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. 2007 Jun 1;6(2):243-9.
eCollection 2007.

Effects of age increment and 36-week exercise training on antioxidant enzymes and apoptosis in rat heart tissue

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Effects of age increment and 36-week exercise training on antioxidant enzymes and apoptosis in rat heart tissue

Nasser Ahmadiasl et al. J Sports Sci Med. .

Abstract

This 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 pointsExercise training induces activity of myocardial SOD.Long-term regular moderate-intensity exercise decreases the rate of myocardial apoptosis.Short-term regular moderate-intensity exercises do not change the rate of myocardial anti oxidant capacity and apoptosis.

Keywords: Oxidative stress; apoptosis; exercises training; heart; superoxide dismutase.

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Figures

Figure 1.
Figure 1.
Effects of 12, 24 and 36-week training protocols on levels of thiobarbituric acid-reactive substances (TBARS) in rat myocardium. Results are mean ± SD of independent preparations. ** Significant differences between the 24 and 36-week groups and the corresponding 12-week groups (p < 0.01).
Figure 2.
Figure 2.
Effects of 12, 24 and 36-week training protocols on antioxidant enzymes activity in rat myocardium. (a) Superoxide dismutase (SOD), (b) Catalase (CAT), and (c) glutathione peroxidase (GPX). # p < 0.05 compared with trained group. * p < 0.05 between the 24 and 36-week groups and the corresponding 12-week groups .
Figure 3.
Figure 3.
Effects of 12, 24 and 36-week training protocols on apoptosis in rat myocardium. Results are mean ± SD of independent preparations. # Significant difference between the trained and their sedentary groups (p < 0.05).

References

    1. Aebi H. (1984) Catalase in vitro. Methods in enzymology 105, 121-126 - PubMed
    1. Alessio H.M. (1993) Exercise-induced oxidative stress. Medicine and science in sports and exercise 25, 218-224 - PubMed
    1. Atalay M., Sen C.K. (1999) Physical exercise and antioxidant defences in the heart. Annals of the New York Academy of Science 874, 169-177 - PubMed
    1. Beere H.M., Wolf B.B., Cain K., Mosser D.D., Mahboubi A., Kuwana T., Tailor P., Morimoto R.I., Cohen G. M., Green D.R. (2000) Heat-shock protein 70 inhibits apoptosis by preventing recruitment of procaspase-9 to the Apaf-1 apoptosome. Nature cell biology 2, 469-475 - PubMed
    1. Bejma J., Ramires P., Ji L.L. (2000) Free radical generation and oxidative stress with ageing and exercise: differential effects in the myocardium and liver. Acta physiologica Scandinavica 169, 343-353 - PubMed

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