VITAMIN E > Nutrition > Antioxidants > Article

A. Background


Vitamin E is one of four fat-soluble vitamins. The vitamin is synthesized by plants, and has eight different isoforms (vitamers) divided into two classes of four vitamers each. The compounds are comprised of a 6-chromanol ring and an isoprenoid side chain. Compounds having saturated side chains are classified as tocols. The second class of compounds, known as tocotrienols (trienols), have unsaturated side chains (9). The groups attached to the R1, R2 and R3 positions on the 6-chromanol ring determine whether the vitamer is identified as alpha, beta, gamma, or delta. A large body of the research currently focuses on the alpha tocopherol form of vitamin E, which is the most biologically active (31,32). Recently gamma tocopherol has been a topic of interest by many researchers. However, those studies fall outside of the scope of this review and will not be addressed. Discussion of vitamin E within the current literature review is limited to the alpha tocopherol form of the vitamer, unless otherwise noted.

Dietary Function

Vitamin E is integral part of cellular membranes whose main role is to defend the cell against oxidation. Within cells and organelles (e.g. mitochondria) vitamin E is the first line of defense against lipid peroxidation. The vitamin also plays a very important function in lending red blood cells (RBC) flexibility as they make their way through the arterial network. Vitamin E has not yet been shown to have any significant functions outside of these two roles.


Synthetic vitamin E, designated dl-alpha-tocopherol, is the less expensive cousin of the naturally occurring form, d-alpha tocopherol. The natural form of the vitamin is synthesized only by plants and is found predominantly in plant oils. Vitamin E (tocopherol) is also present in high amounts within the chloroplast and therefore the leaves of most plants. In contrast, the tocotrienols are synthesized and found in the germ and bran sections of the plant (9). The fat-soluble property of vitamin E allows it to be stored within fatty tissue of animals and humans. Therefore a diet that includes meat supplies additional vitamin E. However, the amount of vitamin E obtained in a meat inclusive diet is less than the amount supplied by plant sources.

B. Metabolism

Absorption and Bioavaliability

Absorption of vitamin E is highly dependent upon the same processes that are utilized during fatty acid digestion and metabolism. Common, and critical, to both fat and vitamin E absorption are micelle and chylomicron formation. A lack of any component of these transporters will inhibit carrier formation and in turn vitamin E absorption. Bile acids are considered essential for vitamin E absorption and micelle formation. Once formed, the micelle is then able to cross the unstirred water layer and release its contents into the enterocyte. An understanding of the movement of vitamin E through the enterocyte to date has been elusive to researchers (32). Many researchers believe that a transfer protein is involved, but the protein has yet to be isolated or discovered. After passing through the enterocyte the vitamin E is packaged into a chylomicron and readied for circulation. Once in the blood 15 to 45% of the total vitamin E intake can be absorbed by the cells. Researchers have found that the uptake of vitamin E correlates negatively with increasing doses of vitamin E (19,32).


Upon reaching the basolateral surface of the enterocyte vitamin E is packaged into chylomicrons and then transported throughout the body via the circulation. Within five minutes of formation chylomicrons are broken down by lipoprotein lipase and the contents are dispersed towards a variety of paths. The vitamin E in the chylomicron equilibrates with both High-Density Lipoproteins (HDL) and Low-Density Lipoproteins (LDL) (9). From the HDL all circulating lipoproteins eventually receive vitamin E, as HDL readily transfers the compound to the lipoproteins at a rate equivalent to 10% of the plasma vitamin E per hour (32). The vitamin E remaining in the chylomicron becomes a chylomicron remnant and travels back to the liver for re-uptake in a process that has garnered much research, but so far is poorly understood. Once in the liver the vitamin E is packaged into Very Low Density Lipoproteins (VLDL) and excreted back into the circulation. Being the most biologically active of the eight vitamers, (9,16,19,32), alpha tocopherol is sequestered by the liver and constitutes over 80% of the total vitamin E packaged into the VLDL and secreted by the liver (32). The predominant transfer of the alpha vitamer is performed by alpha tocopherol transfer protein (ATTP). As the VLDL are broken down by lipoprotein lipase, Low Density Lipoproteins (LDL) are formed and from these lipoproteins the vitamin E is transferred to HDL and eventually incorporated into either circulating lipoproteins or peripheral tissue. Any of the previously mentioned lipoproteins have the ability to transfer vitamin E to the tissue as needed (9,32). A final mechanism for vitamin E is uptake by the peripheral tissue from the chylomicron via lipoprotein lipase activity. Unlike re-uptake of vitamin E by the chylomicron remnant, uptake of the vitamer by peripheral tissue is better understood. After vitamin E has been transferred to the LDL from the chylomicron two receptors (LDL dependent receptor and LDL independent receptor) within the tissue play a key role in the uptake of vitamin E into the cell (32).


