Abstract
Introduction: Hypobaric hypoxia and heightened metabolic rate increase free radical production. Purpose: We tested the hypothesis that antioxidant supplementation would reduce oxidative stress associated with increased energy expenditure (negative energy balance) at high altitude (HA 4300 m). Methods: For 12 d at sea level (SL), 18 active men were fed a weight-stabilizing diet. Testing included fasting blood and 24-h urine samples to assess antioxidant status [plasma α-tocopherol, β-carotene, lipid hydroperoxides (LPO), and urinary 8-hydroxydeoxyguanosine (8-OHdG)] and a prolonged submaximal (55% V̇o2peak) oxidative stress index test (OSI) to evaluate exercise-induced oxidative stress (plasma LPO, whole blood reduced and oxidized glutathione, glutathione peroxidase, and urinary 8-OHdG). Subjects were then matched and randomly assigned to either a placebo or antioxidant supplement group for a double-blinded trial. Supplementation (20,000 IU of β-carotene, 400 IU α-tocopherol acetate, 500 mg ascorbic acid, 100 μg selenium, and 30 mg zinc, or placebo) was begun 3 wk prior to and throughout a 14-d HA intervention. At HA, subjects' daily energy intake and expenditure were adjusted to achieve a caloric deficit of approximately 1400 kcal. Fasting blood and 24-h urine samples were collected throughout HA and the OSI test was repeated on H A day 1 and day 13. Results: Resting LPO concentrations increased and urinary 8-OHdG concentrations decreased over HA with no effect of supplementation. Prolonged submaximal exercise was not associated with increased concentrations of oxidative stress markers at SL or HA. Conclusions: Antioxidant supplementation did not significantly affect markers of oxidative stress associated with increased energy expenditure at HA.
Original language | English |
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Pages (from-to) | 881-888 |
Number of pages | 8 |
Journal | Aviation Space and Environmental Medicine |
Volume | 75 |
Issue number | 10 |
State | Published - Oct 2004 |
Keywords
- DNA damage
- Free radical
- Glutathione
- Hypoxia
- Lipid peroxidation