Dept. of Molecular and Cellular Sport Medicine, German Sport Univ. Cologne, Carl-Diem-Weg 6, 50933 Cologne, Germany.
J Appl Physiol (1985). 2011 Nov;111(5):1431-40. doi: 10.1152/japplphysiol.01392.2010. Epub 2011 Aug 11.
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° 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 1-6) 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 4-6 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 4-6 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.
锰依赖性超氧化物歧化酶（SOD2）表达减少的特征是心脏氧化应激增加。氧化应激也在体育锻炼的情况下被描述过。我们研究了 8 周的 1 小时/天、15 米/分钟、5 天/周、5°角度的跑步机运动（EX）对 SOD2 敲除（SOD2_EX）和野生型（WT_EX）雄性小鼠的心脏功能[心率（HF）、超声心动图、形态测量]、氧化应激[活性氧（ROS）]和抗氧化防御能力（过氧化物酶 1-6）的影响，与未经训练的同龄动物（WT_CON；SOD2_CON）相比。在 SOD2_CON 中，心脏重量、心肌细胞直径和心脏 ROS 明显增大，而过氧化物酶同功酶 4-6 降低。血管与心肌细胞的比例、心脏 VEGF 浓度和心脏功能在 SOD2_CON 和 WT_CON 中相似。两组均能很好地耐受运动方案。在 WT 中，运动显著增加了血管与心肌细胞的比例和 ROS 的产生，下调了过氧化物酶同功酶 4-6 和 VEGF 的生成。与 SOD2_CON 相比，SOD2_EX 的血管与心肌细胞的比例、心脏 VEGF 浓度和心脏 ROS 没有改变，但观察到心脏过氧化物酶 1 和 4 的显著上调。与 WT_EX 的结果相似，SOD2_EX 中的过氧化物酶 3 也被上调。慢性运动使 SOD2_EX 中的（不良）适应性肥厚转变为代偿性扩张性心脏表型。总之，SOD2 的下调会导致心脏不良适应性肥厚。在这种情况下，尽管抗氧化防御系统的上调，体育锻炼仍会导致心脏重构的进一步恶化。
