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Background: Assessment of the athlete's heart is challenging because of a phenotypic overlap between reactive physiological adaptation and pathological remodelling. The potential value of myocardial deformation remains controversial in identifying early cardiomyopathy., Aim: To identify the echocardiographic phenotype of athletes using advanced two-dimensional speckle tracking imaging, and to define predictive factors of subtle left ventricular systolic dysfunction., Methods: In total, 191 healthy male athletes who underwent a preparticipation medical evaluation at Nancy University Hospital between 2013 and 2020 were included. Clinical and echocardiographic data were compared with 161 healthy male subjects from the STANISLAS cohort. Borderline global longitudinal strain value was defined as<17.5%., Results: Athletes demonstrated lower left ventricular ejection fraction (57.9±5.3% vs. 62.6±6.4%; P<0.01) and lower global longitudinal strain (17.5±2.2% vs. 21.1±2.1%; P<0.01). No significant differences were found between athletes with and without a borderline global longitudinal strain value regarding clinical characteristics, structural echocardiographic features and exercise capacity. A borderline global longitudinal strain value was associated with a lower endocardial global longitudinal strain (18.8±1.2% vs. 22.7±1.9%; P=0.02), a lower epicardial global longitudinal strain (14.0±1.1% vs. 16.6±1.2%; P<0.01) and a higher endocardial/epicardial global longitudinal strain ratio (1.36±0.07 vs. 1.32±0.06; P<0.01). No significant difference was found regarding mechanical dispersion (P=0.46)., Conclusions: Borderline global longitudinal strain value in athletes does not appear to be related to structural remodelling, mechanical dispersion or exercise capacity. The athlete's heart is characterized by a specific myocardial deformation pattern with a more pronounced epicardial layer strain impairment., (Copyright © 2024 Elsevier Masson SAS. All rights reserved.)

Background: Exercise-induced cardiac remodeling can be profound, resulting in clinical overlap with dilated cardiomyopathy, yet the significance of reduced ejection fraction (EF) in athletes is unclear. The aim is to assess the prevalence, clinical consequences, and genetic predisposition of reduced EF in athletes., Methods: Young endurance athletes were recruited from elite training programs and underwent comprehensive cardiac phenotyping and genetic testing. Those with reduced EF using cardiac magnetic resonance imaging (defined as left ventricular EF <50%, or right ventricular EF <45%, or both) were compared with athletes with normal EF. A validated polygenic risk score for indexed left ventricular end-systolic volume (LVESVi-PRS), previously associated with dilated cardiomyopathy, was assessed. Clinical events were recorded over a mean of 4.4 years., Results: Of the 281 elite endurance athletes (22±8 years, 79.7% male) undergoing comprehensive assessment, 44 of 281 (15.7%) had reduced left ventricular EF (N=12; 4.3%), right ventricular EF (N=14; 5.0%), or both (N=18; 6.4%). Reduced EF was associated with a higher burden of ventricular premature beats (13.6% versus 3.8% with >100 ventricular premature beats/24 h; P =0.008) and lower left ventricular global longitudinal strain (-17%±2% versus -19%±2%; P <0.001). Athletes with reduced EF had a higher mean LVESVi-PRS (0.57±0.13 versus 0.51±0.14; P =0.009) with athletes in the top decile of LVESVi-PRS having an 11-fold increase in the likelihood of reduced EF compared with those in the bottom decile ( P =0.034). Male sex and higher LVESVi-PRS were the only significant predictors of reduced EF in a multivariate analysis that included age and fitness. During follow-up, no athletes developed symptomatic heart failure or arrhythmias. Two athletes died, 1 from trauma and 1 from sudden cardiac death, the latter having a reduced right ventricular EF and a LVESVi-PRS >95%., Conclusions: Reduced EF occurs in approximately 1 in 6 elite endurance athletes and is related to genetic predisposition in addition to exercise training. Genetic and imaging markers may help identify endurance athletes in whom scrutiny about long-term clinical outcomes may be appropriate., Registration: URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=374976&isReview=true; Unique identifier: ACTRN12618000716268., Competing Interests: Disclosures None.

