Abstract
PURPOSE: Ascorbic acid (vitamin C) is a major antioxidant in the airways. Data on the effect of antioxidants on exercise-induced asthma (EIA) is equivocal. Therefore, the aim of this study was to determine the effects of ascorbic acid (vitamin C) supplementation on the severity of EIA. METHODS: Eight subjects with EIA participated in a randomized, placebo controlled double-blind cross-over trial. Subjects entered the study on their normal diet and were then placed on either 2 weeks of ascorbic acid supplementation (1500mg/day) or placebo, followed by a 1 week washout period, before crossing over to the alternative diet. Pre- and post-exercise pulmonary function was assessed at the conclusion of each treatment period. In addition, urine samples were collected pre- and post-exercise and assayed for the presence of pro inflammatory mediators, cysteinyl leukotrienes (LT) C4-E4 and 9α, 11β- prostaglandin (PG) F2 which have been implicated in the pathogenesis of EIA. Urine was assayed for hydrogen peroxide (H2O2), as a marker of oxidative stress. Diet was monitored through 24-hour dietary recall to ensure that diet was not significantly different between the trials. Pre- and post exhaled breath nitric oxide (FENO) was measured as a noninvasive indicator of airway inflammation. RESULTS: Ascorbic acid supplementation significantly reduced (p <0.05) the mean maximum fall in post-exercise FEV1 (−6.4 ± 2.4%) compared to normal diet (−14.3 ± 1.6%) and placebo (−12.9 ± 2.4%). Post-exercise FENO was reduced on ascorbic acid supplementation (23.8 ± 7.7 ppb) as compared to normal diet (48.4 ±16.3 ppb) and placebo (34.1 ± 7.8 ppb). Ascorbic acid supplementation induced significant reductions (p <0.05) in urinary LTC4-E4 on the ascorbic acid supplementation (5.3 ±1.7 ng/mmol of creatinine) compared to the normal diet (15.0 ±4.0 ng/mmol/creatinine) and placebo (11.1 ±3.1 ng/mmol/creatinine). Similarly, urinary 9α, 11β-PGF was significantly reduced on the ascorbic acid supplementation (8.5 ±1.7 ng/mmol/creatinine) compared to the normal diet (20.0 ±4.5 ng/mmol/creatinine) and placebo (13.0 ± 1.8 ng/mmol). Furthermore, significant reductions (p <0.05) in urinary HO were observed on the ascorbic acid supplementation (5.6 ± 1.3 mmol/L) compared to placebo (23.6 ±5.1 mmol/L) and normal diet (12.6 ±2.9 mmol/L). CONCLUSION: These data indicate that high dose ascorbic acid supplementation reduces the severity of EIA. This reduction in the severity of EIA may occur through a mechanism by which ascorbic acid reduces reactive oxygen species, thereby leading to a reduction in bronchoconstrictive mediators.
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