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Handbook of Vitamin C Research

Handbook of Vitamin C Research

Handbook of Vitamin C Research

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24Kelsey H. Fisher-Wellman and Richard J. BloomerConcentric, Short Duration ProtocolsChronic ingestion <strong>of</strong> various antioxidants mixtures has been shown to attenuate variousmarkers <strong>of</strong> aerobic exercise-induced oxidative damage [90,130,140-142], almost withoutexception [143]. With respect to lipid peroxidation, Bryant and coworkers [130] reported anincrease in exercise (90 minute cycle ride at 60-70% VO 2max ) induced lipid peroxidation(MDA), which was prevented following three weeks <strong>of</strong> supplementation with 1000mg <strong>of</strong>vitamin C + 200IU <strong>of</strong> vitamin E/day in trained men. Moreover, in this same study,supplementation with vitamin C alone (1000mg/day for 3 weeks) resulted in an exacerbatedincrease in MDA, suggesting that chronic administration <strong>of</strong> vitamin C alone may not bewarranted [130]. In a similar study conducted by Kanter et al. [90] attenuation in exerciseinducedlipid peroxidation (assessed via MDA and expired pentane) was reported followingtreatment with a vitamin C (250mg) vitamin E (148mg), and beta-carotene (7.5mg) mixture.In opposition to the above findings, no effect <strong>of</strong> supplementation has been reported by twoinvestigators for exercise-induced MDA formation, despite the use <strong>of</strong> comparable exercise(30 minute run at 80% VO 2max ) and treatment (1000mg vitamin C + 400IU vitamin E/day for14 days) protocols [141,142]. Additionally, Meijer et al. [144] reported no effects <strong>of</strong>antioxidant supplementation (200mg vitamin C + 100mg vitamin E + 2mg beta-carotene/dayfor 12 weeks) on exercise-induced (45 minute cycle ride at 50% max workload) antipyrine(indirect marker or hydroxyl radical formation) and TBARS formation in a population <strong>of</strong> 60year old men and women.With respect to oxidative damage to other biomolecules (protein, glutathione, DNA),three other investigators have reported an attenuation in exercise-induced protein [142] andglutathione [140,141] oxidation following chronic ingestion <strong>of</strong> a vitamin C and vitamin Emixture (1000mg vitamin C + 400IU vitamin E/day for 14 days) [141,145], as well as vitaminC in combination with glutathione (2000mg vitamin C + 1g GSH/day for 7 days) [140]. Theexercise protocol utilized by Sastre et al. [140] consisted <strong>of</strong> a GXT performed on a treadmill.Regarding DNA oxidation or markers <strong>of</strong> muscle injury, no study to our knowledge hasreported a protective effect <strong>of</strong> antioxidant supplementation (including vitamin C)[141,143,145]. Null findings in relation to DNA oxidation may have resulted from the use <strong>of</strong>a less taxing exercise protocol, evident by a failure to induce an increase in 8-OHdG[141,145].Taken together, it appears that chronic ingestion <strong>of</strong> various antioxidant mixtures, whichcontain vitamin C, possess the potential to attenuate lipid peroxidation, as well as protein,andglutathione oxidation, despite having no effect on DNA oxidation. Although other variablesare likely involved (i.e., the direct scavenging <strong>of</strong> the excess antioxidants), these attenuatingeffects may be due to an increase in the activity <strong>of</strong> various antioxidant enzymes followingsupplementation. That is, perhaps antioxidant supplementation serves to increase the activity<strong>of</strong> endogenous antioxidant defenses, as has been reported by Tauler et al. [146]. In this studyan increase in GPx and CAT both at rest and in response to acute exercise (GXT) wasreported following supplementation with a vitamin C, vitamin E, and beta-carotene mixture(250mg vitamin E + 15mg beta-carotene/day for 90 days + 500mg vitamin C for last 15 days)[146]. Based on these findings, perhaps the excess availability <strong>of</strong> non-enzymatic antioxidants

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