Background: Athlete's heart is associated with physiological electrical and structural remodelling. Despite the plethora of data published on male athletes, solid data derived from female athletes, compared to male counterparts or sedentary women, are still scarce., Objectives: We aimed to analyze the electrical, structural, and functional characteristics of athlete's heart in female and male athletes vs sedentary controls., Methods: Olympic athletes and sedentary controls were evaluated by resting ECG and echocardiography. Athletes were divided into 4 different sports groups., Results: The study population included 1096 individuals (360 female athletes, 410 male athletes, 130 sedentary women and 196 sedentary men). Female athletes had lower resting heart rate, longer PR interval, higher voltage of R, and T waves and more frequently incomplete RBBB, left ventricular (LV) hypertrophy, early repolarization, and anterior T-wave inversion as compared to controls. Biventricular cavity dimensions and LV wall thickness were greater in female athletes than in female controls. However, women showed a lower degree of training-induced structural remodelling than men. In female athletes, both cavity dimensions and LV wall thickness increased from those engaged in skill and power to mixed and endurance disciplines. However, in female athletes, contrary to males, the ECG changes were not significantly different according to the different types of sport discipline., Conclusions: Highly-trained women demonstrate relevant training-induced electrical and structural remodelling. However, the type of sport did not influence ECG parameters in women, contrary to men, while it impacted biventricular morphologic remodelling, with endurance athletes showing the greatest degree of adaptation., Competing Interests: Declaration of competing interest None declared., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The integration of artificial intelligence (AI) technologies is evolving in different fields of cardiology and in particular in sports cardiology. Artificial intelligence offers significant opportunities to enhance risk assessment, diagnosis, treatment planning, and monitoring of athletes. This article explores the application of AI in various aspects of sports cardiology, including imaging techniques, genetic testing, and wearable devices. The use of machine learning and deep neural networks enables improved analysis and interpretation of complex datasets. However, ethical and legal dilemmas must be addressed, including informed consent, algorithmic fairness, data privacy, and intellectual property issues. The integration of AI technologies should complement the expertise of physicians, allowing for a balanced approach that optimizes patient care and outcomes. Ongoing research and collaborations are vital to harness the full potential of AI in sports cardiology and advance our management of cardiovascular health in athletes., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: There are various changes in cardiac physiology in athletes compared to the normal population. These physiological changes may differ according to the exercise content. The aim of this study was to compare the effects of different exercise methods on the heart., Methods: A total of 122 male athletes from various sports were evaluated. Depending on the sorts of sports, these participants were split into aerobic, mixed, and resistance groups. Each athlete had to meet the inclusion criteria of having participated in the present sport for at least a year and having trained for at least 600 minutes per week over the previous three months. Transthoracic echocardiography was used to investigate the effects of different exercise types., Results: The aerobic group's heart rate and ejection fraction were found to be lower than those of the resistance and mixed groups (F(2.105)=23.487, P=0.001). The end-diastolic thicknesses of the interventricular septum (8.7 SD 0.8 vs. 10.0 SD 0.7), interventricular septum (11.3 SD 0.9 vs. 13.0 SD 0.9), left ventricular posterior wall (8.6 SD 0.7 vs. 9.9 SD 0.8), and interventricular septum (11.1 SD 0.9 vs. 13.3 SD 0.9) were all found to be lower in the aerobic group than in the resistance group (P=0.0001). The effect of resistance exercise on heart rate was not observed as clearly as other groups., Conclusions: Resistance exercise has a more dominant effect on ventricular thickness than aerobic exercise. In mixed exercise groups, this increase in thickness is similar to resistance exercise. The content of the training should be considered in the evaluation of the athlete's heart. Identifying the subgroups of the athlete's heart will be useful in the differentiation of pathologies and also in the follow-up of the athletes.

Background: Physical activity contributes to changes in cardiac morphology, which are known as "athlete's heart". Therefore, these modifications can be characterized using different imaging modalities such as echocardiography, including Doppler (flow Doppler and Doppler myocardial imaging) and speckle-tracking, along with cardiac magnetic resonance, and cardiac computed tomography., Main Text: Echocardiography is the most common method for assessing cardiac structure and function in athletes due to its availability, repeatability, versatility, and low cost. It allows the measurement of parameters like left ventricular wall thickness, cavity dimensions, and mass. Left ventricular myocardial strain can be measured by tissue Doppler (using the pulse wave Doppler principle) or speckle tracking echocardiography (using the two-dimensional grayscale B-mode images), which provide information on the deformation of the myocardium. Cardiac magnetic resonance provides a comprehensive evaluation of cardiac morphology and function with superior accuracy compared to echocardiography. With the addition of contrast agents, myocardial state can be characterized. Thus, it is particularly effective in differentiating an athlete's heart from pathological conditions, however, is less accessible and more expensive compared to other techniques. Coronary computed tomography is used to assess coronary artery anatomy and identify anomalies or diseases, but its use is limited due to radiation exposure and cost, making it less suitable for young athletes. A novel approach, hemodynamic forces analysis, uses feature tracking to quantify intraventricular pressure gradients responsible for blood flow. Hemodynamic forces analysis has the potential for studying blood flow within the heart and assessing cardiac function., Conclusions: In conclusion, each diagnostic technique has its own advantages and limitations for assessing cardiac adaptations in athletes. Examining and comparing the cardiac adaptations resulting from physical activity with the structural cardiac changes identified through different diagnostic modalities is a pivotal focus in the field of sports medicine., (© 2023. The Author(s).)

Routine or vigorous training, particularly in competitive and elite athletes practicing dynamic sports, leads to a constellation of structural and functional cardiovascular adaptations, facilitating an increased capacity to deliver oxygen to the working muscles during sustained physical exertion. Cardiopulmonary exercise testing is the most accurate and objective method to assess performance in athletes. Although still underutilized, it provides a window into the unique cardiovascular response to exercise in athletes, integrating parameters obtained by the traditional exercise test with breath-by-breath analysis of oxygen consumption, carbon dioxide production, ventilation, and other derived parameters. This review aimed to describe the several applications of cardiopulmonary exercise testing in athletes with a principal focus on the ability to identify cardiovascular adaptations and differentiate an athlete's heart from early cardiomyopathy. In this context, cardiopulmonary exercise testing provides many applications involving exercise physiology in athletes, allowing a precise evaluation of cardiovascular efficiency, the entity of the adaptations, the response to a training program, and identifying early modifications that could reveal early cardiomyopathy. Therefore, thanks to its several applications, this pivotal test allows us to obtain essential information about the athlete's physiology and differentiate between the expected response of a trained athlete from early cardiomyopathy.

