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study investigated the onset of age-related changes in the myocardial
antioxidant enzymes and apoptosis and the vulnerability of the myocardium
to oxidative stress following exercise training. Few studies have
investigated the influence of the most prevalent life-prolonging strategy
physical exercise, on the age increment alterations in the myocardial
antioxidant enzymes and apoptosis at mid age and to determine whether
exercise-induced antioxidant defense system could attenuate lipid
peroxidation. Thirty six male Wistar rats were randomly assigned to
exercise trained (n = 18) and sedentary (n = 18) groups. The rats
in the training group went under 12, 24 and 36 weeks of moderate exercise
trainings (25 m·min-1 for 60-min with a 0% slope). Six
sedentary controls were killed together with each exercise group at
the end of the training programs. Levels of thiobarbituric acid-reactive
substances (TBARS) and catalase (CAT) activity in myocardial homogenates
were unchanged by training irrespective of the protocol duration.
However, an increased content of the TBARS was detected in hearts
from both the 24 and 36-week trained and sedentary control rats when
compared with their corresponding 12-week groups (p<0.01). The
activity of superoxide dismutase (SOD) remained unchanged after the
12-week training period whereas a significant increase was observed
in heart homogenates of 24-week trained animals as compared with their
sedentary controls (p<0.05). The activity of glutathione peroxidase
(GPX) remained unchanged. The rates of apoptosis which was detected
by ELISA assays, were significantly modified after 24 and 36-week
of training (p<0.05). These results demonstrate that a long-term
endurance training (24 weeks) induced increases in SOD activities
in rat myocardium and elicited a marked reduction in apoptosis rate.
However, a shorter training program (12 weeks) was not effective in
increasing heart antioxidant defenses.
KEY
WORDS: Oxidative stress, superoxide dismutase, apoptosis, heart,
exercises training.
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