oxides and hydrogen peroxide. A protective
effect of dietary restriction under such conditions
has been also evident (Sohal et al. 1994). In rats,
dietary restriction has been shown to suppress
ROS generation in hepatic microsomes. Interest-
ingly, a synergistic effect of dietary restriction
and exercise was observed to protect mito-
chondrial membrane fluidity against oxidative
damage (Kim et al. 1996a). Another study investi-
gated the effect of dietary restriction and physi-
cally active lifestyle on lipid peroxidation and
antioxidant defences of the rat heart. Diet
restricted rats were fed 60% of the ad libitumlevel
for 18.5 months. Both dietary restriction and a
physically active lifestyle decreased lipid peroxi-
dation damage in cardiac mitochondria. Dietary
restriction significantly increased the activities of
cytosolic antioxidant enzymes such as superox-
ide dismutase, selenium dependent GSH peroxi-
dase and GSH S-transferase. It is thus evident
that long-term dietary restriction and a physi-
cally active life style may alleviate the extent of
free radical damage in the heart by strengthening
endogenous antioxidant defences (Kim et al.
1996b).
Food deprivation, on the other hand, may
adversely affect liver GSH reserves and whole-
body GSH metabolism. Starvation is followed by
lowered GSH levels in the plasma, lung and
skeletal muscles (Cho et al. 1981; Lauterburg et al.
1984). The influences of food deprivation and
refeeding on GSH status, antioxidant enzyme
activity and lipid peroxidation in response to an
acute bout of exercise have been investigated in
the liver and skeletal muscles of male rats. Food
deprivation depleted tissue GSH stores and
caused increased lipid peroxidation in the liver
and skeletal muscles. Leeuwenburgh and Ji
(1996) showed that both food deprivation–
refeeding and exhaustive exercise influence liver
and skeletal muscle GSH status and that these
changes may be controlled by hepatic GSH syn-
thesis and release due to hormonal stimulation.
Antioxidant nutrients
The chemical nature of any antioxidant deter-
mines its solubility, and thus its localization in
biological tissues. For example, lipid-soluble
antioxidants are localized in membranes and
function to protect against oxidative damage of
membranes. Water-soluble antioxidants, located,
for example, in the cytosol, mitochondrial matrix
or extracellular fluids, may not have access to
ROS generated in membranes. Vitamins E and A,
coenzyme Q, carotenoids, flavonoids, and poly-
phenols represent the most extensively studied
naturally occurring fat-soluble antioxidants.
Vitamin C, GSH, uric acid and lipoic acid are the
most commonly known water-soluble antioxi-
dants. The antioxidants that have been tested in
exercise studies are briefly introduced in the fol-
lowing section.Vitamin E
Vitamin E refers to all tocol and tocotrienol
derivatives which exhibit the biological activity
ofa-tocopherol (Sheppard et al. 1993). The form
of vitamin E that has most biological activity is
RRR-a-tocopherol, previously known as d-a-
tocopherol. Vitamin supplements are marketed
as mixed tocopherols, a-tocopherol or esterified
derivatives, e.g. a-tocopheryl-acetate, -nicotinate
or -succinate. Edible vegetable oils are the richest
natural source of vitamin E. Unprocessed cereal
grains and nuts are also good sources of vitamin
E. Animal sources of vitamin E include meat,
especially fat. One of the most significant proper-
ties of vitamin E is that it is an antioxidant.
Vitamin E especially protects polyunsaturated
fatty acids within phospholipids of biological
membranes and in plasma lipoproteins (Burton
et al. 1983). The phenolic moiety of tocopherol
reacts with peroxyl (ROO•, where R=alkyl
residue) radicals to form the corresponding
organic hydroperoxide and the tocopheroxyl
radical (Fig. 22.2). In this radical form,vitamin E
is not an effective antioxidant, and when suffi-
ciently accumulated may even have toxic pro-
oxidant effects. The effect of vitamin E on the
oxidation of various biological molecules, mem-
branes and tissues have been extensively
studied. Vitamin E suppresses the oxidative
damage of biological membranes, lipoproteins
and tissues. Tocopherols are unstable and are