The term 'athletic heart syndrome' (AHS) is used to describe specific circulatory and morphological changes in individuals who participate in sports competitions. The syndrome is characterized by normal cardiac function and reversible myocardial remodelling.The incidence and severity of the post-COVID-19 cardiac pathology in active athletes are so far unclear. One of the complications involving the heart is myocarditis. We present a case of a 23-year-old rower after having a moderate COVID-19 infection. Electrocardiograms showed evidence of a shift in conduction and rhythm disturbances ranging from Group 1 (normal ECG findings) to Group 2 (abnormal ECG findings) on the background of an AHS. Echocardiography (with new methods of evaluating deformity - Global Longitudinal Strain) revealed an area with mildly reduced left ventricular deformity around the apex. To assess the subtle alterations in the myocardium, magnetic resonance imaging was used and focal myocarditis was detected. In our patient, considering the degree of severity of his COVID-19 infection - a moderate one, a decision was taken to perform a clinical and instrumental reassessment of his cardiovascular complications 6 months after the infection.This clinical case presents two substantial issues. First, is the AHS more susceptible to rhythm and conduction disturbances after a COVID-19 infection than that of a person who does not actively participate in sports? Second, what the reversibility or the definitive nature of these disturbances is, and how this impacts the prognosis associated with an active sporting activity., (This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Three-dimensional echocardiography (3DE) is the most accurate cardiac ultrasound technique to assess cardiac structure. 3DE has shown close correlation with cardiac magnetic resonance imaging (CMR) in various populations. There is limited data on the accuracy of 3DE in athletes and its value in detecting alterations during follow-up. Indexed left and right ventricular end-diastolic volume (LVEDVi, RVEDVi), end-systolic volume, ejection fraction (LVEF, RVEF) and left ventricular mass (LVMi) were assessed by 3DE and CMR in two-hundred and one competitive endurance athletes (79% male) from the Pro@Heart trial. Sixty-four athletes were assessed at 2 year follow-up. Linear regression and Bland-Altman analyses compared 3DE and CMR at baseline and follow-up. Interquartile analysis evaluated the agreement as cardiac volumes and mass increase. 3DE showed strong correlation with CMR (LVEDVi r = 0.91, LVEF r = 0.85, LVMi r = 0.84, RVEDVi r = 0.84, RVEF r = 0.86 p < 0.001). At follow up, the percentage change by 3DE and CMR were similar (∆LVEDVi r = 0.96 bias - 0.3%, ∆LVEF r = 0.94, bias 0.7%, ∆LVMi r = 0.94 bias 0.8%, ∆RVESVi r = 0.93, bias 1.2%, ∆RVEF r = 0.87 bias 0.4%). 3DE underestimated volumes (LVEDVi bias - 18.5 mL/m 2 , RVEDVi bias - 25.5 mL/m 2 ) and the degree of underestimation increased with larger dimensions (Q1vsQ4 LVEDVi relative bias - 14.5 versus - 17.4%, p = 0.016; Q1vsQ4 RVEDVi relative bias - 17 versus - 21.9%, p = 0.005). Measurements of cardiac volumes, mass and function by 3DE correlate well with CMR and 3DE accurately detects changes over time. 3DE underestimates volumes and the relative bias increases with larger cardiac size., (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

Hypertrophic cardiomyopathy (HCM) is a common cause of sudden cardiac death in athletes. Cardiac Magnetic Resonance (CMR) imaging is considered an excellent tool to differentiate between HCM and athlete's heart. The aim of this systematic review was to highlight the novel CMR-derived parameters with significant discriminative capacity between the two conditions. A systematic search in the MEDLINE, EMBASE and Cochrane Reviews databases was performed. Eligible studies were considered the ones comparing novel CMR-derived parameters on athletes and HCM patients. Therefore, studies that only examined Cine-derived volumetric parameters were excluded. Particular attention was given to binary classification results from multi-variate regression models and ROC curve analyses. Bias assessment was performed with the Quality Assessment on Diagnostic Accuracy Studies. Five (5) studies were included in the systematic review, with a total of 284 athletes and 373 HCM patients. Several novel indices displayed discriminatory potential, such as native T1 mapping and T2 values, LV global longitudinal strain, late gadolinium enhancement and whole-LV fractal dimension. Diffusion tensor imaging enabled quantification of the secondary eigenvalue angle and fractional anisotropy in one study, which also proved capable of reliably detecting HCM in a mixed athlete/patient sample. Several novel CMR-derived parameters, most of which are currently under development, show promising results in discerning between athlete's heart and HCM. Prospective studies examining the discriminatory capacity of all promising modalities side-by-side will yield definitive answers on their relative importance; diagnostic models can incorporate the best performing variables for optimal results.

Purpose of Review: The athlete's heart exhibits unique structural and functional adaptations in the setting of strenuous and repetitive athletic training which may be similarly found in pathologic states. The purpose of this review is to highlight the morphologic and functional changes associated with the athlete's heart, with a focus upon the insights that echocardiography provides into exercise-induced cardiac remodeling., Recent Findings: Recent studies are aiming to investigate the long-term effects and clinical consequences of an athlete's heart. The "gray-zone" continues to pose a clinical challenge and may indicate scenarios where additional imaging modalities, or longitudinal follow-up, provide a definitive answer. Echocardiography is likely to remain the first-line imaging modality for the cardiac evaluation of elite athletes. Multimodality imaging combined with outcome and long-term follow-up studies both during training and after retirement in both men and women may help further clarify the remaining mysteries in the coming years., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The pathophysiological mechanisms underlying the development of the athlete's heart are still poorly understood. To characterize the intracavitary blood flows in the right ventricle (RV) and right-ventricular outflow tract (RVOT) in 2 healthy probands, patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and 2 endurance athletes, we performed 4D-MRI flow measurements to assess differences in kinetic energy and shear stresses. Time evolution of velocity magnitude, mean kinetic energy (MKE), turbulent kinetic energy (TKE) and viscous shear stress (VSS) were measured both along the whole RV and in the RVOT. RVOT regions had higher kinetic energy values and higher shear stresses levels compared to the global averaging over RV among all subjects. Endurance athletes had relatively lower kinetic energy and shear stresses in the RVOT regions compared to both healthy probands and ARVC patients. The athlete's heart is characterized by lower kinetic energy and shear stresses in the RVOT, which might be explained by a higher diastolic compliance of the RV., (© 2022. The Author(s).)

