to the antoxidant properties of colostrom, and oxidative stress during sport activities and imbalance supplement to reduce and inhibition of oxidative stress.
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