Natural vitamin E exists in eight different forms, four tocopherols (a-, b-, g-, and d-) and four tocotrienols (a-, b-, g-, and d-). Alpha-tocopherol is considered the only form of vitamin E that is biologically active in the human body. The main function of vitamin E is its role as an antioxidant. Free radicals are produced in the body during normal metabolism and exposure to various environmental factors. As a peroxyl radical scavenger, it protects unsaturated lipid components in cells and plasma from free-radical attack by itself becoming oxidized. The antioxidant capacity of vitamin E is lost by oxidation with free radicals, but vitamin E can be reduced by other antioxidants such as vitamin C, regenerating the antioxidant capacity of vitamin E. Besides its antioxidant activity, vitamin E has been shown to have anti-atherogenic and anti-inflammatory effects through its modulation of some molecular signaling pathways.
Although vitamin E deficiency is rare in humans, it has been observed in individuals with genetic abnormalities in a-tocopherol transfer protein, fat malabsorption syndromes, or protein-energy malnutrition. Newborn babies may be at risk of vitamin E deficiency because the vitamin does not cross the placenta. Symptoms of vitamin E deficiency include degeneration of the sensory nerves (peripheral neuropathy), impaired balance and coordination (ataxia), muscle weakness (myopathy), and damage to the retina of the eye (pigmented retinopathy). Previously, vitamin E activity in foods and dietary recommendations were reported as a-tocopherol equivalents (a-TE) based on the biological activity of tocopherols and tocotrienols in rats. However, it is now known that a-tocopherol is biologically active in humans because only a-tocopherol is repackaged into lipoproteins by the hepatic a-tocopherol transfer protein. DRIs for vitamin E published by the IOM in 2000 were expressed as mg a-tocopherol, and the U.S. Department of Agriculture has updated its nutrient database for vitamin E expressing content in mg a-tocopherol. Alpha-tocopherol in natural foods is in the form of the isomer RRR-a-tocopherol (formally d-a-tocopherol). The synthetic form of vitamin E is all-rac-a-tocopherol, formally dl-a-tocopherol, containing all eight isomers of a-tocopherol (RRR-, RSR-, RRS-, RSS, SRR-, SSR-, SRS-, and SSS-a-tocopherol) in the mixture. Both natural and synthetic forms are used for vitamin E supplementation of foods and supplements, Natural vitamin E exists in eight different forms, four tocopherols (a-, b-, g-, and d-) and four tocotrienols (a-, b-, g-, and d-). Alpha-tocopherol is considered the only form of vitamin E that is biologically active in the human body. The main function of vitamin E is its role as an antioxidant. Free radicals are produced in the body during normal metabolism and exposure to various environmental factors. As a peroxyl radical scavenger, it protects unsaturated lipid components in cells and plasma from free-radical attack by itself becoming oxidized.
The antioxidant capacity of vitamin E is lost by oxidation with free radicals, but vitamin E can be reduced by other antioxidants such as vitamin C, regenerating the antioxidant capacity of vitamin E. Besides its antioxidant activity, vitamin E has been shown to have anti-atherogenic and anti-inflammatory effects through its modulation of some molecular signaling pathways. Although vitamin E deficiency is rare in humans, it has been observed in individuals with genetic abnormalities in a-tocopherol transfer protein, fat malabsorption syndromes, or protein-energy malnutrition. Newborn babies may be at risk of vitamin E deficiency because the vitamin does not cross the placenta. Symptoms of vitamin E deficiency include degeneration of the sensory nerves (peripheral neuropathy), impaired balance and coordination (ataxia), muscle weakness (myopathy), and damage to the retina of the eye (pigmented retinopathy).
Previously, vitamin E activity in foods and dietary recommendations were reported as a-tocopherol equivalents (a-TE) based on the biological activity of tocopherols and tocotrienols in rats.18 However, it is now known that a-tocopherol is biologically active in humans because only a-tocopherol is repackaged into lipoproteins by the hepatic a-tocopherol transfer protein.19 DRIs for vitamin E published by the IOM in 2000 were expressed as mg a-tocopherol, and the U.S. Department of Agriculture has updated its nutrient database for vitamin E expressing content in mg a-tocopherol. Alpha-tocopherol in natural foods is in the form of the isomer RRR-a-tocopherol (formally d-a-tocopherol). The synthetic form of vitamin E is all-rac-a-tocopherol, formally dl-a-tocopherol, containing all eight isomers of a-tocopherol (RRR-, RSR-, RRS-, RSS, SRR-, SSR-, SRS-, and SSS-a-tocopherol) in the mixture. Both natural and synthetic forms are used for vitamin E supplementation of foods and supplements, in cellular membranes, may lower the oxidative stress associated with exercise. In vitamin E-deficient rats, exercise increased susceptibility to free radical damage and declined exercise endurance capacity. Supplementation of vitamin E alone or in combination with other antioxidants such as vitamin C and carotenoids has been shown to result in inconclusive results varying from reduced lipid peroxidation to no effects for protecting against exerciseinduced lipid peroxidation. Several studies have reported that vitamin E supplementation has an effect in attenuating exercise-induced lipid peroxidation in aerobic or endurance exercise, but not strength training, by decreasing lipid peroxidation markers such as malondiadehyde, F2-isoprostanes, or breath pentane. However, the vitamin E effects in antioxidant combinations on exercise-induced oxidative stress have been shown to produce inconsistent results.17 Athletes often use vitamin E supplementation to prevent exercise-induced muscular damages and fatigue. Damage to skeletal muscle cell membranes by exercise-induced oxidative stress can impair cell viability, resulting in necrosis and an acute-phase inflammatory response.
