Pittaras Andreas, Faselis Charles, Doumas Michael, Grassos Charalampos, Kokkinos Peter
Department of Cardiology, Washington DC Veterans Affairs Medical Center, Washington, DC 20422, USA.
School of Medicine and Health Sciences, George Washington University, Washington, DC 20052, USA.
Rev Cardiovasc Med. 2023 May 11;24(5):142. doi: 10.31083/j.rcm2405142. eCollection 2023 May.
Chronic and intense exercise programs lead to cardiac adaptations, followed by increased left ventricular wall thickness and cavity diameter, at times meeting the criteria for left ventricular hypertrophy (LVH), commonly referred to as "". Recent studies have also reported that extremely vigorous exercise practices have been associated with heightened left ventricular trabeculation extent, fulfilling noncompaction cardiomyopathy criteria, as part of exercise-induced structural adaptation. These changes are specific to the exercise type, intensity, duration, and volume and workload demands imposed on the myocardium. They are considered physiologic adaptations not associated with a negative prognosis. Conversely, hypertrophic cardiac adaptations resulting from chronic elevations in blood pressure (BP) or chronic volume overload due to valvular regurgitation, lead to compromised cardiac function, increased cardiovascular events, and even death. In younger athletes, hypertrophic cardiomyopathy (HCM) is the usual cause of non-traumatic, exercise-triggered sudden cardiac death. Thus, an extended cardiac examination should be performed, to differentiate between HCM and non-pathological exercise-related LVH or athlete's heart. The exercise-related cardiac structural and functional adaptations are normal physiologic responses designed to accommodate the increased workload imposed by exercise. Thus, we propose that such adaptations are defined as "eutrophic" hypertrophy and that LVH is reserved for pathologic cardiac adaptations. Systolic BP during daily activities may be the strongest predictor of cardiac adaptations. The metabolic demand of most daily activities is approximately 3-5 metabolic equivalents (METs) (1 MET = 3.5 mL of kg of body weight per minute). This is similar to the metabolic demand of treadmill exercise at the first stage of the Bruce protocol. Some evidence supports that an exercise systolic BP response 150 mmHg at the end of that stage is a strong predictor of left ventricular hypertrophy, as this BP reflects the hemodynamic burden of most daily physical tasks. Aerobic training of moderate intensity lowers resting and exercise systolic BP at absolute workloads, leading to a lower hemodynamic burden during daily activities, and ultimately reducing the stimulus for LVH. This mechanism explains the significant LVH regression addressed by aerobic exercise intervention clinical studies.
长期高强度的运动计划会导致心脏适应性变化，随后左心室壁厚度和腔径增加，有时符合左心室肥厚（LVH）的标准，通常称为“”。最近的研究还报告称，作为运动诱导的结构适应性变化的一部分，极度剧烈的运动与左心室小梁化程度增加有关，符合非致密性心肌病的标准。这些变化特定于运动类型、强度、持续时间以及施加于心肌的容量和工作量需求。它们被认为是与不良预后无关的生理适应性变化。相反，由于血压（BP）长期升高或瓣膜反流导致的慢性容量超负荷引起的肥厚性心脏适应性变化，会导致心脏功能受损、心血管事件增加，甚至死亡。在年轻运动员中，肥厚型心肌病（HCM）是非创伤性、运动诱发的心源性猝死的常见原因。因此，应进行全面的心脏检查，以区分HCM与非病理性运动相关的LVH或运动员心脏。运动相关的心脏结构和功能适应性变化是正常的生理反应，旨在适应运动带来的工作量增加。因此，我们建议将这种适应性变化定义为“营养良好性”肥厚，而LVH则保留用于病理性心脏适应性变化。日常活动期间的收缩压可能是心脏适应性变化的最强预测指标。大多数日常活动的代谢需求约为3 - 5代谢当量（METs）（1 MET = 每分钟每千克体重3.5毫升）。这与布鲁斯方案第一阶段跑步机运动的代谢需求相似。一些证据支持，在该阶段结束时运动收缩压反应超过150 mmHg是左心室肥厚的有力预测指标，因为这个血压反映了大多数日常体力任务的血流动力学负担。中等强度的有氧运动训练会降低绝对工作量下的静息和运动收缩压，导致日常活动期间的血流动力学负担降低，并最终减少LVH的刺激因素。这一机制解释了有氧运动干预临床研究中显著的LVH逆转现象。