Regular exercise promotes structural, functional, and electrical remodeling of the heart, often referred to as the "athlete's heart," with intense endurance sports being associated with the greatest degree of cardiac remodeling. However, the extremes of exercise-induced cardiac remodeling are potentially associated with uncommon side effects. Atrial fibrillation is more common among endurance athletes and there is speculation that other arrhythmias may also be more prevalent. It is yet to be determined whether this arrhythmic susceptibility is a result of extreme exercise remodeling, genetic predisposition, or other factors. Gender may have the greatest influence on the cardiac response to exercise, but there has been far too little research directed at understanding differences in the sportsman's vs sportswoman's heart. Here in part 4 of a 4-part seminar series, the controversies and ambiguities regarding the athlete's heart, and in particular, its arrhythmic predisposition, genetic, and gender influences are reviewed in depth., Competing Interests: Funding Support and Author Disclosures Dr La Gerche is supported by the National Heart Foundation of Australia. Dr Fatkin is supported by the Victor Chang Cardiac Research Institute, Heart Foundation, NSW Health, NHMRC. Dr Heidbuchel is supported by the Fund for Scientific Research, Flanders, with sports cardiology related grants T003717N and G099222N; has received personal lecture and consultancy fees from Abbott, Biotronik, Daiichi-Sankyo, Pfizer-Bristol Myers Squibb, Medscape, and Springer Healthcare Ltd; and has received unconditional research grants through the University of Antwerp and/or the University of Hasselt from Abbott, Bayer, Biotronik, Biosense Webster, Boston Scientific, Boehringer Ingelheim, Daiichi-Sankyo, Fibricheck/Qompium, Medtronic, and Pfizer-Bristol Myers Squibb, all outside the scope of this work. Dr Baggish has received funding to study topics relevant to this publication from the National Institute of Health/ National Heart, Lung, and Blood Institute, the National Football Players Association, and the American Heart Association; and receives compensation for his role as team cardiologist from the U.S. Olympic Committee / U.S. Olympic Training Centers, U.S. Soccer, U.S. Rowing, the New England Patriots, the Boston Bruins, the New England Revolution, and Harvard University. Prof Kovacic acknowledges research support from the National Institutes of Health (R01HL148167), New South Wales health grant RG194194, the Bourne Foundation and Agilent; and is the recipient of an Agilent Thought Leader Award (January 2022), which includes funding for research that is unrelated to the current paper. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Besides the health benefits of regular exercise, high-level training-above an optimal level-may have adverse effects. In this study, we investigated the effects of long-term vigorous training and its potentially detrimental structural-functional changes in a small animal athlete's heart model. Thirty-eight 4-month-old male guinea pigs were randomized into sedentary and exercised groups. The latter underwent a 15-week-long endurance-training program. To investigate the effects of the intense long-term exercise, in vivo (echocardiography, electrocardiography), ex vivo, and in vitro (histopathology, patch-clamp) measurements were performed. Following the training protocol, the exercised animals exhibited structural left ventricular enlargement and a significantly higher degree of myocardial fibrosis. Furthermore, resting bradycardia accompanied by elevated heart rate variability occurred, representing increased parasympathetic activity in the exercised hearts. The observed prolonged QTc intervals and increased repolarization variability parameters may raise the risk of electrical instability in exercised animals. Complex arrhythmias did not occur in either group, and there were no differences between the groups in ex vivo or cellular electrophysiological experiments. Accordingly, the high parasympathetic activity may promote impaired repolarization in conscious exercised animals. The detected structural-functional changes share similarities with the human athlete's heart; therefore, this model might be useful for investigations on cardiac remodeling.

Background: Physiological cardiac remodelling in highly trained athletes may overlap with dilated cardiomyopathy (DCM)., Objectives: The aim of this study was to investigate the role of the electrocardiogram (ECG) in differentiating between physiological and pathological remodelling., Methods: The study population consisted of 30 patients with DCM who revealed a pathogenic variant at genetic testing and 30 elite athletes with significant cardiac remodelling defined by a left ventricular (LV) end-diastolic diameter >62 mm and/or LV ejection fraction between 45% and 50%., Results: The ECG was abnormal in 22 (73%) patients with DCM. The most common abnormalities were low voltages (n = 14, 47%), lateral T-wave inversion (TWI) (n = 6, 20%), ventricular ectopic beats (n = 5, 17%) and anterior TWI (n = 4, 13). Two athletes revealed an abnormal ECG: complete left bundle branch block (LBBB) in one case and atrial flutter in the other. The sensitivity, specificity and accuracy of the ECG in differentiating DCM from physiological adaptation to exercise in athletes was 73% (confidence interval [CI]: 54%-88%), 93% (CI: 78%-99%) and 0.83 (CI: 0.71-0.92) respectively., Conclusions: While the ECG is usually normal in athletes exhibiting significant LV dilatation and/or systolic dysfunction, this test is often abnormal in patients with DCM harbouring a pathogenic variant. Low voltages in the limb leads and lateral TWI are the most common abnormalities., (© 2022 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.)

