How to interpret right ventricular remodeling in athletes

Abstract

Long‐lasting athletic training induces an overload on the heart that leads to structural, functional, and electrical adaptive changes known as the “athlete's heart.” The amount of this heart remodeling has been traditionally considered balanced between the left and the right heart chambers. However, during intense exercise, the right heart is exposed to a disproportional afterload and wall stress which over a long period of time could lead to more pronounced exercise‐induced changes. Highly trained athletes, especially those involved in endurance sport disciplines, can develop marked right ventricular (RV) remodeling that could raise the suspicion of an underlying RV pathology including arrhythmogenic cardiomyopathy (ACM). The distinction between physiological and pathological RV remodeling is essential as ACM is a common cause of sudden cardiac death in athletes, and high‐intensity exercise training has demonstrated to accelerate its phenotypic expression and worsen its prognosis. The distinction between physiological and pathological RV remodeling is essential since ACM is a common cause of sudden cardiac death in athletes, and high‐intensity exercise training has demonstrated to accelerate the phenotypic expression and worsen the prognosis. This article outlines the physiological adaptation of the RV to acute exercise, the subsequent physiological structural and functional changes induced by athletic training and provides useful tips of how to differentiate between physiological RV remodeling and a cardiomyopathy phenotype.

Effect of Exercise-Induced Reductions in Blood Volume on Cardiac Output and Oxygen Transport Capacity

“…Over the years, it has been well established that cardiac output (Q) is a major limiting factor for the maximum oxygen uptake (VO 2max ) during exercise (Bassett and Howley, 2000;Stöhr et al, 2011;Lundby et al, 2017).Q equals the product of heart rate (HR) and stroke volume (SV), and is largely determined by a harmonic structural and functional adaption of the heart, where especially cardiac compliance is a prerequisite for large end-diastolic volumes (Levine, 2008;Magder, 2016). If these prerequisites are given, the heart, e.g., the athletic heart-which is characterized by greater dimensions, specifically harmonically increased leftventricular dimensions (Baggish and Wood, 2011;La Sanz-de Garza et al, 2020)-has a greater ability to use the Frank-Starling-mechanism. This well described mechanism allows for an efficient realization of SV due to a preload mediated stretch of the myocardium (Woodiwiss and Norton, 1995).…”

Comparative characteristics of changes in central hemodynamics during early recovery after different exercise regimes

“…During the Martin test, we did not find any significant changes in adBP. However, cardiac output increased, and TPVR, respectively, decreased, which is a physiologically appropriate response of the cardiovascular system to exercise [5,17,23].…”

Intrinsic Exercise Capacity and Mitochondrial DNA Lead to Opposing Vascular-Associated Risks

“…However, in highly trained endurance athletes where the RV dilation is prominent, a slight reduction in RV global systolic function assessed by RV FAC may be shown. 30 , 31 On the contrary, resistance training, such as weight lifting and wrestling, may lead to increased cardiac mass without LV chamber dilation, referred to as concentric hypertrophy. 29 In this study, we used untrained animals to understand the influence of innate aerobic capacity on the cardiovascular system.…”