Vitamin E is a lipid soluble vitamin and therefore over 90% of total body vitamin E is found in the adipose tissue (19,32). Over 90% of this pool are found as a part of an adipocyte fat droplet whereas the remaining amount is found mainly in adipocyte cellular membrane. The storage ratios of vitamin E are also very difficult to alter. It takes over two years to alter the ratio of alpha to gamma isoforms. Previous studies have shown that the ratio is altered as the alpha vitamer replaces the gamma vitamer, which is reduced by 70% (31). Concentrations of vitamin E cover a wide range in body tissues. In the plasma the concentration of vitamin E is approximately 27 umol/l. Within skeletal muscle protein the vitamin E concentration varies considerably depending upon the type of muscle (19). Although a large majority of vitamin E is found in adipose tissue (230 nmol/g wet weight) (19) there is no single organ that functions to store and release vitamin E as needed. The actual mechanisms regarding vitamin E release from the tissue is unknown at this time. While it seems likely that vitamin E is released during lipolysis associated with exercise this may not be true. Research has shown that even during times of weight reduction vitamin E is not released from the adipose cells (32). Therefore, the factors that regulate bioavliability of vitamin E from adipose tissue are not known.


Vitamin E is excreted mainly via bile, urine, feces, and the skin. The vitamin is oxidized and forms hydroquinone and then is conjugated to form glucuronate. Once formed the glucuronate can be excreted into bile or further degraded in the kidneys and excreted in the urine. Kinetic studies have shown that a maximal binding capacity for alpha tocopherol may exist (~50 mg) within the plasma, thereby leading to fecal excretion of excess vitamin E (32). Because of the poor intestinal absorption of vitamin E, fecal excretion is the main route of vitamin E elimination. Synthetic and less common vitamers (e.g. gamma) are also likely excreted in bile during the secretion of new VLDL molecules from the liver (32).

Physiological Role

A review of current literature suggests that the primary role of vitamin E within the body is to function as an antioxidant. Vitamin E is considered to be the major chain breaking antioxidant in membranes (23). Oxidation has been linked to numerous possible conditions / diseases including: cancer, aging, arthritis, and cataracts. Platelet hyper- aggregation, which can lead to atherosclerosis, may also be prevented via vitamin E involvement (22). Vitamin E helps to reduce production of prostaglandins such as thromboxane, that cause platelet clumping. Thromboxane is formed from arachidonic acid, which is high in western diets (22). Vitamin E also acts as a cell membrane stabilizer, which is postulated by some researchers to be the primary mechanism for its prevention of muscle damage (19,31). The vitamin possibly stabilizes the membrane by increasing the "orderliness of membrane lipid packaging." This affect allows for a tighter packing of the membrane and in turn greater stability to the cell (31). Since 1922 vitamin E deficiency studies have been conducted to determine more distinct and physiologically specific roles for the vitamin. Deficiency studies have been performed to determine the biologic activity of vitamin E, or the ability of the vitamin to "reverse or prevent specific vitamin-E deficiency symptoms." (32). To date these studies have only been able to produce speculative and inconclusive results at best. Human subjects suffering from anemia and muscular dystrophy have been supplemented with Vitamin E as a possible simple mechanism of reversing the diseases. These trials were deemed unsuccessful, except in extreme cases of childhood and infant anemia (32). Even today, after 75 years of research, the physiological role of vitamin E still remains elusive. Many researchers now believe that the biological role of vitamin E may be solely as an antioxidant.

