| Despite
the knowledge on the antiatherogenic effects of exercise, the mechanism
by which exercise reduces atherogenic risk remains unknown. In this
study, we investigated the hypothesis that chronic exercise-induced
oxidative stress may increase plasma total antioxidant capacity and
antioxidant defense in the red cells. For 8 weeks, 60 male Dutch rabbits
were fed rabbit chow with or without the addition of 2% cholesterol.
The animals were further divided into rest and exercise groups (n
= 15 for each group). Animals in exercise groups ran on a rodent treadmill
at 15 m/min for 10 to 60 minutes gradually for 5 days per week for
a total of 8 weeks. At the end of experiments, blood samples were
collected and glutathione peroxidase (GPX), superoxide dismutase (SOD),
and catalase (CAT) activities were determined in red blood cells.
Total antioxidant capacity (TAC), malondialdehyde (MDA) and total
thiol (T-SH) levels were measured in plasma. Thoracic aorta and carotid
arteries were isolated for histological examination to evaluate atherosclerosis.
Eight weeks of chronic exercise reduced atherogenic diet-induced atherosclerotic
lesions in all the arteries studied, along with positive changes in
cholesterol profile, especially increase of serum HDL-C level. Plasma
MDA, TAC and T-SH concentrations were enhanced by exercise in both
control and hypercholesterolemic diet groups. Erythrocyte catalase
activity was significantly increased by chronic exercise (p < 0.05),
whereas total SOD activity rose with exercise only in the control
group. Surprisingly, GPX activity was significantly reduced (P <
0.05) in response to exercise in the control group and also in the
high cholesterol diet group. Exercise is a useful tool for the prevention
and regression of atherosclerosis which is evident by our findings
of the enhancement of plasma TAC and positive change in serum cholesterol
profile. However, the effect of exercise on red cell antioxidant activities
is limited in the hypercholesterolemic animals compared to control
animals, possibly in part because of alterations in the ability to
adapt to exercise-induced oxidative stress in high cholesterol diet.
KEY
WORDS: Chronic exercise, antioxidant, malondialdehyde, thiol,
atherosclerosis.
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