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Mechanisms and Biomarkers (WG 4) page 23
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Exercise and oxidative stress
An elevated metabolic rate as a result of exercise can dramatically increase oxygen
consumption and hence reactive oxygen species that may lead to oxidative stress. This is
particularly shown during unaccustomed and strenuous exercise (Sen, 1995). Using animal
models it has been shown that strenuous in vivo exercise indeed enhances reactive oxygen
species production detected in muscle homogenates and detected by electron spin resonance
techniques (Davies et al., 1982; Kumar et al., 1992) or a fluorimetric method using
dichlorofluorescin (Bejma and Ji, 1999). As stated before, most of the oxygen is metabolised
in the mitochondria and during its reduction a certain amount of oxygen not consumed is
liberated as reactive oxygen species. During maximal exercise, whole-body oxygen
consumption may increase up to 20 fold whereas in muscle fibre may be up to 100 fold. One
may expect a proportional increase of reactive oxygen species. However, no clear data
demonstrated such an increase and some even showed that this may not be the case as isolated
mitochondria reactive oxygen species production from exercised muscle did not differ from
that of rested one (Bejma and Ji, 1999). The mitochondrial theory is indirectly supported by
the increase of mitochondrial lipid peroxidation (Ji et al., 1988), decreased GSH redox status
in muscle (Leichtweis et al., 1997) and training adaptation of mitochondrial antioxidant
enzymes (Higuchi et al., 1985). Another source of free radicals is the one produced by
xanthine oxidase during conversion of hypoxanthine to xanthine and uric acid. Such a process
has been described during ischaemia-reperfusion of tissues. After intense muscular
contraction, accumulation of uric acid strongly support the activation of xanthine oxidase
which is found increased 10 fold in the plasma. Whether such an activation normally occurred
during aerobic exercise remains to be demonstrated. Another potential source of free radicals
is the activation of neutrophils during the inflammatory response following muscle damage
arising from oxidative stress or simply mechanical forces (Ji, 1999). The occurrence of
oxidative stress after exercise may result from the activation of immune cells. It was shown
for instance that phagocytosis and superoxide anion production by neutrophils were increased
at 24 hours postexercise. This long delay together with the time necessary for neutrophils to
infiltrate the tissue suggest that immmune cells are not a primary source of free radicals but
they serve as an important secondary source of free radical production during endurance
exertion and also during recovery. The role of antioxidants is first investigated on rats fed
vitamin E deficient diet and it was shown that endurance performance decreased and lipid
peroxidation increased. Interestingly, an acute bout of exercise in contrast to chronic exercise
did not decrease tissue vitamin E level, indicating that physiological levels of vitamin E are