C. Dietary Reference Intake (DRI)

Current DRI

In 1968 the RDA for vitamin E was established at 300 IU (300 mg) for a 65 kg adult male (21). This daily level was very difficult to reach unless a diet high in polyunsaturated fatty acids was consumed (31). From 1 mg of vitamin E approximately .3 (32) to .5 is in the alpha vitamer form and therefore readily absorbed. The other vitamers are not stored as efficiently and usually excreted (31,32). Therefore a new RDA was set based on the alpha-tocopherol form of the vitamin. In 1989 the RDA for Vitamin E was set at 10 mg alpha tocopherol for men and 8 mg of alpha-tocopherol for women (32). In the year 2000 all RDA values were in the process of being replaced by Dietary Reference Intakes (DRI). The DRI has been established at 15 IU of alpha-tocopherol. The revised DRI levels are the same for both men and women (21).


Anemia, muscle necrosis, and fetal death have been observed in over fifteen different vitamin-E-deficient animal species. Extrapolation of these results to humans has been difficult though. Humans who have fat malabsorption do suffer from the same symptoms shown in rats, but to a lesser degree. These manifestations are exhibited early in childhood. Some of the symptoms include decreased sensory perception, muscle weakness, scoliosis, and muscle structural abnormalities. These symptoms can usually be reversed using vitamin E supplementation (31) Vitamin E deficient diets fed to adult humans have resulted in the formation of very few deficiency symptoms. Bunnell et al. (1) has shown that prisoners performing strenuous physical labor while fed a vitamin-E deficient diet for 13 months exhibited no deficiency symptoms. Consequently, unless fat malabsorption problems exist vitamin E deficiency is not likely to be a concern.


Vitamin E toxicity has rarely been documented in humans. Doses up to 1600 I.U. have been commonly administered in studies without observable adverse side effects. Toxicity may be difficult because of the wide variation in daily blood vitamin E levels. Increasing vitamin E levels in muscle tissue is especially difficult to attain and therefore toxic levels are difficult to achieve. Meydani et al. (17) gave 800 I.U. of vitamin E to experimental subjects for 48 days and only saw a 37% increase in plasma alpha tocopherol levels. It should be noted that this increase was achieved at the expense of gamma tocopherol, which decreased by over 70%. The tocopherol binding protein is likely to control the amount of vitamin E that can be physiologically stored. Excess amounts of the vitamin are likely excreted by the body via methods mentioned earlier. The binding protein may actually exhibit a protective role via this mechanism but this hypothesis deserves further investigation.


