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.
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.
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.
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).
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).
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.
Dietary Reference Intake (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).
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.
Vitamin E and Exercise
Effects of Exercise
on Vitamin E Requirements
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.
of Oxidative Stress / Lipid Peroxidation
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
E in Exercise Recovery
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
Summary and Current Recommendations
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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