Sanz-de la Garza Maria, Rubies Cira, Batlle Montserrat, Bijnens Bart H, Mont Lluis, Sitges Marta, Guasch Eduard
Cardiovascular Institute, Hospital Clínic, Universitat de Barcelona, Barcelona, Catalonia, Spain.
Institut d'Investigacions Biomédiques August Pi i Sunyer, Barcelona, Catalonia, Spain.
Am J Physiol Heart Circ Physiol. 2017 Sep 1;313(3):H459-H468. doi: 10.1152/ajpheart.00763.2016. Epub 2017 May 26.
Arrhythmogenic right ventricular (RV) remodeling has been reported in response to regular training, but it remains unclear how exercise intensity affects the presence and extent of such remodeling. We aimed to assess the relationship between RV remodeling and exercise load in a long-term endurance training model. Wistar rats were conditioned to run at moderate (MOD; 45 min, 30 cm/s) or intense (INT; 60 min, 60 cm/s) workloads for 16 wk; sedentary rats served as controls. Cardiac remodeling was assessed with standard echocardiographic and tissue Doppler techniques, sensor-tip pressure catheters, and pressure-volume loop analyses. After MOD training, both ventricles similarly dilated (16%); the RV apical segment deformation, but not the basal segment deformation, was increased [apical strain rate (SR): -2.9 ± 0.5 vs. -3.3 ± 0.6 s, SED vs. MOD]. INT training prompted marked RV dilatation (26%) but did not further dilate the left ventricle (LV). A reduction in both RV segments' deformation in INT rats (apical SR: -3.3 ± 0.6 vs. -3.0 ± 0.4 s and basal SR: -3.3 ± 0.7 vs. -2.7 ± 0.6 s, MOD vs. INT) led to decreased global contractile function (maximal rate of rise of LV pressure: 2.53 ± 0.15 vs. 2.17 ± 0.116 mmHg/ms, MOD vs. INT). Echocardiography and hemodynamics consistently pointed to impaired RV diastolic function in INT rats. LV systolic and diastolic functions remained unchanged in all groups. In conclusion, we showed a biphasic, unbalanced RV remodeling response with increasing doses of exercise: physiological adaptation after MOD training turns adverse with INT training, involving disproportionate RV dilatation, decreased contractility, and impaired diastolic function. Our findings support the existence of an exercise load threshold beyond which cardiac remodeling becomes maladaptive. Exercise promotes left ventricular eccentric hypertrophy with no changes in systolic or diastolic function in healthy rats. Conversely, right ventricular adaptation to physical activity follows a biphasic, dose-dependent, and segmentary pattern. Moderate exercise promotes a mild systolic function enhancement at the right ventricular apex and more intense exercise impairs systolic and diastolic function.
已有报道称，规律训练会引发致心律失常性右心室（RV）重塑，但运动强度如何影响这种重塑的存在及程度仍不清楚。我们旨在评估长期耐力训练模型中右心室重塑与运动负荷之间的关系。将Wistar大鼠按中等强度（MOD；45分钟，30厘米/秒）或高强度（INT；60分钟，60厘米/秒）的工作量训练16周；久坐不动的大鼠作为对照。采用标准超声心动图和组织多普勒技术、传感器尖端压力导管以及压力-容积环分析来评估心脏重塑情况。经过中等强度训练后，两个心室同样扩张（约16%）；右心室心尖段变形增加，但基底段变形未增加[心尖应变率（SR）：-2.9±0.5对-3.3±0.6秒，SED对MOD]。高强度训练促使右心室显著扩张（约26%），但未使左心室进一步扩张。高强度训练组大鼠的两个右心室段变形均降低（心尖SR：-3.3±0.6对-3.0±0.4秒，基底SR：-3.３±0.7对-2.7±0.6秒，MOD对INT），导致整体收缩功能下降（左心室压力最大上升速率：2.53±0.15对2.17±0.116毫米汞柱/毫秒，MOD对INT）。超声心动图和血流动力学结果一致表明高强度训练组大鼠右心室舒张功能受损。所有组的左心室收缩和舒张功能均保持不变。总之，我们发现随着运动剂量增加，右心室重塑反应呈双相且不均衡：中等强度训练后的生理适应在高强度训练时变为不良适应，包括右心室不成比例的扩张、收缩力下降和舒张功能受损。我们的研究结果支持存在一个运动负荷阈值，超过该阈值心脏重塑会变得适应不良。运动可促进健康大鼠左心室离心性肥厚，而收缩或舒张功能无变化。相反，右心室对体力活动的适应遵循双相、剂量依赖性和节段性模式。适度运动可促进右心室心尖部轻度收缩功能增强，而更剧烈的运动则会损害收缩和舒张功能。