Sports Cardiology practice commonly involves the evaluation of athletes for genetically determined cardiac conditions that may predispose to malignant arrhythmias, heart failure, and sudden cardiac death. High-level exercise can lead to electrical and structural cardiac remodelling which mimics inherited cardiac conditions (ICCs). Differentiation between 'athlete's heart' and pathology can be challenging and often requires the whole armamentarium of available investigations. Genetic studies over the last 30 years have identified many of the genetic variants that underpin ICCs and technological advances have transformed genetic testing to a more readily available and affordable clinical tool which may aid diagnosis, management, and prognosis. The role of genetic testing in the evaluation and management of athletes with suspected cardiac conditions is often unclear beyond the context of specialist cardio-genetics centres. This document is aimed at physicians, nurses, and allied health professionals involved in the athlete's care. With the expanding role and availability of genetic testing in mind, this document was created to address the needs of the broader sports cardiology community, most of whom work outside specialized cardio-genetics centres, when faced with the evaluation and management of athletes with suspected ICC. The first part of the document provides an overview of basic terminology and principles and offers guidance on the appropriate use of genetic testing in the assessment of such athletes. It outlines key considerations when contemplating genetic testing, highlighting the potential benefits and pitfalls, and offers a roadmap to genetic testing. The second part of the document presents common clinical scenarios in Sports Cardiology practice, outlining the diagnostic, prognostic, and therapeutic implications of genetic testing, including impact on exercise recommendations. The scope of this document does not extend to a comprehensive description of the genetic basis, investigation, or management of ICCs., Competing Interests: Conflicts of interest: none declared., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Aims: While left ventricular (LV) adaptation to regular, intense exercise has been thoroughly studied, data concerning the right ventricular (RV) mechanical changes and their continuum with athletic performance are scarce. The aim of this study was to characterize biventricular morphology and function and their relation to sex, age, and sports classes in a large cohort of elite athletes using three-dimensional (3D) echocardiography., Methods and Results: Elite, competitive athletes (n = 422) and healthy, sedentary volunteers (n = 55) were enrolled. Left ventricular and RV end-diastolic volumes (EDVi) and ejection fractions (EFs) were measured. To characterize biventricular mechanics, LV and RV global longitudinal (GLS) and circumferential strains (GCS) were quantified. All subjects underwent cardiopulmonary exercise testing to determine peak oxygen uptake (VO2/kg). Athletes had significantly higher LV and RV EDVi compared with controls (athletes vs. controls; LV EDVi: 81 ± 13 vs. 62 ± 11 mL/m2, RV EDVi: 82 ± 14 vs. 63 ± 11 mL/m2; P &lt; 0.001). Concerning biventricular systolic function, athletes had significantly lower resting LV and RV EF (LV EF: 57 ± 4 vs. 61 ± 5%; RV EF: 55 ± 5 vs. 59 ± 5%; P &lt; 0.001). The exercise-induced relative decrease in LV GLS (9.5 ± 10.7%) and LV GCS (10.7 ± 9.8%) was similar; however, the decrement in RV GCS (14.8 ± 17.8%) was disproportionately larger compared with RV GLS (1.7 ± 15.4%, P &lt; 0.01). Right ventricular EDVi was found to be the strongest independent predictor of VO2/kg by multivariable linear regression., Conclusion: Resting LV mechanics of the athlete's heart is characterized by a balanced decrement in GLS and GCS; however, RV GCS decreases disproportionately compared with RV GLS. Moreover, this mechanical pattern is associated with better exercise capacity., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background/purpose: Sport-specific adaptations of athlete's hearts are still under investigation. This study sought to 1) identify athlete groups with similar characteristics by clustering echocardiographic data; 2) externally validate the data-driven clusters with sport classifications of various dynamic or static loads to support the conventional hypothesis-driven approach in delineating the athlete's heart., Methods: Anthropometric, echocardiographic and electrocardiographic assessments were collected during the 2017 Summer Universiade in Taiwan. Besides standard echocardiography and strain measurements, ventricular-arterial coupling (VAC) was assessed by the ratio of effective arterial elastance (Ea) to left ventricular end-systolic elastance (Ees) as calculated by a modified single-beat algorithm., Results: We grouped 598 elite athletes (348 male, age 23 ± 2.5 years, across 24 disciplines) using Mitchell's classification. The hypothesis-driven analysis showed dynamic training-related adaptations in heart rate and morphology, including ventricular size, mass, and stroke volume. In comparison, the unsupervised approach found two clusters for each sex. Male athletes participating in high dynamic-load exercises had larger chambers, supranormal diastolic functions, depressed Ees, lower Ea and preserved optimal VAC implicating the resting status of a reservoir-rich pump, which affirmed sport-specific adaptation. The female athletes could be clustered with more noticeable functional alterations, such as depressed biventricular strain. However, the imbalanced number between clusters impeded the validation of load-related remodeling., Conclusion: Hierarchical clustering could analyze complicated multiparametric interactions among numerous echocardiography-derived phenotypes to discern the adaptive propensity of the athlete's heart. The endorsement or generation of hypotheses by a data-driven approach can be applied to various domains., Competing Interests: Declaration of competing interest None., (Copyright © 2021 Formosan Medical Association. Published by Elsevier B.V. All rights reserved.)

