- that physical exercise induces blood GSH
oxidation even at submaximal intensities. This
response is relatively rapid and can be observed
after only a few minutes of exercise. Given the
critical role of GSH in the antioxidant defence
network and other physiological functions, this
effect of exercise on blood GSH may be expected
to have important implications (Sen & Packer
1999).
Exercise training
In 1973, Caldarera et al. were the first to show that
acute exercise increases catalase activity in rat
liver, heart and skeletal muscle. Since then a rela-
tively large number of studies have shown
that endurance exercise training regimes may
strengthen antioxidant defences in organs such
as the skeletal muscle, heart and liver (Ji 1994;
Ohnoet al. 1994; Sen & Hanninen 1994; Powers
& Criswell 1996). Results from needle biopsy
samples collected from the vastus lateralis
muscle of healthy men showed that individuals
with high aerobic capacity had significantly
greater activities of catalase and superoxide dis-
mutase in their muscles. A strong positive corre-
lation (r=0.72,P<0.01) between the subject’s
maximum oxygen uptake and muscle catalase
was noted. A similar correlation was also
observed between the subject’s maximum
oxygen uptake and muscle superoxide dismu-
tase (r=0.60,P<0.05). The study also found that
there was a rank order relationship between
tissue oxygen consumption and antioxidant
enzyme activity (Jenkins et al. 1984). In a study on
exercise-induced oxidative stress in diabetic
young men, we observed that levels of lipid per-
oxidation by-products in the resting plasma, and
the exercise-induced increase in plasma lipid
peroxidation by-products, strongly correlated
(r=–0.82 and 0.81, respectively) with the aerobic
capacity of the individuals, suggesting a protec-
tive effect of physical fitness (Laaksonen et al.
1996). It has been observed that GSH-dependent
antioxidant defence in the skeletal muscle is
tightly regulated by the state of physical activity;
endurance training enhances and chronic
inactivity diminishes such protection (Sen et al.
1992).
Compared with information on the effect
of endurance training on tissue antioxidant
defences, very limited information is currently
available on the effect of sprint training. Criswell
et al. (1993) studied the effect of 12-week interval
training and observed favourable changes in the
skeletal muscle of rat. It was proposed that 5-min
interval high-intensity training was superior
to moderate-intensity continuous exercise in
upregulating muscle antioxidant defences. In
another study, it was observed that sprint train-
ing of rats significantly increased the total GSH
pool of skeletal muscles (Fig. 22.1) and GSH per-
oxidase activity of the heart and skeletal muscle.
Skeletal muscle or heart superoxide dismutase
activity was not influenced by sprint training
(Atalayet al. 1997). Similar results were observed
in a human study testing the effect of sprint cycle
training on skeletal muscle antioxidant enzymes.
After 7 weeks, sprint training significantly
increased activities of GSH peroxidase and GSH
reductase in muscle (Hellsten et al. 1996). Thus,
habitual physical exercise is crucial to maintain
and promote our natural capacity to defend
against the ravages of reactive oxygen.Nutrition
The 1988 United States Surgeon General’s report
on Nutrition and Health state that ‘for the two
out of three adult Americans who do not smoke
and do not drink excessively, one personal choice
seems to influence long-term health prospect
more than any other: what we eat’. As discussed
above, in several conditions including physical
exercise and cigarette smoking, generation of
ROS in tissues may overwhelm endogenous
antioxidant defence systems (Table 22.2).
Epidemiological studies have emphasized the
relevance of antioxidants in the prevention of
health disorders that may have an oxidative
stress-related aetiology (Sies 1997). It is not only
what we eat but also how much we eat that may
have marked implications in the management of
oxidative stress. Dietary restriction is known