{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T03:37:24Z","timestamp":1771472244932,"version":"3.50.1"},"reference-count":64,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p>A reduced expression of the manganese-dependent superoxide dismutase (SOD2) is characterized by increased cardiac oxidative stress. Oxidative stress has also been described in situations of physical exercise. We investigated the influence of physical exercise (EX; treadmill 1 h\/day at 15 m\/min, 5 days\/wk, at an angle of 5\u00b0 for a duration of 8 wk) on cardiac function [heart frequency (HF), echocardiography, morphometry], oxidative stress [reactive oxygen species (ROS)], and antioxidative defence capacity (peroxiredoxin 1\u20136) in male SOD2-knockout (SOD2_EX) and wild-type mice (WT_EX) compared with untrained age-matched animals (WT_CON; SOD2_CON). In SOD2_CON, heart weight, cardiomyocyte diameter, and cardiac ROS were significantly larger and peroxiredoxin isoforms 4\u20136 lower than in WT_CON. The vessel-to-cardiomyocyte ratio, cardiac VEGF-concentration, and cardiac function were similar in SOD2_CON and WT_CON. Both groups tolerated the exercise protocol well. In WT, exercise significantly increased vessel-to-cardiomyocyte ratio and ROS-generation and downregulated peroxiredoxin isoforms 4\u20136 and VEGF generation. The vessel-to-cardiomyocyte ratio, cardiac VEGF concentration, and cardiac ROS were not altered in SOD2_EX compared with SOD2_CON, but a significant upregulation of cardiac peroxiredoxin 1 and 4 was observed. Similar to the result observed in WT_EX, peroxiredoxin 3 was upregulated in SOD2_EX. Chronic exercise shifted the (mal)adaptive hypertrophic into a compensated dilated cardiac phenotype in SOD2_EX. In conclusion, downregulation of SOD2 induces a maladaptive cardiac hypertrophy. In this situation, physical exercise results in a further deterioration of cardiac remodeling despite an upregulation of the antioxidative defense system.<\/jats:p>","DOI":"10.1152\/japplphysiol.01392.2010","type":"journal-article","created":{"date-parts":[[2011,8,12]],"date-time":"2011-08-12T04:22:08Z","timestamp":1313122928000},"page":"1431-1440","source":"Crossref","is-referenced-by-count":26,"title":["Exercise-induced adaptations of cardiac redox homeostasis and remodeling in heterozygous SOD2-knockout mice"],"prefix":"10.1152","volume":"111","author":[{"given":"L.","family":"Richters","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Sport Medicine, Institute of Cardiology and Sport Medicine, German Sport University Cologne, Cologne;"},{"name":"Department of Obstetrics and Gynecology, University Hospital of Cologne, Cologne, 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