Background: Both hypertension and age-related impairment of the cardiac condition are known to be improved by regular physical training. As relatively few studies have been reported about the older, hypertensive patients, the aim of this study was to establish cardiac benefits of active lifestyle in these subjects., Methods: Two-dimensionally guided M-mode, Doppler- and tissue Doppler echocardiography was performed in 199 normo- and hypertensive, active and sedentary older (age >60 years) men (N.=111) and women (N.=88). Results were compared either by ANOVA, or by Kruskall-Wallis test., Results: The Left Ventricular Muscle Index (LVMI), which is higher in young active than in sedentary persons, proved to be smaller in the active than sedentary older subjects: men normotensives: actives 83 vs. sedentary ones 98, hypertensives: actives 88 vs. sedentary ones 107, women normotensives: actives 77 vs. sedentary ones 89 g/m 3 . Diastolic function was better in the active groups demonstrated both by the ratio of the early to atrial peak blood flow velocities (men: normotensives: actives 1.03 vs. sedentary ones 0.76, women normotensives: actives 1.21 vs. sedentary ones 0.9, hypertensives: actives 1.04 vs. sedentary ones 0.88). The tissue Doppler results were also better in the active groups; the difference between the active and sedentary groups was more marked in the normotensive male groups than in the hypertensive ones., Conclusions: Active lifestyle prevents age-related pathological LV hypertrophy, and attenuates the LV diastolic dysfunction.

Providing medical care for an athlete can be challenging in many aspects. One specific aspect is the athlete's cardiovascular system. Athletic training and physical activity certainly can improve cardiovascular health, but it can also cause cardiac adaptations and place athletes at risk for sudden cardiac arrest. When an athlete has cardiac symptoms, a concerning family history, abnormal cardiac testing, or an underlying cardiac condition, a wide range of professionals are needed to appropriately care for the athlete under evaluation., Competing Interests: Disclosure The authors have nothing to disclose., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Cardiac magnetic resonance (CMR) is a second-line imaging test in cardiology. Balanced enlargement of heart chambers called athlete's heart (AH) is a part of physiological adaptation to regular physical activity. The aim of this study was to evaluate the diagnostic utility of CMR in athletes with suspected structural heart disease (SHD) and to analyse the relation between the coexistence of AH and SHD. We wanted to assess whether the presence of AH phenotype could be considered as a sign of a healthy heart less prone to development of SHD. This retrospective, single centre study included 154 consecutive athletes (57 non-amateur, all sports categories, 87% male, mean age 34 ± 12 years) referred for CMR because of suspected SHD. The suspicion was based on existing guidelines including electrocardiographic and/or echocardiographic changes suggestive of abnormality but without a formal diagnosis. CMR permitted establishment of a new diagnosis in 66 patients (42%). The main diagnoses included myocardial fibrosis typical for prior myocarditis ( n = 21), hypertrophic cardiomyopathy ( n = 17, including 6 apical forms), other cardiomyopathies ( n = 10) and prior myocardial infarction ( n = 6). Athlete's heart was diagnosed in 59 athletes (38%). The presence of pathologic late gadolinium enhancement (LGE) was found in 41 patients (27%) and was not higher in athletes without AH (32% vs. 19%, p = 0.08). Junction-point LGE was more prevalent in patients with AH phenotype (22% vs. 9%, p = 0.02). Patients without AH were not more likely to be diagnosed with SHD than those with AH (49% vs. 32%, p = 0.05). Based on the results of CMR and other tests, three patients (2%) were referred for ICD implantation for the primary prevention of sudden cardiac death with one patient experiencing adequate intervention during follow-up. The inclusion of CMR into the diagnostic process leads to a new diagnosis in many athletes with suspicion of SHD and equivocal routine tests. Athletes with AH pattern are equally likely to be diagnosed with SHD in comparison to those without AH phenotype. This shows that the development of AH and SHD can occur in parallel, which makes differential diagnosis in this group of patients more challenging.

The changes of the athlete's heart are not well defined and characterized in children. We aimed to describe the morphological changes of the heart related to sport in young athletes. We evaluated a group of 331 young athletes under 18 years (mean 11.9 ± 3.2) who practice tennis: 58 (16.52%), football: 118 (33.62%), basketball: 16 (4.56%), athletics: 40 (11.4%), and swimming: 99 (28.21%). Type of sport, years of practice, and duration of the training were collected. All children underwent echocardiography with the following M-mode parameters: left atrium diameter (LAD), interventricular septum (IVS), and left ventricle posterior Wall (LVPW), diastolic diameter of the left ventricle (LVDD), and right ventricle outflow tract (RVOT). The major finding of our study was that 20% of the children had a Z score > 2 for the IVS and that increased to 30% for the children playing tennis or swimming. Also, other changes like LA and RVOT dilatation were observed in about 10 and 14% of the cases, respectively. Taken together, these figures indicate that cardiac remodeling is frequent in children. Further studies are needed to establish consensus-based criteria of athlete's heart in young children., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Whilst the athlete's heart has been extensively described, less work has focused on the potential for elite athletes to demonstrate further cardiac remodelling upon an increase in training volume. Moreover, little work explored potential side-specific cardiac remodelling. Therefore, we examined the impact of an increase in training volume across 9-months in elite rowers on left- and right-sided cardiac structure, function and mechanics (i. e. longitudinal, radial and circumferential strain, twist and strain-volume loops). As part of the preparations to the 2012 Olympic Games, twenty-seven elite rowers (26.4±3.7years, 19 male) underwent echocardiography prior to and post (9 months) an increase in training volume (24 to 30-35 h weekly). Training increased left ventricular structure, including wall thickness, diameter, volume, mass and LV twist (all p<0.05). Female rowers demonstrated larger adaptation in left ventricular diameter and mass compared to male rowers (both p<0.05). No changes were observed in other measures of left ventricular function in both sexes (all p>0.05). The 9-month intervention showed no change in right ventricular/atrial structure, function or mechanics (all p>0.05). In conclusion, our data revealed that 9-month increased training volume in elite rowers induced left-sided (but not right-sided) structural remodelling, concomitant with an increase in left ventricular twist, with some changes larger in women., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

