making up fish oil are highly polyunsaturated,
concerns have been raised regarding increased
oxidative stress from fish oil intake (Hu et al.
1989; Nalbone et al. 1989; Leibovitz et al. 1990;
Demozet al. 1992, 1994). Furthermore, fish oils
induce peroxisomal b-oxidation, in which fatty-
acyl oxidation yields hydrogen peroxide (H 2 O 2 )
as a normal by-product, and upregulate the
activity of the H 2 O 2 decomposing enzyme cata-
lase (Aarsland et al. 1990; Demoz et al. 1992, 1994).
Under normal conditions, up to 20% of cellular
O 2 consumption has in fact been estimated to
occur in the peroxisome (Chance et al. 1979). The
beneficial effects of regular exercise on cardio-
vascular and overall mortality (Paffenbarger et
al.1984) may be decreased by uncontrolled exer-
cise-induced oxidative stress. This may be par-
ticularly concerning in groups predisposed to
oxidative stress, including that induced by fish
oil (Hu et al. 1989; Nalbone et al. 1989; Leibovitz
et al. 1990). Sen et al. (1997a) assessed the effect of
fish oil and vitamin E supplementation com-
pared to placebo soy oil and vitamin E supple-
mentation on physiological antioxidant defences
and resting and exercise-induced oxidative stress
in rat liver, heart and skeletal muscle. The effects
of 8-week vitamin E and fish oil supplementation
on resting and exercise-induced oxidative stress
was examined. Lipid peroxidation was 33%
higher in fish oil fed rats than in the placebo
group in the liver, but oxidative protein damage
remained similar in both liver and red gastro-
cnemius muscle. Vitamin E supplementation
markedly decreased liver and muscle lipid per-
oxidation induced by fish oil diet. Vitamin E sup-
plementation also markedly decreased oxidative
protein damage in the liver and muscle. Exhaus-
tive treadmill exercise increased liver and muscle
lipid peroxidation, and muscle oxidative pro-
tein damage. Vitamin E effectively decreased
exercise-induced lipid peroxidation and protein
oxidation (Sen et al. 1997a).
A limited number of studies have examined
the effect of vitamin E supplementation in
humans. Exercise performance and physical
fitness have multifactorial determinants and
may not serve as reasonable end points to test the
306 nutrition and exercise
efficacy of antioxidant supplementation. Vitamin
E supplementation (900 IU · day–1for 6 months)
in trained swimmers did not alter their swim
performance nor their lactate response in plasma
(Lawrence et al. 1975). Neither did vitamin E
supplementation (800 IU · day–1for 4 weeks) alter
the work load needed to run at 80% V.
o2max.in
trained and untrained males (Goldfarb et al.
1989). Volunteers given 400 IU vitamin E per day
for 6 weeks showed no influence on cycle time,
swim time, or step time (Sharman et al. 1976).
Additionally no changes in V.
o2max., a marker of
physical fitness, was noted in humans following
vitamin E supplementation (Watt et al. 1974;
Goldfarbet al. 1989; Sumida et al. 1989). However,
Cannonet al. (1990) reported that supplementa-
tion of 400 IU vitamin E daily for 48 days
decreased the amount of creatine kinase leakage
from muscles during recovery from a downhill
run. Sumida et al. (1989) examined the effects of
4 weeks of vitamin E supplementation in
21 healthy college-aged males. The subjects
ingested 300 mg of vitamin E daily and blood
levels of several enzymes and lipid peroxides
were determined before and for up to 3 h after
cycling exercise to exhaustion. Exercise increased
the level of lipid peroxidation by-products in
plasma immediately after the cycling and
returned to normal at 1 and 3 hours of recovery.
Vitamin E supplementation significantly de-
creased the resting level of plasma lipid perox-
ides. Meydani et al. (1993) reported that urinary
excretion of lipid peroxidation by-products
tended to be lower in vitamin E-supplemented
individuals (400-IU doses, twice daily, for 48
days) than in the corresponding placebo group,
but this effect was only significant 12 days after
downhill running. The subjects ran at 16% down-
hill inclination at 75% of their maximum heart
rate for three 15-min periods. Muscle biopsies
were obtained from the vastus lateralis of young
subjects. It was observed that exercise increased
the level of lipid peroxidation by-products in
the muscle of the placebo group, whereas in the
muscle of the vitamin E-supplemented group,
no such oxidative lipid damage was evident.
Another study examined the effect of vitamin E