Free Radicals, Exercise, and Antioxidants - Setanta College

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180 McBride and Kraemer Vitamin E. There are several nonenzymatic antioxidant substances in the body that can be supplemented easily. Probably the most focused on and important is vitamin E (tocopherols). It has been shown that this lipid-soluble vitamin is an effective antioxidant within the cell membrane (7, 30). The ability of vitamin E to prevent oxidation of unsaturated fatty acids is believed to be its primary function in the body (26). The absence of vitamin E results in the abnormal structure and function of cellular organelles and the cell membrane itself (26). Vitamin E supplementation in humans originally developed in the search for a treatment of muscle diseases. In animal models muscular dystrophy is associated with vitamin E deficiency myopathy (5). The protective mechanism of vitamin E has been shown in several animal models that used contractile activity as a stimulus for muscle damage. Vitamin E status in rats has been highly correlated with the susceptibility of that animal to damage from muscle contractions (31). In addition, studies have shown the protective effect of oral vitamin E supplementation (51). As previously mentioned, models looking at the effects of vitamin E supplementation on muscle damage have involved muscle contraction. Vitamin E exerts its major effect by the oxidation of free radicals (65). The mechanisms of ischemia-reperfusion injury have been the foundation for which the damaging effects of free radical formation may be seen. In rats, tissue markers for free radical generation significantly increase during ischemia-reperfusion injury. Supplementation of free radical scavengers significantly decrease this marker (59). It has been shown that free radicals are mediators of ischemia-reperfusion injury and that antioxidants such as vitamin E are effective in attenuating this injury (14, 40). Inflammation that may accompany this type of injury is directly linked to the formation of free radicals, which results in tissue injury (71). Ischemia reperfusion and inflammation are 2 conditions that are related to in vivo environmental situations found at the site of the muscle during exercise. This may implicate vitamin E supplementation as an effective means of reducing exercise-induced muscle damage due to free radical formation. Vitamin C. Vitamin C or L-ascorbic acid has also been implicated as an antioxidant. Vitamin C may be involved in the regeneration of vitamin E (47). Ascorbic acid has been shown to be involved in a key pathway related to the generation of vitamin E (58). A recent study has shown that ascorbate is an effective antioxidant in human plasma (19). It is suggested that ascorbate is a potent reducing agent and that it is effective in the quenching of free radicals. In addition, ascorbate is vital in the protection of retinoids, carotenoids, tocopherols, B complex vitamins, and lipids (8). Vitamin A. There has been recent confusion over how to identify vitamin A because of the varying forms that exist in nature (8). Vitamin A is a retinol Table 1. Forms of vitamin E and their biological activities. Vitamer IU·mg 1 RRR-D-alpha-tocopherol RRR-D-beta-tocopherol RRR-D-alpha-tocopherol acetate RRR-D-alpha-tocopherol succinate 1.49 0.75 1.36 1.21 Tocopherol equivalents 1.00 0.49 1.03 1.03 and is related to but different from retinoids and carotenoids (8). Beta carotene, which is commonly mistaken as a vitamin A equivalent, is actually 2 retinols with the alcohol groups removed. It is classified as a carotenoid (8). Beta carotene has been identified as a possible antioxidant because of its ability to scavenge singlet oxygen (8, 33). On demand beta carotene can be broken down into 2 retinol equivalents (RE) if other sources of vitamin A are not available (8). This mechanism is how beta carotene has been identified as a vitamin A precursor. Much less work has been done with vitamin A compared with vitamin E and C as a protective antioxidant in relation to exercise. Antioxidant Supplementation and Exercise Several studies have focused attention on the effects of dietary antioxidants in relation to exercise (15, 22, 24, 37, 41, 47, 69). The amount of each of these vitamins to be given has been questioned. The National Research Council recommendations for vitamins E, A, and C are 8–10 mg·d1 as RRR-D-alpha-tocopherol, 800–1,200 retinol equivalents (RE)·d1 , and 30–80 mg·d1 as ascorbic acid, respectively (8). There has been much confusion as to the appropriate units for these vitamins and how to express them. Vitamin E should be expressed in milligrams or tocopherol equivalents (TE). One TE is equivalent to 1 mg of RRRalpha-D-tocopherol (8). It must be noted that other forms of vitamin E are not based on a 1-mg to 1-TE ratio (Table 1). This means that milligram dosages from different vitamer forms result in different biological activities. Therefore, if reporting vitamin E dosages in milligrams the vitamer source must also be reported. Almost no toxicity or adverse effects have been reported with oral administration of vitamin E in any vitamer form in doses up to 1,600 mg·d1 (8). Vitamin A should be expressed in RE. Precursor forms have very different ratios in relation to 1 RE (8). One retinol equivalent is equal to 6 g of beta carotene as ingested orally as a precursor to vitamin A. However, 1 RE is equal to 12 g of an ingested mixed provitamin A carotenoid (8). Beta carotene can be reported in milligrams. Vitamin C can also simply be referred to in units of milligrams but should be appropriately referred to as ascorbic acid. It has been suggested that doses over 1,000% of the recommended daily allowance (RDA) are not toxic for