Aims: We sought to investigate the correlation between speckle-tracking echocardiography (STE)-derived myocardial work (MW) and invasively measured contractility in a rat model of athlete's heart. We also assessed MW in elite athletes and explored its association with cardiopulmonary exercise test (CPET)-derived aerobic capacity., Methods and Results: Sixteen rats underwent a 12-week swim training program and were compared to controls (n = 16). STE was performed to assess global longitudinal strain (GLS), which was followed by invasive pressure-volume analysis to measure contractility [slope of end-systolic pressure-volume relationship (ESPVR)]. Global MW index (GMWI) was calculated from GLS curves and left ventricular (LV) pressure recordings. In the human investigations, 20 elite swimmers and 20 healthy sedentary controls were enrolled. GMWI was calculated through the simultaneous evaluation of GLS and non-invasively approximated LV pressure curves at rest. All subjects underwent CPET to determine peak oxygen uptake (VO2/kg). Exercised rats exhibited higher values of GLS, GMWI, and ESPVR than controls (-20.9 ± 1.7 vs. -17.6 ± 1.9%, 2745 ± 280 vs. 2119 ± 272 mmHg·%, 3.72 ± 0.72 vs. 2.61 ± 0.40 mmHg/μL, all PExercise < 0.001). GMWI correlated robustly with ESPVR (r = 0.764, P < 0.001). In humans, regular exercise training was associated with decreased GLS (-17.6 ± 1.5 vs. -18.8 ± 0.9%, PExercise = 0.002) but increased values of GMWI at rest (1899 ± 136 vs. 1755 ± 234 mmHg·%, PExercise = 0.025). GMWI exhibited a positive correlation with VO2/kg (r = 0.527, P < 0.001)., Conclusions: GMWI precisely reflected LV contractility in a rat model of exercise-induced LV hypertrophy and captured the supernormal systolic performance in human athletes even at rest. Our findings endorse the utilization of MW analysis in the evaluation of the athlete's heart., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.

Background: Sports training triggers exercise-induced cardiac remodeling (EICR). Sprint- and endurance-trained master athletes are exposed to different hemodynamic stimuli accompanied by aging. The aim of this study was to compare EICR types in light of the Morganroth hypothesis, frequency of abnormalities, and relationships between cardiac traits and age., Methods: In this observational cross-sectional study, echocardiographic examinations were conducted in 143 sprint-trained (age range, 36-83 years) and 114 endurance-trained (age range, 38-85 years) competitive master athletes. Structural and functional characteristics were compared with population reference values, and EICR types were identified. Athletic groups were compared using t tests and χ 2 tests. Relationships with age were assessed using linear regression., Results: In the sprint group, 51.0% of athletes had normal cardiac geometry (nonhypertrophic heart), 4.2% had eccentric hypertrophy, 36.4% had concentric remodeling, and 8.4% had concentric hypertrophy. In their endurance-trained peers, these proportions were 22.8%, 16.7%, 36.8%, and 23.7%, respectively. Many athletes in both groups had structural abnormalities, as assessed using population norms (up to ~81% for septal thickness) but their resting cardiac function was normal. The relationships of structural and functional cardiac characteristics with age were mostly weak to moderate and did not differ between training modalities., Conclusions: Even though many endurance- and sprint-oriented master athletes exceed population norms for cardiac structure, they do not go beyond the "gray zone" and preserve normal cardiac function. Therefore, physiologic adaptations, rather than pathologic abnormalities, are expected in aging but still active athletes. Inconsistent with the Morganroth hypothesis, EICR is shifted toward normal geometry in sprinters and toward concentric remodeling and hypertrophy in endurance runners. A better understanding of the mechanisms behind cardiac remodeling during aging is needed to adequately predict EICR types in master athletes., (Copyright © 2021 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)

Participation in regular exercise of moderate intensity is associated with a plethora of systemic benefits, including a reduction in risk factors for coronary atherosclerosis; however, intensive exercise may paradoxically culminate in sudden cardiac arrest among individuals harboring arrhythmogenic substrates. The precise mechanism for arrhythmogenesis is likely multifactorial, however, surges in catecholamines, electrolyte shifts, acid-base disturbances, increased core temperature and demand myocardial ischemia are potential contributors. Although most deaths occur in middle aged and older males with atherosclerotic coronary artery disease, a significant proportion also affect young athletes with inherited or congenital cardiac abnormalities. The impact of such catastrophes on society, particularly when a young high-profile athlete is affected could be considered a justified reason for identifying individuals who may be at risk. Given the rarity of deaths in young athletes, only the simplest screening test, such as the 12-lead electrocardiography (ECG) may be considered to be cost effective. The ECG is effective for detecting serious electrical diseases in young athletes such as congenital electrical accessory pathways and ion channel diseases but can also identify athletes with potential life-threatening structural diseases such as hypertrophic and arrhythmogenic cardiomyopathy. One of the concerns about ECG screening is that regular intensive exercise results in several physiological alterations in cardiac structure and function that are reflected on the athlete's ECG. Sinus bradycardia, first-degree atrioventricular block, incomplete right bundle branch block, minor J-point elevation and large QRS voltages are common. Conversely, some repolarization anomalies affecting the ST segment, T waves and QT interval may overlap with patterns observed in patients with serious cardiac diseases. The situation is complicated further because age, sex and ethnicity of the athletes also influence the ECG and there is a risk that erroneous interpretation could have serious consequences. This review will describe the normal electrical patterns of the "athlete's heart" and provide insights into differentiation physiological electrical patterns from those observed in serious cardiac disease.

