Zanchi Nelo Eidy, Bechara Luiz Roberto Grassmann, Tanaka Leonardo Yuji, Debbas Victor, Bartholomeu Teresa, Ramires Paulo Rizzo
Laboratory of Biochemistry of Exercise, School of Physical Education and Sport, University of São Paulo, Av. Prof. Mello Moraes, 65, São Paulo, SP 05508-900, Brazil.
Eur J Appl Physiol. 2008 Dec;104(6):1045-52. doi: 10.1007/s00421-008-0861-0. Epub 2008 Sep 2.
Myocardial infarction (MI) has been associated with increases in reactive oxygen species (ROS). Exercise training (ET) has been shown to exert positive modulations on vascular function and the purpose of the present study was to investigate the effect of moderate ET on the aortic superoxide production index, NAD(P)H oxidase activity, superoxide dismutase activity and vasomotor response in MI rats. Aerobic ET was performed during 11 weeks. Myocardial infarction significantly diminished maximal exercise capacity, and increased vasoconstrictory response to norepinephrine, which was related to the increased activity of NAD(P)H oxidase and basal superoxide production. On the other hand, ET normalized the superoxide production mostly due to decreased NAD(P)H oxidase activity, although a minor SOD effect may also be present. These adaptations were paralleled by normalization in the vasoconstrictory response to norepinephrine. Thus, diminished ROS production seems to be an important mechanism by which ET mediates its beneficial vascular effects in the MI condition.
心肌梗死（MI）与活性氧（ROS）增加有关。运动训练（ET）已被证明对血管功能有积极调节作用，本研究的目的是探讨中度ET对MI大鼠主动脉超氧化物生成指数、NAD(P)H氧化酶活性、超氧化物歧化酶活性和血管舒缩反应的影响。进行了为期11周的有氧ET。心肌梗死显著降低了最大运动能力，并增加了对去甲肾上腺素的血管收缩反应，这与NAD(P)H氧化酶活性增加和基础超氧化物生成有关。另一方面，ET使超氧化物生成正常化，这主要是由于NAD(P)H氧化酶活性降低，尽管可能也存在轻微的超氧化物歧化酶效应。这些适应性变化与对去甲肾上腺素的血管收缩反应正常化同时出现。因此，减少ROS生成似乎是ET在MI状态下介导其有益血管效应的重要机制。
