Free radical changes in rat muscle tissue after exercise

Arslan, Serkan; Erdem, Sevim; Kılınç, Kamer; Sívrí, A.; Tan, Ersin; Hasçelik, H. Zafer

doi:10.1007/s002960000094

Cited by 8 publications

(4 citation statements)

References 25 publications

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“…In the present study, we demonstrated that the 8-week exercise training in rats did not alter SOD, CAT and GPx activities in the kidney. These results are consistent with those of others, in which regular training was shown to have little eVect on renal, myocardial and hepatic anti-oxidant enzyme systems while a signiWcant up-regulation of antioxidant enzymes was demonstrated in skeletal muscles, which were actively involved in exercise (Ji 1993;Hong and Johnson 1995;Benderitter et al 1996;Oh-ishi et al 1997;Liu et al 2000;Pohlman and Harlan 2000;Arslan et al 2001;Gunduz et al 2004). The results suggest that exerciseinduced oxidative stress could be a prominent damaging factor in organs actively involved in exercise, such as skeletal muscle and, thus, adaptive processes in these tissues might require increased activity of antioxidant enzymes.…”

Section: Discussionsupporting

confidence: 94%

“…The available data suggest that regular training reduces the capacity of some tissues to release ROS and leads to adaptation of antioxidative mechanisms, which Wnally may contribute to a limitation of exercise-induced oxidative damage (Niess et al 1999). It has been reported that regular training could increase antioxidant defense capacity and, therefore, could protect against cellular stress in the working skeletal muscle, whereas it has little eVect on the hepatic and myocardial antioxidant enzyme system (Benderitter et al 1996;Arslan et al 2001;Pohlman and Harlan 2000;Pedersen and HoVman-Goetz 2000;Rus et al 2003). The variability of response of diVerent tissues to exhaustive and regular exercise depends on their variable past exposures to oxidative stress and/or to their intrinsic oxidant status (Ji 1996(Ji , 2002Liu et al 2000).…”

Section: Introductionmentioning

confidence: 98%

“…Imbalance between formation of ROS and antioxidative defense mechanisms leads to oxidative stress, which is known to be an activator of apoptotic processes (Phaneuf and Leeuwenburgh 2000;Galle 2001). Augmented oxidative stress has been shown to occur during strenuous exercise and has the potential to induce apoptosis in skeletal muscle, peripheral blood cells, and thymocytes (Lin et al 1999;Azenabor and HoVman-Goetz 1999;Phaneuf and Leeuwenburgh 2000;Liu et al 2000;Arslan et al 2001).…”

Section: Introductionmentioning

confidence: 98%

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Effects of adaptive exercise on apoptosis in cells of rat renal tubuli

et al. 2006

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Regular exercise is known to improve physiological and functional capacity of many organs due to adaptive processes. We have previously shown that acute exercise in untrained rats results in apoptosis of renal tubular cells and that the apoptotic process seems to be associated with stimulation of angiotensin II, AT1 and AT2 receptors. In this study, we examined the influence of regular training on apoptosis and the role of angiotensin II receptors and antioxidant enzymes in mediating the adaptive response in renal tubular cells. We measured apoptosis, expression of AT1 and AT2 receptors, level of lipid peroxidation (TBARS) and activities of antioxidant enzymes, SOD, GPx and CAT in kidneys of sedentary rats that were exposed to acute exercise and rats that were trained for 8 weeks. In untrained animals, the acute exercise resulted in increased apoptosis and increased expression of AT1 and AT2 receptors in renal tubular cells, while in the rats exposed to the 8-week regular training, there were no changes in apoptosis nor AT1 and AT2 receptor expression as compared to the sedentary animals. The TBARS levels were significantly increased in acutely exercised rats, while in rats pre-exposed to the training they remained unchanged. The acute exercise, as well as regular training, did not change SOD, CAT or GPx activities. These findings suggested that the acute exercise-induced apoptosis in renal tubules could involve action of AT1 and AT2 receptors as well as oxidative stress, while the regular training was shown to prevent apoptosis in renal tubular cells via modulated expression of AT1 and AT2 receptors.

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Section: Discussionsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 98%

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Effects of adaptive exercise on apoptosis in cells of rat renal tubuli

et al. 2006

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“…Mitochondria are the source and target of ROS because complexes I and III of the electron transport chain are the main sites of mitochondrial superoxide production [ 38 , 60 ] . The magnitude of changes in exercise induced ROS depends on the type of muscle fi bre [ 7 ] as cellular Ca 2+ overload activates the degradation of muscle proteins and membrane phospholipids via Ca 2+ dependent proteolytic and phospholipolytic pathways [ 6 ] . Ca 2+ overload results in the uptake of Ca 2+ into mitochondria [ 99 ] , reduces mitochondrial capacity to synthesize ATP and causes damage of mitochondrial membranes.…”

Section: Exhaustive Exercise and Rosmentioning

confidence: 99%

Muscle Protein Turnover in Endurance Training: a Review

2011

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There has been much debate about skeletal muscle capacity to adapt to long-lasting endurance exercise. Exercise in the aerobic zone of metabolism does not result in hypertrophy of skeletal muscle fibres but increases their oxidative capacity. The duration and intensity of an exercise session determines the time period of depressed muscle protein synthesis and increased degradation rate during the recovery period after exercise. Protein turnover characterizes the renewal processes of muscle proteins and the functional capacity of muscle. The turnover rate of myofibrillar proteins is slow in comparison with mitochondrial proteins and depends on the oxidative capacity of muscle fibres. The turnover rate of myofibrillar proteins in the same muscle is different and is also different within the myosin molecule between myosin heavy and light chain isoforms. The turnover rate of muscle proteins in endurance training shows the adaptation of skeletal muscle to long-lasting exercise via remodelling of muscle structures. Adaptational coordination between myofibrillar and mitochondrial compartments shows the physiological role and adaptational capacity of skeletal muscle to endurance training. It is challenging to use muscle protein turnover for the purposes of monitoring the training process of endurance athletes, optimizing training programs and preventing overtraining.

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