Oxidative Balance in Rats during Adaptation to Swimming Load

Elikov, A. V.

doi:10.1007/s10517-016-3570-4

Cited by 6 publications

(5 citation statements)

References 2 publications

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“…). Furthermore, a study comparing a protocol of moderate physical training in both previously trained and untrained rats found that the untrained group had lower levels of anti‐oxidant parameters in response to oxidative stress (Elikov, ). In this regard, we also found that Mn‐SOD and Cu/Zn‐SOD expression were significantly reduced in the carotid artery in the trained group.…”

Section: Discussionmentioning

confidence: 99%

Chronic exercise impairs nitric oxide pathway in rabbit carotid and femoral arteries

Marchio

Guerra-Ojeda

Vila

et al. 2018

The Journal of Physiology

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The present study aimed to evaluate the effects of chronic exercise on vasodilator response in two different arteries. Rings of carotid and femoral arteries from control and trained rabbits were suspended in organ baths for isometric recording of tension. Endothelial nitric oxide synthase (eNOS), Cu/Zn and Mn-superoxide dismutase (SOD), and large conductance calcium activated potassium (BKCa) channel protein expression were measured by western blotting. In the carotid artery, training reduced the relaxation to ACh (10 to 3 × 10 m) that was reversed by N-acetylcysteine (10 m). l-NAME (10 m) reduced the relaxation to ACh in both groups, although the effect was lower in the trained group (in mean ± SEM, 39 ± 2% vs. 28 ± 3%). Physical training did not modify the relaxation to ACh in femoral arteries, although the response to l-NAME was lower in the trained group (in mean ± SEM, 41 ± 5% vs. 17 ± 2%). Charybdotoxin (10 m) plus apamin (10 m) further reduced the maximal relaxation to ACh only in the trained group. The remaining relaxation in both carotid and femoral arteries was abolished by KCl (2 × 10 m) and BaCl (3 × 10 m) plus ouabain (10 m) in both groups. Physical training decreased eNOS expression in both carotid and femoral arteries and Cu/Zn and Mn-SOD expression only in the carotid artery. BKCa channels were overexpressed in the trained group in the femoral artery. In conclusion, chronic exercise induces endothelial dysfunction in the carotid artery as a result of oxidative stress. In the femoral artery, it modifies the vasodilator pathways, enhancing the participation of BKCa channels, thus compensating for the impairment of NO-mediated vasodilatation.

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Section: Discussionmentioning

confidence: 99%

Chronic exercise impairs nitric oxide pathway in rabbit carotid and femoral arteries

Marchio

Guerra-Ojeda

Vila

et al. 2018

The Journal of Physiology

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“…It consisted of a swimming exercise in a tank with controlled temperature (31°C) carrying constant loads of 10% of the body weight (17) that were fixed on mice tails. Exhaustion was characterized by the animal losing the coordinated movements and not returning to the surface within 7 s. The animals were submitted to the exercise only once on day 0.…”

Section: Methodsmentioning

confidence: 99%

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

Furtado

Hartmann

Martins

et al. 2018

Braz J Med Biol Res

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When exercises are done in intense or exhaustive modes, several acute biochemical mechanisms are triggered. The use of cryotherapy as cold-water immersion is largely used to accelerate the process of muscular recovery based on its anti-inflammatory and analgesic properties. The present study aimed to study the biochemical effects of cold-water immersion treatment in mice submitted to exercise-induced exhaustion. Swiss albino mice were divided into 4 treatment groups: control, cold-water immersion (CWI), swimming exhaustive protocol (SEP), and SEP+CWI. Treatment groups were subdivided into times of analysis: 0, 1, 3, and 5 days. Exhaustion groups were submitted to one SEP session, and the CWI groups submitted to one immersion session (12 min at 12°C) every 24 h. Reactive species production, inflammatory, cell viability, and antioxidant status were assessed. The SEP+CWI group showed a decrease in inflammatory damage biomarkers, and reactive species production, and presented increased cell viability compared to the SEP group. Furthermore, CWI increased acetylcholinesterase activity in the first two sessions. The present study showed that CWI was an effective treatment after exercise-induced muscle damage. It enhanced anti-inflammatory response, decreased reactive species production, increased cell viability, and promoted redox balance, which could decrease the time for the recovery process.

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“…It should be taken into consideration that pro-oxidants detected in blood plasma and erythrocytes reflect the redox state of all components which are included in the motor act during physical exercise. In that sense it's logical to expect the different values of parameters of oxidative stress response measured in heart and in plasma (Elikov 2016). Furthermore, Hu et al (2000) observed no change in the lipid peroxidation level in heart, which may be explained by a shorter period of swimming training (7 days, 45 minutes per day) insufficient to establish positive adaptations to exercise.…”

Section: Levels Of Reduced Glutathione (Gsh)mentioning

confidence: 98%

“…On the contrary, excessive production of ROS leads to a contractile dysfunction which is followed by muscle weakness and fatigue (Powers and Jackson 2008;Rahal et al 2014). It has been established that swimming training causes changes in antioxidant enzymes, alters muscle gene expression, thus contributing to exercise-induced adaptations to skeletal muscle (Venditti and Di Meo 1997;Elikov 2016;Ruzicic et al 2016). However it should be taken into consideration that various factors influence the oxidative stress response to swimming training, such as type of exercise, intensity, duration, gender and age of athletes etc.…”

Section: Introductionmentioning

confidence: 99%

Comparison of training and detraining on redox state of rats: gender specific differences

Bradić¹,

Ruzicić²,

Jeremić³

et al. 2018

gpb

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Given the fact that oxidative stress response induced by training/detraining has still not been clarified and may be influenced by gender, the aim of our investigation was to compare the effects of swimming training and detraining on oxidative and antioxidative parameters in rats, with a special focus on sex differences. Wistar albino rats (n = 64) were divided into 4 groups: control, trained group, groups exposed to 2 and 4 weeks of detraining. Each group included two subgroups: males and females. After sacrificing, hearts were isolated and retrogradely perfused according to Langendorff technique. Levels of superoxide anion radical, hydrogen peroxide, nitrites and thiobarbituric acid reactive substances were measured in plasma and coronary venous effluent, while reduced glutathione, activities of superoxide dismutase and catalase were measured in erythrocytes. Our results indicate that swimming training doesn't promote oxidative damage, nor act protectively within the heart. However, 2 and 4 weeks of detraining led to a partial lost in exercise-induced adaptation. It seems that moderate-intensity physical exercise of sufficient duration leads to beneficial adaptations, which may be partially lost during detraining period. Positive antioxidative effects of training remained longer in males. Findings of present study may help in elucidation of training and detraining effects on modulation of redox homeostasis, especially from aspect of gender differences.

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Oxidative Balance in Rats during Adaptation to Swimming Load

Cited by 6 publications

References 2 publications

Chronic exercise impairs nitric oxide pathway in rabbit carotid and femoral arteries

Chronic exercise impairs nitric oxide pathway in rabbit carotid and femoral arteries

Cryotherapy: biochemical alterations involved in reduction of damage induced by exhaustive exercise

Comparison of training and detraining on redox state of rats: gender specific differences

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