Effects of sprint exercise on oxidative stress in skeletal muscle and liver

Kayatekin, Berkant Muammer; Gönenç, Sevil; Açıkgöz, Osman; Uysal, Nazan; Dayı, Ayfer

doi:10.1007/s00421-002-0607-3

Cited by 64 publications

(49 citation statements)

References 19 publications

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“…−1 (30 mins swimming followed by 10 minutes rest) for 28 days as per the design of previous workers (Kayatekin et al, 2002) and some modification of our technique (Misra et al, 2005). Group 5: Extract pretreated cum co-treated swimming (EPCS) -preconditioning by extract treatment at the same dose as group 3 for 15 days prior to swimming followed by swimming as per the protocol of group 4 and composite extract co-administration through gavage at the above dose throughout 28 days of swimming.…”

Section: Group 4: Forced Swimming (Fs) -Intermittent Swimming 8 H Daymentioning

confidence: 99%

Protection of swimming-induced oxidative stress in some vital organs by the treatment of composite extract of Withania somnifera, Ocimum sanctum and Zingiber officinalis in male rat

Misra

Maiti²,

Ghosh³

2010

Afr. J. Trad. Compl. Alt. Med.

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Composite methanolic extract of roots of Withania somnifera, leaves of Ocimum sanctum, and rhizomes of Zingiber officinalis was administered by gavage at the dose of 40 mg 100 g −1 body weight day −1 to rat orally for 15 days prior to experimentation followed by co-administration of above extract at the same dose for 28 days of swimming to find out the remedial effect of this extract on exhaustive physical exercise-induced oxidative damage. Swimming resulted significant diminution (p<0.05) in the activities of catalase and superoxide dismutase along with elevation (p<0.05) in the levels of thiobarbituric acid reactive substances and conjugated dienes in cardiac, skeletal, hepatic tissues, cerebrum and cerebellum in respect to control. The levels of all these parameters were resettled significantly (p<0.05) towards the extract pretreated cum co-treated swimming group. The antioxidative potency of this composite extract was compared with standard non-enzymatic antioxidant (vitamin-E) in forced swimming state. The above extract has no general toxic effect as reflected here from the study of transaminase activities in liver and kidney. Results lead to conclude that the composite extract of above three plant parts has a therapeutic protective effect on forced swimming-induced oxidative stress in vital organs.

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Section: Group 4: Forced Swimming (Fs) -Intermittent Swimming 8 H Daymentioning

confidence: 99%

Protection of swimming-induced oxidative stress in some vital organs by the treatment of composite extract of Withania somnifera, Ocimum sanctum and Zingiber officinalis in male rat

Misra

Maiti²,

Ghosh³

2010

Afr. J. Trad. Compl. Alt. Med.

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“…Exercise is beneficial to patients with metabolic syndrome, and can markedly increase glycemic control (15,16). Exercise stimulates glucose uptake and increases insulin sensitivity in the muscle and other peripheral tissues (16).…”

mentioning

confidence: 99%

Acute Oxidative Stress Can Reverse Insulin Resistance by Inactivation of Cytoplasmic JNK

Berdichevsky

Guarente

Bose

2010

Journal of Biological Chemistry

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Chronic oxidative stress results in decreased responsiveness to insulin, eventually leading to diabetes and cardiovascular disease. Activation of the JNK signaling pathway can mediate many of the effects of stress on insulin resistance through inhibitory phosphorylation of insulin receptor substrate 1. By contrast, exercise, which acutely increases oxidative stress in the muscle, improves insulin sensitivity and glucose tolerance in patients with Type 2 diabetes. To elucidate the mechanism underlying the contrasting effects of acute versus chronic oxidative stress on insulin sensitivity, we used a cellular model of insulin-resistant muscle to induce either chronic or acute oxidative stress and investigate their effects on insulin and JNK signaling. Chronic oxidative stress resulted in increased levels of phosphorylated (activated) JNK in the cytoplasm, whereas acute oxidative stress led to redistribution of JNK-specific phosphatase MKP7 from the nucleus into the cytoplasm, reduction in cytoplasmic phospho-JNK, and a concurrent accumulation of phospho-JNK in the nucleus. Acute oxidative stress restored normal insulin sensitivity and glucose uptake in insulin-resistant muscle cells, and this effect was dependent on MKP7. We propose that the contrasting effects of acute and chronic stress on insulin sensitivity are driven by changes in subcellular distribution of MKP7 and activated JNK.Chronic oxidative stress is one of the major sources of metabolic abnormalities associated with Type 2 diabetes (1-3). High glucose and fatty acid levels lead to increased production of reactive oxygen species (ROS), 2 which can cause insulin resistance in peripheral metabolic tissues. This leads to decreased glucose uptake in muscle and adipose tissue, and eventually, pancreatic ␤ cell failure, glucose intolerance, and frank diabetes (4 -8).The mechanistic link between increased ROS levels and insulin resistance is activation of several signaling pathways, primarily mitogen-activated protein kinases (MAPK) pathways. JNK (Jun N-terminal kinases) are MAP kinases activated by cellular stresses, including oxidative stress, and play a role in apoptosis and survival, stress resistance, and immune response (9). Upstream signaling leading to JNK activation involves stress-induced MAPK kinases MEKK4 and MEKK7, as well as scaffold protein JIP (JNK-interacting protein) (10). Activation of JNK leads to dimerization followed by translocation into the nucleus, where it can phosphorylate its downstream target c-Jun, leading to activation of stress response and apoptotic pathways. JNKs are specifically dephosphorylated and inactivated by MAP kinase phosphatase 7 (MKP7), which also acts as a shuttle protein and was proposed to be involved in JNK nucleocytoplasmic translocation (11).Obesity increases JNK activation in muscle and adipose tissue in mice. Genetic ablation or pharmacological inhibition of JNK results in marked improvement of insulin sensitivity in mouse models of diet-induced obesity and insulin resistance (6, 12, 13). Mechanistically, J...

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“…Information on the production of ROS as a result of acute anaerobic exercise is lacking compared with aerobic exercise (Groussard, 2003). However, these studies generally show an increase of the oxidative stress after supramaximal exercise such as intermittent running, sprints, jumps or sets of jumps, resistance or Wingate tests on an ergocycle (Groussard, 2003;Chen et al, 2001;Kayatekin et al, 2002;Goldfarb et al, 2005, Ramel et al, 2004.…”

Section: Anaerobic Exercisementioning

confidence: 99%