High-intensity interval training, but not continuous training, reverses right ventricular hypertrophy and dysfunction in a rat model of pulmonary hypertension
High-intensity interval training, but not continuous training, reverses right ventricular hypertrophy and dysfunction in a rat model of pulmonary hypertension
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DOI：
10.1152/ajpregu.00358.2016
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发表时间：
2017-02-01
影响因子：
2.8
通讯作者：
Lahm, Tim
中科院分区：
文献类型：
--
作者：
Brown, Mary Beth;Neves, Evandro;Lahm, Tim
运动对肺动脉高压（PAH）有益，尽管迄今为止的研究表明对与该疾病相关的肺动脉压升高或适应不良的右心室（RV）肥大几乎没有影响。对于慢性左心室衰竭，高强度间歇训练（HIIT）比常规持续运动训练（CExT）促进更大的内皮刺激和上级获益;然而，尚未对HIIT进行PAH检测。因此，我们在野百合碱（MCT）诱导的轻度PAH大鼠模型中研究了HIIT与CExT的急性和慢性反应。进行6周的跑台训练（5次/周），作为30 min HIIT或60 min低强度CExT。为了表征对两种方法的急性血流动力学反应，使用长期植入式遥测技术在MCT前和MCT后2、4、6和8周获得了跑步期间同时肺和体循环压力的新记录。MCT诱导的最大有氧运动能力降低通过HIIT和CExT得到改善，肺血管重塑不太明显，未观察到RV炎症或细胞凋亡增加。最重要的是，只有HIIT降低了RV收缩压、RV肥大和总肺阻力，并促使心脏指数升高，这是由RV增加的正性肌力物质爱帕琳和减少的纤维化补充的。HIIT提示在运行过程中显着脉动肺动脉压，并与6周后更大的肺内皮型一氧化氮合酶。我们得出结论，HIIT可能上级CExT改善PAH患者的血流动力学和适应不良的RV肥大。HIIT的上级结果可能是由于肺血管内皮对脉动HIIT刺激的适应性更好。
Exercise is beneficial in pulmonary arterial hypertension (PAH), although studies to date indicate little effect on the elevated pulmonary pressures or maladaptive right ventricle (RV) hypertrophy associated with the disease. For chronic left ventricle failure, high-intensity interval training (HIIT) promotes greater endothelial stimulation and superior benefit than customary continuous exercise training (CExT); however, HIIT has not been tested for PAH. Therefore, here we investigated acute and chronic responses to HIIT vs. CExT in a rat model of monocrotaline (MCT)induced mild PAH. Six weeks of treadmill training (5 times/wk) were performed, as either 30 min HIIT or 60 min low-intensity CExT. To characterize acute hemodynamic responses to the two approaches, novel recordings of simultaneous pulmonary and systemic pressures during running were obtained at pre-and 2, 4, 6, and 8 wk post-MCT using long-term implantable telemetry. MCT-induced decrement in maximal aerobic capacity was ameliorated by both HIIT and CExT, with less pronounced pulmonary vascular remodeling and no increase in RV inflammation or apoptosis observed. Most importantly, only HIIT lowered RV systolic pressure, RV hypertrophy, and total pulmonary resistance, and prompted higher cardiac index that was complemented by a RV increase in the positive inotrope apelin and reduced fibrosis. HIIT prompted a markedly pulsatile pulmonary pressure during running and was associated with greater lung endothelial nitric oxide synthase after 6 wk. We conclude that HIIT may be superior to CExT for improving hemodynamics and maladaptive RV hypertrophy in PAH. HIIT's superior outcomes may be explained by more favorable pulmonary vascular endothelial adaptation to the pulsatile HIIT stimulus.