all 3 vitamins (38). It is unclear at this time what the optimal dosage of these vitamins would be or in what combination to reduce lipid peroxidation during exercise. Few studies have looked carefully at comparing the effectiveness of each of these vitamins individually and in different combined ratios. This makes it unclear as to how antioxidant supplementation should be approached. One study reported that a mixture of 592 mg of vitamin E, 1,000 mg of vitamin C, and 30 mg of beta carotene resulted in a decreased level of a lipid peroxidation marker after exercise (33). A study involving vitamin E supplementation stated that 300 mg of vitamin E given for 4 weeks reduced exercise-induced lipid peroxidation (64). A study involving resistance exercise has also reported the effectiveness of vitamin E supplementation in reducing MDA and creatine kinase levels (44). In general, the supplementation has been implemented for a period of 2–4 weeks before exercise. These studies give indication that these vitamins are effective in decreasing lipid peroxidation. However, specific dosage recommendations cannot be made. It must be noted that to compare dosages studies need to more accurately report the exact form from which these vitamins were derived. As shown previously, different precursor forms of vitamins result in varying ratios of actual vitamin formation in the body. Many studies have reported vitamin dosages in an improper form. Practical Applications The literature reviewed suggests that high-intensity exercise can result in the production of free radicals (32, 39, 44). In addition, it appears that at a minimum these free radicals can cause significant disruption to muscle cell membranes (32, 44). This may indicate that, especially in the early phases of a new and unfamiliar exercise program, antioxidant supplementation is necessary to combat excessive free radical–mediated tissue damage. This is further supported by investigations reporting the effectiveness of antioxidant supplementation on decreasing free radical–mediated tissue damage with intense exercise (33, 44, 64). Vitamin E, vitamin C, and beta carotene have been identified as potent antioxidants, as covered previously. The following provides some information pertaining to an antioxidant supplementation program. Vitamin E Five times the RDA for vitamin E may be necessary for prevention of free radical damage (16). Intense exercise by athletes may result in free radical production 3 times that of sedentary individuals (50). Because of these findings, it has been stated at the Colgan Institute that 1,200–2,000 IU (equivalent to 800–1,350 mg of RRR-D-alpha-tocopherol or 800–1,350 TE) of vita- Free Radicals 181 min E have been taken daily by athletes (13). This may be a necessary dosage to counter free radical formation during exercise. Vitamin C As stated earlier the RDA for vitamin C is 60 mg. It has been suggested that this is based on an inaccurate and antiquated method for calculating vitamin C requirements (13). Dosages given to athletes have been reported to be 2–12 g·d 1 . A consensus on reviews has shown complete safety with dosages of vitamin C of 1–5 g·d 1 (8). For musculoskeletal healing dosages of 500–1,000 mg 2–4 times daily have been taken in the form of ascorbic acid (8). Beta Carotene The amount of beta carotene that would be necessary for it to be a significant contributor to antioxidation is unknown. The RDA for vitamin A is approximately 800–1,200 RE·d 1 . Toxicity has been reported in rare instances at levels of 25,000 IU, which is approximately 7,500 RE (7,500 g of retinol, 9,000 g of retinyl acetate, and 13,500 g of retinyl palmitate) (8, 23). A safe dosage would fall somewhere between these 2 values. However, it is beta carotene and not vitamin A that acts as an antioxidant, but specific values for beta carotene are not clear. Recommended dosage for vitamin A in RE·d 1 is 1,000. This would equal 6 mg·d 1 of beta carotene. Beta carotene has been shown to be safe at any dose. Adverse effects such as oily diarrhea have been reported but only at absurdly high levels (8). The suggested dosage of vitamin A for effective injury repair assistance is 25,000 IUs or 7,500 REs, which would be approximately 45 mg·d 1 of beta carotene (8). Conclusion It now appears that free radical–mediated tissue damage may be a new variable in the way tissue remodeling occurs after intense exercise (44). Thus, future areas of research must focus on the effect of antioxidant supplementation and determine if it is in fact desirable to curtail tissue damage after intense exercise. It is possible that free radical–mediated tissue damage is a vital and necessary component of the tissue remodeling process. However, it is most likely that the shock of a new and unfamiliar exercise bout leads the body to overcompensate in the restructuring phase of muscle tissue following exercise (12, 17, 45). Excessive free radical production during intense exercise or from the oxidative burst of neutrophils following exercise could lead to damage far beyond what was caused by the mechanical forces of the exercise bout (36). High doses of anitoxidants before an unfamiliar exercise bout may combat the body’s natural overcompensation response due to the fact that free radical production may be a primary player in this overcompensation mechanism. Future study will need to assess the via-
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Free Radicals, Exercise, and Antioxidants - Setanta College

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