Atrial Adaptations and Total Cardiac Volume in Athletes

Frequent and high-intensity exercise is associated with a range of structural, functional, and electrical cardiac adaptations that enhance cardiac performance. The structural changes primarily involve proportional cardiac four-chamber enlargement and increased left ventricular mass [1]. Functionally, the resting heart rate is usually lower in athletes versus age- and sex-matched non-athlete, although maximal heart rates tend to be similar [2]. Although this allows for a potentially greater heart rate rise with exercise, it is the significantly greater left ventricular size and stroke volume of athletes that is the main determinant of their higher cardiac outputs [1]. Left ventricular wall thickness is either preserved or marginally increased. The most commonly observed electrical changes are identified on a resting 12-lead electrocardiogram. These include relatively longer PR intervals, higher voltage of R, and T waves and more frequently incomplete right bundle branch block (RBBB), left ventricular (LV) hypertrophy, early repolarization, and anterior (typically V1–3) T-wave inversion as compared to non-athletes [3, 4]. The degree of cardiac remodeling is subject to marked individual variation which is heavily influenced by the type of exercise (endurance vs. strength), height, sex, genetics, ethnicity and the exercise dose (= intensity × time) [1].

Although these adaptations are usually benign and enhance cardiac performance, they can sometimes lead to difficulties in differentiating a genuine athletic heart (AH) from an underlying cardiomyopathy (the so-called “grey zone”) [2]. This is particularly noticeable where phenotypic expression of cardiomyopathy is more covert (e.g., mild concentric hypertrophic cardiomyopathy or mild left ventricular dysfunction with a dilated cardiomyopathy) or where there has been extreme exercise-related remodeling. Consequently, there is a need to accurately define the phenotype of the AH in order to improve the clinical precision of differentiating it from a true cardiomyopathy.

In a very recent publication in our Journal, Stadter and Keller present the results of an observational study designed to better understand the potential differences in cardiac structure and function among athletes determined to have an AH versus those who did not [5]. They conducted a retrospective analysis of pre-participation screening data collected on 648 adult athletes at University Hospital Heidelberg (Germany) between April 2020 and October 2021. All of the participants underwent standard transthoracic echocardiography, cardiopulmonary exercise testing (adapted to the athlete's sport), basic height and weight assessment, and body fat estimation using calipometry. Their primary aim was to examine the differences in atrial adaptations between those with and without a defined AH and explore the baseline factors influencing potential differences [5]. The case definition of an AH was based on the estimated total cardiac volume (TCV) indexed to body weight. An AH was defined as a physiologically increased TCV of >13.0 mL/kg in men and >12.0 mL/kg in women [6].

In their study, the median age of their cohort was 24.0 (interquartile range (IQR) 20.0–31.00) years-old and included 206 (31.9%) females. They found that 118 (18.3%) out of the 646 athletes investigated had an AH based on their estimated TCV. The median TCV was significantly greater in athletes with an AH than those without [5]. Those with an AH had a significantly lower body weight, body mass index (BMI), body fat%, and significantly higher peak oxygen consumption (VO₂) than those without an AH and were more likely to participate in endurance and game sports. Notable differences in echocardiography included significantly greater left ventricular size and mass, absolute and weight-adjusted TCV, bi-atrial sizes, and tricuspid annular plane excursion (TAPSE) and lower mitral E/Eʹ in those with an AH. Echocardiographic factors significantly and independently (adjusted for age, sex, and BMI) associated with AH included LV mass (odds ratio (OR) 1.05; 95% CI 1.04–1.06), left atrial (OR 1.29; 95% CI 1.19–1.39), right atrial area (OR 1.28; 95% CI 1.19–1.38) peak VO₂ (OR 1.19; 1.12–1.25), TAPSE (OR 3.33; 1.94–5.73) and lower E/Eʹ (OR 0.80; 95% CI 0.68–0.95).

These majority of these findings are not new. It has been well reported that athletes have larger atria than that of non-athletes of similar age and sex [7, 8]. Although the majority of this data relates to left atrial size, there is now a considerable amount of contemporaneous data demonstrating right atrial dilation with normal function in the AH [7, 9]. Nevertheless, this article supports existing evidence and is one of the largest studies to examine right atrial sizes in athletes and the findings were consistent in both males and females (Drs Stadter and Keller 2024).

It is important to note that in their study the investigators first calculated the left ventricular end diastolic volume on TTE [5]. This was done by first measuring the end-diastolic left ventricular diameter in the parasternal M-mode at the papillary muscle and at the mitral valve level and the measurement of the maximum longitudinal diameter from the apex of the left ventricle to mitral annular level [10]. These data were then used to estimate the TCV using a regression equation based on the recognized and published correlation between TTE-measured left ventricular volume and the TCV measured radiographically [6]. Although this approach reflects the validation work underpinning this method, this research was conducted more than 25 years ago in which the heart volume was estimated using chest x-rays [10]. Consequently, there are several points relating to the definition of an AH used in this study that need to be mentioned.

First, only a structural criterion was used to define cases of an AH in this study and based on TCV. Yet, it is now well established, that the AH also encapsulates functional and electrical cardiac changes. Secondly, the use of volume calculations derived from linear measurements, as done in this study, while consistent with the validation work can be unreliable, because it relies on the assumption of a fixed geometric left ventricular shape [11]. This is less likely to be an issue in genuine cases of AH where there tends to be more harmonious left ventricular dilatation. However, with pathological left ventricular dilatation, there is frequently unequal left ventricular dilatation undermining linear calculations [11]. The investigators do acknowledge this as a limitation. For this reason, it is strongly recommended that TTE volumetric measurements of the left ventricle should be based on tracings of the endocardium using both apical two- and four-chamber views [12].

Thirdly, the estimation of TCV in this study was based solely on the calculated left ventricular volume data and not a summation of four-chamber measurements. The inclusion of data on the right ventricle size (and preferably function) is paramount and bi-atrial sizes are preferable. The right heart is exposed to a disproportional afterload and wall stress during exercise. Owing to its complex geometry right ventricular remodeling following intense exercise can be highly variable and its accurate distinction from right ventricular cardiomyopathy is paramount [11]. Finally, the reliability of multiplane chest radiography to accurately determine TCV is outdated and unreliable. Cardiac magnetic resonance imaging cMRI) and computerized tomography have been shown to be far superior modalities for TCV quantification [13]. It is interesting and reassuring that the median TCV of participants with an AH was 969.4 (IQR: 853.1–1083.0) mL which is remarkably similar to that observed among 71 athletes (947 ± 169 mL) of similar age and sex using cMRI of the entire heart from base of the atria to the ventricular apices in another study [14].

Overall, the authors should be congratulated on presenting a comprehensive and rather unique insight into the AH using a rather singular structural case definition. Although the quantification of TCV is being increasingly appreciated in the field of cardiac transplant, its translation to the athlete heart is in its infancy. Further validation work on the accuracy of TTE to gold standard TCV data in athletes is needed.