D. Vitamin E and Exercise

Effects of Exercise on Vitamin E Requirements

Early studies showing that vitamin E could improve exercise performance (7) were often flawed because of the lack of double blind protocols and measurement standards. An initial hypothesis to interpret these results was that vitamin E "improved myocardial efficiency" (oxygen delivery and offloading). This hypothesis labeled vitamin E as an "ergogenic" aid (7,31). These earlier studies should be interpreted with skepticism, however, because they were not well designed or controlled. A stronger body of evidence became available between 1970 - 1980 (25,26,35) suggesting that vitamin E has no ergogenic benefits. Sharman et al. (25) performed one of the first well-designed studies addressing vitamin E as an ergogenic aid. The researchers studied two experimental groups of swimmers, receiving either vitamin E (400 mg) or a placebo daily for six weeks. At baseline, the 15 trained swimmers showed no difference in a 400-meter swim. After six weeks both groups had significant decreases in time, but exhibited no significant differences when compared to the control group (25). A study done in 1974, by Shephard et al.(26) also found no ergogenic benefits of the vitamin when administered in doses of 1200 mg per day. Swimmers were the subjects of choice in previous studies until 1975, when Watt et al. (35) studied hockey players. He found no difference in aerobic power between groups after 50 days of placebo versus 1200 I.U. vitamin E supplementation. The previously mentioned studies reviewed the effects of dosages from 400-1600 I.U. daily. These dosages are considered sufficient to benefit the antioxidant defense system (2), but have failed to show any ergogenic benefits. These findings suggest that vitamin E supplementation does not provide any ergogenic benefit to the exercising individual. Plasma vitamin E levels have been shown to decrease via endurance training in humans (34). Although vitamin deficiency has been observed in athletes it is at best a marginal deficiency. This is likely attributed to increased turnover rate, excretion (sweat, feces, urine) and adaptation to training (34). The structural changes that occur with chronic exercise (e.g. increased mitochondria) must also not be ignored. The cellular changes may lead to vitamin E being redistributed among the newly formed mitochondria. Therefore, vitamin levels may not actually be decreasing in people who exercise. High-intensity resistance training has also been shown to increase free radical production (19). The vitamin E intake of athletes who resistance train along with any ergogenic benefit deserve further attention. A few studies performed at altitude (>6000 ft) (34) have suggested that vitamin E is beneficial in this environment. Studies have shown that mountain climbers supplemented with vitamin E expired less pentane than those on a placebo. These findings indicate that fewer free radicals were being formed in the supplemented group. A summary of the studies report that supplemented climbers had enhanced performance (31). These results are likely due to the ability of vitamin E to restore red blood cell deformity that is shown at high altitude. This in turn allows for better oxygen delivery as the RBC can flow more easily through the arterial tree. In summary, exercise near sea level has presented a lack of strong evidence supporting ergogenic benefits for vitamin E supplementation. At higher altitude however, vitamin E supplementation may be beneficial to performance, but additional research is needed. Studies to date suggest that eating a well balanced diet will provide adequate amounts of vitamin E to meet needs of both the athlete and the recreational exerciser at working in altitudes less than 6000 ft.

Prevention of Oxidative Stress / Lipid Peroxidation

The effectiveness of vitamin E in preventing exercise-induced oxidative stress (lipid peroxidation) is poorly understood. While more invasive studies can be performed with the rat, the extrapolation of results to humans is often questioned. This has led to the conductance of a number of human studies whose results have varied depending on the variable measured. From human studies the following indicators of oxidative stress have been measured: DNA damage, creatine kinase (CK) leakage, maximum voluntary contraction (MVC), thiobarbituric acid reacting substances (TBARS) and/or conjugated dienes (CD) (10,17). Differing indices of oxidative stress along with a multitude of contrasting design variables (i.e. subject conditions, length of study, dose of vitamin, type of exercise) have created confusion when trying to interpret the role vitamin E plays in preventing oxidative damage. Creatine kinase is a commonly measured indicator of oxidative stress. The enzyme is considered a hallmark for muscle damage as it leaks from the muscle during periods of muscle cell membrane injury. Cannon et al. (4) concluded that 400 I.U. of vitamin E for 48 days reduced the amount of CK leakage in young and old men during recovery from downhill running bouts. In subsequent studies Rokitski et al.(24) concluded that 400 I.U. of vitamin E for 5 months decreases CK leakage in aerobic cyclists. The studies indicate that vitamin E supplementation can help reduce muscle damage caused by free radical damage. Hartmann et al. (12) has shown decreased MDA production in subjects consuming 1200 mg of vitamin E for 14 days prior to a run to exhaustion. In the same study Hartmann et al. (12) noted that DNA damage could occur in white blood cells after exercise. However, the researchers concluded that a 2400 mg dose of vitamin E resulted in decreased damage to the DNA of white blood cells.

