Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart.
ABSTRACT 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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ABSTRACT: To evaluate the influence of aerobic exercise on oxidative stress in mice. The study included twenty female mice Mus musculus-Swiss divided into two groups: sedentary control (GA) and exercise (GB), each containing ten animals. All animals underwent an adaptation period of seven days isolated in individual boxes. After this period, the animals in the exercise group (GB) were trained in angled running wheel with circumference of 25 cm assembled on an articulated axle during five minutes for three consecutive days. On the fourth day, they underwent an exercise program of one session lasting 45 minutes. The evaluation of oxidative stress was performed by determining the levels of malondialhyde derived of lipid peroxidation by the TBA method. The samples were read in a spectrophotometer at 535 nm. No significant difference was observed in the intergroup comparison of MDA levels in the tissues evaluated. A significant difference was observed in the intragroup comparison of MDA levels in the control group (p = 0.0201).The Tukeys' post hoc test indicated significantly lower values of MDA in the smooth muscle in relation to plasma. In the analysis of variance in the exercise group, a significant difference between tissues (p = 0.0009), with significantly lower values in the smooth muscle in relation to plasma (p<0.001) and higher in striated muscle in relation to smooth muscle (p<0.05) was observed. There was no change in the analysis of oxidative stress in mice which were undergone a single session of aerobic exercise.Acta cirurgica brasileira / Sociedade Brasileira para Desenvolvimento Pesquisa em Cirurgia 08/2012; 27(8):544-51. · 0.48 Impact Factor
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ABSTRACT: The central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to re-define 'oxidative stress' as well as to introduce the term 'alterations in redox homeostasis' to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscle-damaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30 s and isometric exercise lasting 1-3 min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, 'exercise-induced oxidative stress' is not an 'oddity' associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.Journal of Experimental Biology 05/2012; 215(Pt 10):1615-25. · 3.24 Impact Factor
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ABSTRACT: Abstract Endurance exercise training is known to promote beneficial adaptations to numerous tissues including the heart. Indeed, endurance exercise training results in a cardioprotective phenotype that resists injury during an ischemia-reperfusion (IR) insult. Because IR-induced cardiac injury is due, in part, to increased production of radicals and other reactive oxygen species, many studies have explored the impact of exercise training on myocardial antioxidant capacity. Unfortunately, the literature describing the effects of exercise on the cardiac antioxidant capacity is widely inconsistent. Nonetheless, a growing body of evidence indicates that regular bouts of endurance exercise promote an increase in the expression of both superoxide dismutase 1 and 2 in cardiac mitochondria. Moreover, emerging evidence suggests that exercise also increases accessory antioxidant enzymes in the heart. Importantly, robust evidence indicates that as few as five consecutive days of endurance exercise training results in a cardiac phenotype that resists IR-induced arrthymthias, myocardial stunning, and infarction. Further, mechanistic studies indicate that exercise induced increases in mitochondrial superoxide dismutase 2 play a key role in this adaptation. Future studies are required to provide a complete picture regarding the cellular adaptations that are responsible for exercise-induced cardioprotection.Free Radical Research 08/2013; · 3.28 Impact Factor