背景:这项研究的目的是开发一种动物模型,以研究长时间的高强度耐力运动是否会引起RV重塑,考虑到Wnt/β-catenin信号传导的参与。
方法:将四周龄雄性Wistar大鼠(100至125g)分为四组(n=8/组):1)16周的高强度(36m/min)运动(INT),2)12周的高强度运动,然后是4周的中等强度(18米/分钟)运动(INT+MOD),3)12周的强化训练,然后是4周的去训练(INT+DT),和4)久坐的大鼠(SED)。锻炼方案每周进行五天,每天一次。超声心动图,实时PCR,西方印迹,在第16周结束时进行组织学染色。
结果:与SED(p=0.006)和INTDT(p=0.035)相比,INT大鼠出现同心肥大,无舒张功能障碍。训练组Wnt1、β-catenin和CyclinD1蛋白显著高于SED大鼠(p<0.001)。有趣的是,INT大鼠的蛋白质水平高于INT+DT和INT+MOD(p<0.001),与SED大鼠相比具有更高的基因表达(p<0.05)。与SED(p=0.046)和INTDT(p=0.034)相比,INT大鼠的胶原蛋白沉积也显着增加。此外,INT+MOD和INT+DT大鼠未显示任何结构不良,功能,或组织学变化。
结论:长期高强度耐力训练似乎通过Wnt/β-catenin信号(浓度依赖性)与RV中胶原蛋白沉积和壁厚增加有关,没有舒张功能的变化。
■在过去的几十年里,关于经过训练的耐力运动员的心血管系统的结构和功能适应是对训练的良性生理反应还是与疾病相关的潜在病理变化,一直存在争议。虽然左心的适应是有据可查的,右心的重塑仍然是一个讨论的主题。为了深入了解持续高强度运动引起右心室(RV)不良重塑的能力,我们进行了一项实验研究,在16周的时间内,雄性大鼠每天剧烈奔跑1小时,并将其与静坐的对照大鼠平行组进行比较。我们的发现表明,剧烈的长期运动会引起形态学变化以及影响RV的纤维化。这些纤维化变化是16周剧烈运动训练方案的结果。如果这些结果在人类身上得到证实,他们提示长时间的高强度耐力运动训练可能导致不良的心脏重构.我们的发现对于评估从事高水平运动训练的个体的心脏重塑具有重要的潜在意义。
BACKGROUND: The aim of this study was to develop an animal model to investigate whether prolonged intensive endurance exercise induces RV remodeling, taking into account the involvement of Wnt/β-catenin signaling.
METHODS: Four-week-old male Wistar rats (100 to 125 g) were assigned to four groups (n = 8/group): 1) sixteen weeks of intensive (36 m/min) exercise (INT), 2) twelve weeks of the intensive exercise followed by four weeks of moderate intensity (18 m/min) exercise (INT + MOD), 3) twelve weeks of the intensive exercise followed by four weeks of detraining (INT + DT), and 4) sedentary rats (SED). The exercise protocols were performed five days a week for one h/day. Echocardiography, real-time PCR, western blotting, and histological staining were performed at the end of week sixteen.
RESULTS: INT rats developed concentric hypertrophy without diastolic dysfunction compared to SED (p = 0.006) and INT + DT (p = 0.035). Wnt1, β-catenin and CyclinD1 proteins in the training groups were significantly higher than SED rats (p < 0.001). Interestingly, INT rats had higher protein levels than INT + DT and INT + MOD (p < 0.001), with higher gene expression compared to SED rats (p < 0.05). There was also a significant increase in collagen deposition in INT rats compared to SED (p = 0.046) and INT + DT (p = 0.034). Furthermore, INT + MOD and INT + DT rats did not show any adverse structural, functional, or histological changes.
CONCLUSIONS: Long-term intensive endurance training seems to be associated with increased collagen deposition and wall thickness in the RV through Wnt/β-catenin signaling (which is concentration dependent), without changes in diastolic function.
UNASSIGNED: Over the past decades, there has been an ongoing debate about whether the structural and functional adaptations of the cardiovascular system in trained endurance athletes are benign physiological responses to training or potentially pathological changes related to disease. While the adaptations of the left heart are well-documented, the remodeling of the right heart remains a subject of discussion. To gain insights into the ability of sustained high-intensity exercise to cause adverse right ventricular (RV) remodeling, we conducted an experimental study in which male rats were trained to run vigorously for 1 h daily over a 16-week period and compared them to a parallel group of sedentary control rats. Our findings revealed that intense long-term exercise induced morphological changes along with fibrosis affecting the RV. These fibrotic changes were a result of the 16-week vigorous exercise training regimen. If these results are confirmed in humans, they suggest that prolonged high-intensity endurance exercise training may lead to adverse cardiac remodeling. Our findings have important potential implications for the assessment of cardiac remodeling in individuals engaged in high-level exercise training.