Sumida et al.(27) has also shown that vitamin E reduces pentane production and lipid peroxidation products from the mitochondria in vitamin E supplemented subjects. The decrease in lipid peroxidation production from the organelle reported by Sumida et al.(27), is likely significant due to the high antioxidant concentration in the mitochondria. Studies have also produced contradictory results. Goldfarb (10) summarizes two studies presented by Lewis and Goldfarb at the Southeast ACSM conference. The two separate studies used supplementation with 400 and 800 I.U. of vitamin E respectively. Each study resulted in no significant change in CK levels versus controls after 100 miles of cycling or 3-4 hours of cycling at 75% of VO2 max. This adaptation to chronic exercise is termed the "repeated bout effect." This effect states that the body is better able to control free radical damage with repeated bouts of exercise. It seems reasonable to assume that Type I and IIa fibers may contain a greater concentration of vitamin E than Type IIb fibers do. This would be because of the high oxidative potential of Type I and IIa fibers. However, evidence to support this has not been conclusive and is disputed in the literature (19). The wide variety of oxidative indices used in research studies has led to some confusion concerning the interpretation of studies. The markers may or may not be elevated after exercise depending on the indicator measured. Regardless of the marker measured, studies seem to indicate that acute, unaccustomed, strenuous, or chronic training sessions increase oxidative stress and hence lipid peroxidation. This phenomenon seems to be somewhat decreased with chronic training (31), although the data addressing this claim is not abundant (19). Results also suggest that weekend athletes or those performing regular strenuous (e.g. marathoners, triathletes) or unaccustomed exercise may be at greater risk for lipid peroxidation. The majority of literature suggests that supplementation with vitamin E does protect against lipid peroxidation (19,23,31).

Vitamin E in Exercise Recovery

Delayed onset of muscle soreness (DOMS) and muscle damage is usually greatest a few days after an unaccustomed or rigorous bout of exercise (5). This may be due to post-exercise elevation of immune system defenses at sites of muscle damage post-exercise (5,30). Utilizing urinary TBARS measurements, Meydani et al. (20) reported that vitamin E treated subjects had a decrease in oxidative stress over 12 days following eccentric exercise (downhill running). Additional research addressing the role vitamin E consumption has during recovery is limited. Vitamin E utilizes vitamin C to regenerate itself back to the original state. Studies involving exercise recovery commonly use a cocktail mixture of vitamins C and E. Studies addressing only the role of vitamin E in exercise recovery are therefore lacking. Summarizing, the role vitamin E plays in exercise recovery is not clear but deserves further attention.

E. Summary and Current Recommendations

In conclusion, the data surrounding vitamin E seems to be contradictory depending on the exercise parameter measured. Disregarding studies before 1970, the consensus is that vitamin E supplementation has no ergogenic or performance enhancing effects. In contrast, vitamin E may help reduce oxidative stress and lipid peroxidation of cellular membranes. However data from different studies are not in agreement because of the parameters measured and the design of the experiment. Regular exercisers are less likely to suffer the consequences of oxidative stress as the body has the ability to adapt to exercise-induced damage with chronic training. Vitamin E likely plays a complementary role in this process. Because of this the so-called "Weekend warriors", and those beginning an exercise program may lack this adaptation mechanism and thereby possibly benefit from supplementation with vitamin E. The current DRI for vitamin E meets the needs of most exercisers and non-exercisers alike and can be achieved through a healthy diet. However, due to the rigorous training and diet of some athletes (high calorie, low fat, high carbohydrate) vitamin E supplementation may be warranted. Recently in April 2000 The National Academy of Sciences (21) established an intake ceiling of 1100 I.U for synthetic and 1500 I.U. for natural vitamin E. These ceilings are approximately one hundred times the DRI. These limits were based on studies showing very high doses of vitamin E caused hemorrhaging in rats. These results have not been duplicated in humans however. Vitamin E supplementation in exercising adults has produced mixed scientific results. The majority of studies show that vitamin E has little to no beneficial effect on exercise-performance related parameters, other than reducing lipid membrane peroxidation. Those who can be classified as "sporadic exercisers" are likely to gain more of this benefit than chronic exercisers. Evidence also suggests that extremely strenuous or unaccustomed exercise overwhelm the antioxidant defense systems (30); therefore, exogenous antioxidants may have a prophylactic effect (14). This topic warrants a more in-depth investigation. Americans can obtain the DRI for vitamin E from a healthy diet. Despite this, vitamin E supplementation by both athletes and non-athletes is a widely employed practice, which addresses exercise and other issues outside the scope of this review. The choice to supplement or not supplement a diet with vitamin E is an individual choice that may go beyond exercise. At this time supplementation up to the ceiling established by the NAS does not appear to be an unhealthy or dangerous practice.

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