2012
DOI: 10.1016/j.lfs.2012.06.028
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Therapeutic action of physical exercise on markers of oxidative stress induced by chronic kidney disease

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Cited by 23 publications
(12 citation statements)
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References 34 publications
(44 reference statements)
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“…The efferent renal arteriole demonstrates a constriction in response to glomerular endothelial injury [ 45 ] and may eventually contribute to further deterioration in eGFR and progression to renal microvascular disease [ 46 ]. A late-onset decrease in oxidative stress and increase in anti-oxidative factors due to exercise training could prevent progressive fibrosis in the kidneys [ 47 , 48 ]. Exercise-induced blood volume expansion likely contributes to increased renal blood flow and shear stress in the kidney at rest and during exercise [ 49 – 51 ], the latter stimulating improvements in endothelial function [ 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…The efferent renal arteriole demonstrates a constriction in response to glomerular endothelial injury [ 45 ] and may eventually contribute to further deterioration in eGFR and progression to renal microvascular disease [ 46 ]. A late-onset decrease in oxidative stress and increase in anti-oxidative factors due to exercise training could prevent progressive fibrosis in the kidneys [ 47 , 48 ]. Exercise-induced blood volume expansion likely contributes to increased renal blood flow and shear stress in the kidney at rest and during exercise [ 49 – 51 ], the latter stimulating improvements in endothelial function [ 52 ].…”
Section: Discussionmentioning
confidence: 99%
“…In rats, moderate-(65% VO 2max ) and high-intensity (75% VO 2max ) chronic aerobic exercise resulted in significantly increased SOD activity, compared to low-intensity (55% VO 2max ) and sedentary conditions [11] in the right ventricle of the heart. In addition, treadmill running performed for 8 weeks (50 min/day, 5 days/wk, 17 m/min) [24] and 14 weeks (60 min/day, 3 days/wk, 30 m/min) [25] resulted in significant increases in kidney-specific SOD activity [24] and CAT activity in the tibialis anterior [25], compared to sedentary rats. Although research suggests increases in exercise intensity results in increased levels of OS and INF, it is the repeated exposure to increased oxidative and inflammatory insult that seems to be responsible for positive exercise-induced adaptations, namely increases in eAO activity [11,25].…”
Section: Quantitative Reverse Transcription Polymerase Chain Reactionmentioning
confidence: 91%
“…In parallel to human data, swimming exercise in rats for 10 weeks increased SOD activity in the diaphragm and kidney (37). Treadmill exercise in rats with either chronic hypertension (38) or chronic renal disease was shown to increase SOD and GPx activity, but not the antioxidant effects of CAT, implicating that the protective effect of regular aerobic exercise on kidney damage occurs by up-regulating SOD and GPx activity (19). In the current study, exercise training did not alter RVHinduced depletion in renal SOD levels.…”
Section: Discussionmentioning
confidence: 65%