The effect of acute vitamin C supplementation in response to oxidative factors after sub maximal exercise in normobaric hypoxia

Background and aim: Maximal exercise in normoxia results in oxidative stress due to an increase in free
radical Production .This increase has negative effect on energy production during exercise and due to
fasting fatigue. However, the effect of a single bout of moderate aerobic exercise performed normobaric
hypoxia on free radical production, lipid per oxidation and total antioxidant capacity (TAC) remains
inconsistent. In this study, we followed the effect of acute vitamin C supplementation in response to
oxidative factors after sub maximal exercise in normobaric hypoxia. Material and method: 11active
male) age: 22.18±2.18 yrs, BMI: 21.99±1.24 kg/m2) was required to exercise on a treadmill at 55% of
VO2mox for 35 minutes hypoxic condition [FiO2 (inspired fraction of O2) =0.14(altitude about 3500
meter). The subject received orally ascorbic acid (1000 mg/ two hours before exercise session). Blood
samples were taken before (fasting) and immediately after exercise. Total antioxidant capacity (TAC),
lipid per oxidation products malondialdehyde (MDA) and uric acid were measured using HPLC and/or
photometric detection. The results obtained were analyzed by two-way analysis ofvariance (ANOVA)
using SPSS statistics software package (version 16) followed by post-hoc Kolmogroph-Smirnov test
where F value was significant. Level of significance was set at p ≤0.05. Results: The main findings show
that moderate intensity exercise in the hypoxia position, increased significantly plasma-volume-corrected
TAC and uric acid concentration (pooled rest compared with exercise P<0.05); However, vitamin C
supplementation did significantly affect MDA concentration (P<0.05). Discussion: These observations
would suggest that single bout of moderate aerobic exercise in normobaric hypoxia increases oxidant and
antioxidant markers in oxidative stress and supplementation vitamin C was an effective preventive agent,
which further supports the oxidative character (beta oxidation) versus lipid per oxidation induced by
hypoxia.