supplementation (800 IU daily for 4 weeks) and
compared that with a placebo treatment in the
same individuals at a specific exercise intensity
(Goldfarbet al. 1989). Subjects were randomly
assigned to either a placebo or vitamin E treat-
ment group in a counterbalanced design. Sub-
jects were exercised for 30 min at 80% V
.
o2max.and
blood was collected before and after the run.
Vitamin E treatment attenuated the level of
resting plasma lipid peroxidation by-products
and also protected against the exercise response.
The effects of 5 months of a-tocopherol supple-
mentation has been studied in 30 top-class
cyclists. Although the supplementation did not
improve physical performance, it was evident
that exercise-induced muscle damage was less
in response to antioxidant supplementation
(Rokitzkiet al. 1994a).
In 1980, the United States daily allowance for
vitamin E was reduced from 30 IU (recom-
mended in 1968) to 15 IU. In the same year it was
estimated that in the United States, the amount of
vitamin E supplied by a ‘normal’ diet is about
11 IU (7.4 mg). Packer and Reznick (1992) have
discussed that such dosages are insufficient for
active athletes and that dosages of up to 400 IU
daily may be reasonable recommendation for
active athletes engaged in moderate to heavy
exercise. Vitamin E is proven to be safe at levels
of intake up to approximately 3000 mg for pro-
longed periods of time (Bendich & Machlin
1988). However, individuals taking anticoagu-
lants should refrain from taking very high doses
(>4000 IU) of vitamin E because vitamin E can act
synergistically with this class of drug (Corrigan
1979).
Vitamin C supplements (3 g · kg–1diet) given to
rats who were placed on a vitamin E-deficient
diet did not alter the run time to exhaustion in the
vitamin E-deficient animals (Gohil et al. 1986).
Vitamin C was unable to counter the deleterious
effects of vitamin E deficiency. In a preliminary
report, the effect of vitamin C supplementation
in humans was documented. A mild protective
effect of vitamin C supplementation, based on
elevated total antioxidant capacity of the plasma,
was observed (Alessio et al. 1993).
Other nutrients that have been ascribed to be
beneficial as antioxidants, such as selenium and
b-carotene, have not been examined individually
but have been assessed in conjunction with either
vitamin E deficiency or in combination with
other antioxidants. The effects of selenium
supplementation (0.5 ppm diet) or deprivation
have been tested in liver, muscle and blood of
swim-exercised rats (Brady et al. 1979). Some rats
were additionally supplemented with vitamin
E (50 IU · kg–1). Selenium supplementation
increased the activity of the hydroperoxide
metabolizing enzyme GSH peroxidase in the
liver. A tight regulation of tissue GSH peroxidase
activity by dietary selenium was observed
because a selenium-deficient diet markedly
downregulated the activity of the enzyme.
Muscle GSH peroxidase activity demonstrated
similar responses to selenium intervention com-
pared with the liver. Increased tissue lipid perox-
idation was evident when both selenium and
vitamin E were deficient. However, selenium
deficiency had little effect when vitamin E was
present. Selenium appeared to have minimal
effects on swim-induced lipid peroxidation in
the liver or muscle. Dietary selenium supple-
mentation in horses (0.15 ppm daily for 4 weeks)
had minimal effects on exercise-induced lipid
peroxidation as indicated by blood level of lipid
peroxidation by-products (Brady et al. 1978). In a
double-blind human study, no effect of selenium
supplementation on human physical perfor-
mance was observed (Tessier et al. 1995). Sele-
nium poisoning is rare in the United States, but
the case of a man who was poisoned by
selenium-containing vitamin tablets has been
described (Clark et al. 1996).
A few studies have examined the effects of
coenzyme Q 10 to determine if additional
amounts of this factor in the electron transport
chain would be beneficial in preventing free
radical damage (Zuliani et al. 1989; Shimomura et
al.1991; Snider et al. 1992). Dietary coenzyme Q 10
supplementation protected against leakage of
creatine kinase and lactate dehydrogenase from
the muscles to serum following downhill run
(Shimomuraet al. 1991). In two human studies,