PDF(Pubmed)
Abstract：
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 \"athlete\'s heart\". 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 O 2 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.
摘要：
慢性和剧烈运动计划会导致心脏适应，随后左心室壁厚度和腔直径增加，有时满足左心室肥厚（LVH）的标准，通常被称为“运动员的心脏”。最近的研究还报告说，剧烈的运动与左心室小梁的增加有关。符合心肌致密化不全标准，作为运动引起的结构适应的一部分。这些变化特定于运动类型，强度,持续时间,以及对心肌的体积和工作量要求。它们被认为是与负面预后无关的生理适应。相反，由于瓣膜反流引起的血压慢性升高（BP）或慢性容量超负荷引起的肥厚性心脏适应，导致心脏功能受损，心血管事件增加，甚至死亡。在年轻的运动员中，肥厚型心肌病（HCM）是非创伤性的常见原因，运动引发的心脏性猝死.因此，应该进行扩展的心脏检查，区分HCM和非病理性运动相关的LVH或运动员心脏。与运动相关的心脏结构和功能适应是正常的生理反应，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定义为“富营养化”肥大，而LVH保留用于病理性心脏适应。日常活动中的收缩压可能是心脏适应的最强预测因子。大多数日常活动的代谢需求约为3-5代谢当量（MET）（1MET=每分钟3.5mLO2kg体重）。这类似于Bruce方案第一阶段跑步机运动的代谢需求。一些证据支持运动收缩压反应≥150mmHg在该阶段结束时是左心室肥大的强预测因子。因为该BP反映了大多数日常身体任务的血液动力学负担。中等强度的有氧训练可降低绝对工作负荷下的静息和运动收缩压，在日常活动中导致较低的血液动力学负担，并最终减少对LVH的刺激。这种机制解释了有氧运动干预临床研究解决的显着LVH消退。
