Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart

Department of Physiology, Faculty of Medicine, Ataturk University, 25240, Erzurum, Turkey.
Comparative Biochemistry and Physiology - Part A Molecular & Integrative Physiology (Impact Factor: 1.97). 03/2006; 143(2):239-45. DOI: 10.1016/j.cbpa.2005.12.001
Source: PubMed


We investigated whether 8-week treadmill training strengthens antioxidant enzymes and decreases lipid peroxidation in rat heart. The effects of acute exhaustive exercise were also investigated. Male rats (Rattus norvegicus, Sprague-Dawley strain) were divided into trained and untrained groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h day(-1), 5 days week(-1) for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted. Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats. The activities of glutathione peroxidase and glutathione reductase enzymes decreased by both acute exercise and training. Glutathione S-transferase and catalase activities were not affected. Total and non-enzymatic superoxide scavenger activities were not affected either. Superoxide dismutase activity decreased by acute exercise in untrained rats; however, this decrease was not observed in trained rats. Our results suggested that rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited.

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    • "Increased oxidative stress, evidenced by lipid peroxidation, has been found in human patients with ARF [15] [16]. Gul et al. found that the " rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited " [17]. It is obvious that LDL oxidation alone does not explain the complex mechanism of oxidative stress and atherosclerosis. "
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    ABSTRACT: Atherosclerotic heart diseases are universal problems in modern society. Oxidative damage to lipids is a primary cause of atherosclerosis. There are many choices for treatment, but no definite recommendations to prevent the occurrence of the disease. There is a relationship between atherosclerotic risk factors and increased vascular production of reactive oxygen species (ROS). Oxidized low-density lipoproteins (LDL) and ROS may directly cause endothelial dysfunction by reducing endothelial nitric oxide (NO) bioavailability. Vitamin E can to some degree prevent the consequences of oxidized LDL, and vitamin C provides NO synthase activity. Although prolonged use of vitamin A, C, and E supplementation in pharmaceutical forms has been proven to be effective in preventing atherosclerosis in animal experiments, this has not yet been demonstrated in clinical trials with human beings. It should be taken into account that the evidence has been gathered from young/adult experimental animals with early stages of arthrosclerosis and from in-vitro studies, while most of the clinical trials have involved older patients with late stages of the disease. Prolonged use of vitamins in the diet has not yet been recommended in human beings. There is some indication that a diet rich in antioxidant fruit and vegetables may be beneficial in the prevention of cardiovascular events.
    Advances in Clinical and Experimental Medicine 12/2012; 21(1):115-23. · 1.10 Impact Factor
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    • "First, free radicals cause metabolic disturbances; both normal and exhaustive exercises can cause an increase in free radicals in hepatic tissues, resulting in hepatocyte damage (Gul et al., 2006; Voces et al., 1999). Second, exercise causes the production and accumulation of products of metabolism, such as lactic acid. "

    Soybean and Health, 09/2011; , ISBN: 978-953-307-535-8
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    • "While many researches did not determine any change in GPx enzyme activity with acute maximal exercise after endurance training period (Miyazaki et al., 2001; Öztaan et al., 2004), some determined an increase (Elosua et al., 2003; Fatouros et al., 2004; Servais et al., 2003), and some determined a decrease (Balakrishnan and Anuradha, 1998; Gül et al., 2006). Similarly again, while some researchers determined no change in CAT enzyme activity (Balakrishnan and Anuradha, 1998; Gül et al., 2006; Miyazaki et al., 2001), there are also other researches who have found an increase (Alessio and Goldfarb, 1988; Poprzecki et al., 1997; Servais et al., 2003). Among possible reasons for the contradictions in studies towards determining exercise-related lipid peroxidation and antioxidant status; the differences between type, duration and intensity of the exercise applied, type of the subjects and their qualities, the periods during which measurements are made before and after exercise and the methods used and doing the research in different configurations and environments may be shown. "
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    ABSTRACT: This study was aimed to investigate the effects of endurance training on lipid peroxidation and antioxidant enzyme levels in young adults. Twenty four male students participated in this study. Subjects were divided into two groups as training group (n=12) and control group (n=12). Subjects in the training groups performed running exercise 25 to 60 min/day, three days/week for eight weeks at an intensity of 50 to 70% of target heart rate. Blood samples collected at rest and after exhaustive exercise before and after 8 weeks, were analyzed for the determination of plasma lipid hydroperoxide (LOOH) level, and activities of glutathione peroxidase (GPx), catalase (CAT) and lactate dehydrogenase (LDH). LOOH level in the training group significantly decreased after the post-training period (p<0.05), but did not alter in the control group (p>0.05). LDH activities significantly increased both control and training groups after the exhaustive exercise (p<0.05). LDH activity was found significantly higher in control group than training group both at rest and after exhaustive exercise (p<0.05). GPx was not significantly altered by training and exhaustive exercise in both groups (p>0.05). In the training group, exhaustive exercise significantly increased CAT level after training period (p<0.05). Consequently, it can be said that endurance training is effective in prevention of lipid peroxidation caused by exhaustive exercise.
    African journal of pharmacy and pharmacology 04/2011; 5(3):437-441. DOI:10.5897/AJPP11.159 · 0.84 Impact Factor
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