A reduced expression of the manganese-dependent superoxide dismutase (SOD2) is characterised 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 a day at 15 m/min, 5 days/week, at an angle of 5° for a duration of 8 weeks) on cardiac function (heart frequency (HF), echocardiography, morphometry), oxidative stress (reactive oxygen species (ROS)) and antioxidative defence capacity (peroxiredoxin 1-6) in male SOD2-knockout (SOD2_EX) and wild-type mice (WT_EX) compared to untrained age-matched animals (WT_CON; SOD2_CON). In SOD2_CON, heart weight, cardiomyocyte diameter and cardiac ROS were significantly larger and peroxiredoxin-isoforms 4-6 lower than in WT_CON. The vessels-per-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 vessels-per-cardiomyocyte ratio and ROS-generation and down-regulated peroxiredoxin isoforms 4-6 and VEGF-generation. The vessels-per-cardiomyocyte ratio, cardiac VEGF concentration and cardiac ROS were not altered in SOD2_EX compared to SOD2_CON but a significant up-regulation of cardiac peroxiredoxin 1 and 4 was observed. Similar to the result observed in WT_EX, peroxiredoxin 3 was up-regulated in SOD2_EX. Chronic exercise shifted the (mal)adaptive hypertrophic into a compensated dilated cardiac phenotype in SOD2_EX. Conclusions: Down-regulation of SOD2 induces a maladaptive cardiac hypertrophy. In this situation, physical exercise results in a further deterioration of cardiac remodelling despite an up-regulation of the antioxidative defense system.
- oxidative stress
- Copyright © 2011, Journal of Applied Physiology