Haykowsky Mark J, Samuel T Jake, Nelson Michael D, La Gerche André
Integrated Cardiovascular Exercise Physiology and Rehabilitation (iCARE) Laboratory, College of Nursing & Health Innovation, University of Texas Arlington, Arlington, TX, USA; Sport Cardiology, Baker Heart and Diabetes Research Institute, Melbourne, Vic, Australia.
Applied Physiology and Advanced Imaging Laboratory, College of Nursing & Health Innovation, University of Texas Arlington, Arlington, TX, USA.
Heart Lung Circ. 2018 Sep;27(9):1037-1041. doi: 10.1016/j.hlc.2018.04.289. Epub 2018 May 1.
In 1975, Morganroth and colleagues reported that the increased left ventricular (LV) mass in highly trained endurance athletes versus nonathletes was primarily due to increased end-diastolic volume while the increased LV mass in resistance trained athletes was solely due to an increased LV wall thickness. Based on the divergent remodelling patterns observed, Morganroth and colleagues hypothesised that the increased "volume" load during endurance exercise may be similar to that which occurs in patients with mitral or aortic regurgitation while the "pressure" load associated with performing a Valsalva manoeuvre (VM) during resistance exercise may mimic the stress imposed on the heart by systemic hypertension or aortic stenosis. Despite widespread acceptance of the four-decade old Morganroth hypothesis in sports cardiology, some investigators have questioned whether such a divergent "athlete's heart" phenotype exists. Given this uncertainty, the purpose of this brief review is to re-evaluate the Morganroth hypothesis regarding: i) the acute effects of resistance exercise performed with a brief VM on LV wall stress, and the patterns of LV remodelling in resistance-trained athletes; ii) the acute effects of endurance exercise on biventricular wall stress, and the time course and pattern of LV and right ventricular (RV) remodelling with endurance training; and iii) the value of comparing "loading" conditions between athletes and patients with cardiac pathology.
1975年,摩根罗斯及其同事报告称,与非运动员相比,高水平耐力运动员左心室(LV)质量增加主要是由于舒张末期容积增加,而力量训练运动员左心室质量增加则完全是由于左心室壁厚度增加。基于观察到的不同重塑模式,摩根罗斯及其同事推测,耐力运动期间增加的“容量”负荷可能与二尖瓣或主动脉瓣反流患者的情况相似,而力量运动期间与进行瓦尔萨尔瓦动作(VM)相关的“压力”负荷可能模拟系统性高血压或主动脉瓣狭窄对心脏施加的压力。尽管在运动心脏病学领域,摩根罗斯假说已被广泛接受了四十年,但一些研究人员质疑是否存在这种不同的“运动员心脏”表型。鉴于这种不确定性,本简要综述的目的是重新评估摩根罗斯假说,内容包括:i)进行短暂VM的力量运动对左心室壁应力的急性影响,以及力量训练运动员左心室重塑的模式;ii)耐力运动对双心室壁应力的急性影响,以及耐力训练后左心室和右心室(RV)重塑的时间进程和模式;iii)比较运动员与心脏疾病患者“负荷”情况的价值。