Reis Junior Dermeval, Antonio Ednei Luiz, de Franco Marcello Fabiano, de Oliveira Helenita Antonia, Tucci Paulo José Ferreira, Serra Andrey Jorge
Cardiology Division, Federal University of São Paulo, São Paulo, Brazil.
Pathology Division, Federal University of São Paulo, São Paulo, Brazil.
Nicotine Tob Res. 2016 Dec;18(12):2268-2272. doi: 10.1093/ntr/ntw180. Epub 2016 Jul 14.
There was no data for cardiac repercussion of exercise training associated with tobacco smoking. This issue is interesting because some smoking people can be enrolled in an exercise-training program. Thus, we evaluated swimming training effects on the function and structural myocardial in rats exposed to tobacco smoking.
Male Wistar rats were assigned to one of four groups: C, untrained rats without exposure to tobacco smoking; E, exercised rats without exposure to tobacco smoking; CS, untrained rats exposed to tobacco smoking; ECS, exercised rats exposed to tobacco smoking. Rats swam five times a week twice daily (60min per session) for 8 weeks. Before each bout exercise, rats breathed smoke from 20 cigarettes for 60min. Twenty-four hours after the last day of the protocol, papillary muscles were isolated for in vitro analysis of myocardial mechanics. The myocardial mass and nuclear cardiomyocyte volume were used as hypertrophy markers, and collagen content was determined by picrosirius red staining.
There was a well-pronounced myocardial hypertrophic effect for two interventions. The exercise blunted myocardial collagen increases induced by tobacco smoking. However, exercise and tobacco-smoking association was deleterious to myocardial performance. Thereby, in vitro experiments with papillary muscles contracting in isometric showed impairment myocardial inotropism in exercised rats exposed to tobacco smoking.
This work presents novel findings on the role of exercise training on cardiac remodeling induced by tobacco smoking. Although exercise has mitigated tissue fibrosis, their association with tobacco smoking exacerbated hypertrophy and in vitro myocardial dysfunction.
This is first study to show that the association of an aerobic exercise training with tobacco smoking intensifies the phenotype of pathological cardiac hypertrophy. Therefore, the combination of interventions resulted in exacerbated myocardial hypertrophy and contractility dysfunction. These findings have significant clinical implication because some smoking people can be enrolled in an exercise-training program.
尚无关于与吸烟相关的运动训练对心脏影响的数据。这个问题很有趣，因为一些吸烟者可以参加运动训练项目。因此，我们评估了游泳训练对暴露于吸烟环境的大鼠心肌功能和结构的影响。
将雄性Wistar大鼠分为四组之一：C组，未暴露于吸烟环境的未训练大鼠；E组，未暴露于吸烟环境的运动大鼠；CS组，暴露于吸烟环境的未训练大鼠；ECS组，暴露于吸烟环境的运动大鼠。大鼠每周游泳5次，每天2次（每次60分钟），持续8周。每次运动前，大鼠吸入20支香烟的烟雾60分钟。在实验方案的最后一天后24小时，分离乳头肌进行心肌力学的体外分析。心肌质量和心肌细胞核体积用作肥大标志物，胶原含量通过天狼星红染色测定。
两种干预措施均有明显的心肌肥大效应。运动减弱了吸烟诱导的心肌胶原增加。然而，运动与吸烟的联合对心肌性能有害。因此，体外等长收缩乳头肌实验显示，暴露于吸烟环境的运动大鼠心肌收缩性受损。
这项工作提出了关于运动训练在吸烟诱导的心脏重塑中作用的新发现。尽管运动减轻了组织纤维化，但运动与吸烟的联合加剧了肥大和体外心肌功能障碍。
这是第一项表明有氧运动训练与吸烟的联合加剧病理性心脏肥大表型的研究。因此，联合干预导致心肌肥大和收缩功能障碍加剧。这些发现具有重要的临床意义，因为一些吸烟者可以参加运动训练项目。