However, the evidence of antioxidant protection provided by vitamin E supplementation on membrane damage following exercise and recovery is limited; thus, further research is needed in this area. Many studies have been conducted to investigate the effects of vitamin E supplementation as an ergogenic aid. Most studies have shown no improvement in exercise performance of humans with vitamin E supplementation.
The current RDAs for vitamin E meet the needs of normal healthy people, but no specific recommendations have been set for athletes. Vitamin E may be of some benefit in endurance exercise to decrease exercise-induced oxidative stress, although vitamin E supplementation seems to have no effect on exercise performance, muscle damage, or recovery. Athletes who consume low intakes of antioxidants including vitamin E may be at risk for the harmful effects of oxygen radicals, and endurance athletes may need more than the recommendation of vitamin E.
The antioxidant capacity of vitamin E is lost by oxidation with free radicals, but vitamin E can be reduced by other antioxidants such as vitamin C, regenerating the antioxidant capacity of vitamin E. Besides its antioxidant activity, vitamin E has been shown to have anti-atherogenic and anti-inflammatory effects through its modulation of some molecular signaling pathways. Although vitamin E deficiency is rare in humans, it has been observed in individuals with genetic abnormalities in a-tocopherol transfer protein, fat malabsorption syndromes, or protein-energy malnutrition. Newborn babies may be at risk of vitamin E deficiency because the vitamin does not cross the placenta. Symptoms of vitamin E deficiency include degeneration of the sensory nerves (peripheral neuropathy), impaired balance and coordination (ataxia), muscle weakness (myopathy), and damage to the retina of the eye (pigmented retinopathy).
Previously, vitamin E activity in foods and dietary recommendations were reported as a-tocopherol equivalents (a-TE) based on the biological activity of tocopherols and tocotrienols in rats.18 However, it is now known that a-tocopherol is biologically active in humans because only a-tocopherol is repackaged into lipoproteins by the hepatic a-tocopherol transfer protein.19 DRIs for vitamin E published by the IOM in 2000 were expressed as mg a-tocopherol, and the U.S. Department of Agriculture has updated its nutrient database for vitamin E expressing content in mg a-tocopherol. Alpha-tocopherol in natural foods is in the form of the isomer RRR-a-tocopherol (formally d-a-tocopherol). The synthetic form of vitamin E is all-rac-a-tocopherol, formally dl-a-tocopherol, containing all eight isomers of a-tocopherol (RRR-, RSR-, RRS-, RSS, SRR-, SSR-, SRS-, and SSS-a-tocopherol) in the mixture. Both natural and synthetic forms are used for vitamin E supplementation of foods and supplements, in cellular membranes, may lower the oxidative stress associated with exercise. In vitamin E-deficient rats, exercise increased susceptibility to free radical damage and declined exercise endurance capacity. Supplementation of vitamin E alone or in combination with other antioxidants such as vitamin C and carotenoids has been shown to result in inconclusive results varying from reduced lipid peroxidation to no effects for protecting against exerciseinduced lipid peroxidation. Several studies have reported that vitamin E supplementation has an effect in attenuating exercise-induced lipid peroxidation in aerobic or endurance exercise, but not strength training, by decreasing lipid peroxidation markers such as malondiadehyde, F2-isoprostanes, or breath pentane. However, the vitamin E effects in antioxidant combinations on exercise-induced oxidative stress have been shown to produce inconsistent results.17 Athletes often use vitamin E supplementation to prevent exercise-induced muscular damages and fatigue. Damage to skeletal muscle cell membranes by exercise-induced oxidative stress can impair cell viability, resulting in necrosis and an acute-phase inflammatory response.
However, the evidence of antioxidant protection provided by vitamin E supplementation on membrane damage following exercise and recovery is limited; thus, further research is needed in this area. Many studies have been conducted to investigate the effects of vitamin E supplementation as an ergogenic aid. Most studies have shown no improvement in exercise performance of humans with vitamin E supplementation.
The current RDAs for vitamin E meet the needs of normal healthy people, but no specific recommendations have been set for athletes. Vitamin E may be of some benefit in endurance exercise to decrease exercise-induced oxidative stress, although vitamin E supplementation seems to have no effect on exercise performance, muscle damage, or recovery. Athletes who consume low intakes of antioxidants including vitamin E may be at risk for the harmful effects of oxygen radicals, and endurance athletes may need more than the recommendation of vitamin E.
