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Since physical exercise has been indicated as cardioprotective, we tested the hypothesis that high\u2010intensity exercise training could reverse the cardiac maladaptations produced by diabetes. For this, diabetes was induced in rats by a single dose of alloxan. Diabetic rats were randomly assigned to a sedentary group or submitted to a program of exercise on a treadmill for 4 weeks at 80% of maximal performance. Another group of normoglycemic rats was used as control. Diabetic rat hearts presented cardiomyocyte hypertrophy and interstitial fibrosis. Chronic exercise reduced both parameters but increased apoptosis. Diabetes increased the myocardial levels of the mRNA and proteins of NADPH oxidases NOX2 and NOX4. These altered levels were not reduced by exercise. Diabetes also increased the level of uncoupled endothelial nitric oxide synthase (eNOS) that was not reversed by exercise. Finally, diabetic rats showed a lower degree of phosphorylated phospholamban and reduced levels of SERCA2 that were not restored by high\u2010intensity exercise. These results suggest that high\u2010intensity chronic exercise was able to reverse remodeling in the diabetic heart but was unable to restore the nitroso\u2010redox imbalance imposed by diabetes.<\/jats:p>","DOI":"10.1155\/2017\/7921363","type":"journal-article","created":{"date-parts":[[2017,6,18]],"date-time":"2017-06-18T21:03:14Z","timestamp":1497819794000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["High\u2010Intensity Exercise Reduces Cardiac Fibrosis and Hypertrophy but Does Not Restore the Nitroso\u2010Redox Imbalance in Diabetic 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