Exercise training is generally beneficial for cardiovascular health, improving stroke volume, cardiac output, and aerobic capacity. Despite these benefits, some evidence indicates that endurance training may increase the risk of atrial fibrillation (AF), particularly in highly trained individuals. Among multiple mechanisms, autonomic tone changes and atrial remodeling have been proposed as main contributors for exercise-induced AF. However, the contribution of local and systemic immunity is poorly understood in the development of atrial arrhythmogenic substrates. Here we aim to update the field of immunomodulation in the context of exercise and AF by compiling and reconciling the most recent evidence from preclinical and human studies and rationalize the applicability of "lone" AF terminology in athletes., Competing Interests: Declaration of Competing Interest None., (Copyright © 2021. Published by Elsevier Inc.)

To provide clinically relevant criteria for differentiation between the athlete's heart and similar appearing hypertrophic (HCM), dilated (DCM), and arrhythmogenic right-ventricular cardiomyopathy (ARVC) in MRI. 40 top-level athletes were prospectively examined with cardiac MR (CMR) in two university centres and compared to retrospectively recruited patients diagnosed with HCM (n = 14), ARVC (n = 18), and DCM (n = 48). Analysed MR imaging parameters in the whole study cohort included morphology, functional parameters and late gadolinium enhancement (LGE). Mean left-ventricular enddiastolic volume index (LVEDVI) was high in athletes (105 ml/m 2 ) but significantly lower compared to DCM (132 ml/m 2 ; p = 0.001). Mean LV ejection fraction (EF) was 61% in athletes, below normal in 7 (18%) athletes vs. EF 29% in DCM, below normal in 46 (96%) patients (p < 0.0001). Mean RV-EF was 54% in athletes vs. 60% in HCM, 46% in ARVC, and 41% in DCM (p < 0.0001). Mean interventricular myocardial thickness was 10 mm in athletes vs. 12 mm in HCM (p = 0.0005), 9 mm in ARVC, and 9 mm in DCM. LGE was present in 1 (5%) athlete, 8 (57%) HCM, 10 (56%) ARVC, and 21 (44%) DCM patients (p < 0.0001). Healthy athletes' hearts are characterized by both hypertrophy and dilation, low EF of both ventricles at rest, and increased interventricular septal thickness with a low prevalence of LGE. Differentiation of athlete's heart from other non-ischemic cardiomyopathies in MRI can be challenging due to a significant overlap of characteristics also seen in HCM, ARVC, and DCM., (© 2021. The Author(s).)

Erythropoietin (EPO) is a haematopoietic hormone that regulates erythropoiesis, but the EPO-receptor (EpoR) is also expressed in non-haematopoietic tissues. Stimulation of the EpoR in cardiac and skeletal muscle provides protection from various forms of pathological stress, but its relevance for normal muscle physiology remains unclear. We aimed to determine the contribution of the tissue-specific EpoR to exercise-induced remodelling of cardiac and skeletal muscle. Baseline phenotyping was performed on left ventricle and m. gastrocnemius of mice that only express the EpoR in haematopoietic tissues (EpoR-tKO). Subsequently, mice were caged in the presence or absence of a running wheel for 4 weeks and exercise performance, cardiac function and histological and molecular markers for physiological adaptation were assessed. While gross morphology of both muscles was normal in EpoR-tKO mice, mitochondrial content in skeletal muscle was decreased by 50%, associated with similar reductions in mitochondrial biogenesis, while mitophagy was unaltered. When subjected to exercise, EpoR-tKO mice ran slower and covered less distance than wild-type (WT) mice (5.5 ± 0.6 vs. 8.0 ± 0.4 km/day, p < 0.01). The impaired exercise performance was paralleled by reductions in myocyte growth and angiogenesis in both muscle types. Our findings indicate that the endogenous EPO-EpoR system controls mitochondrial biogenesis in skeletal muscle. The reductions in mitochondrial content were associated with reduced exercise capacity in response to voluntary exercise, supporting a critical role for the extra-haematopoietic EpoR in exercise performance., (© 2021. The Author(s).)

Cardiac response to prolonged, intense exercise induces phenotypic and physiologic adaptive changes that improve myocardial ability to meet oxygen demands. These adaptations, termed "athletes' heart," have been extensively studied. The importance of this entity arises from the increasing numbers of athletes as well as the drive for physical fitness in the general population leading to adaptive cardiac changes that need to be differentiated from life-threatening cardiovascular diseases. A number of pathologic entities may share phenotypic changes with the athletes' heart such as hypertrophic cardiomyopathy, dilated cardiomyopathy, Marfan's syndrome, and arrhythmogenic right ventricular cardiomyopathy. Cardiologists need to be cognizant of these overlapping findings to appropriately diagnose diseases and prevent catastrophic outcomes especially in young and healthy individuals who may not show any symptoms until they engage in intense exercise. It is equally important to recognize and distinguish normal, exercise-adaptive cardiac changes to provide accurate screening and guidance to young elite athletes. Echocardiography is a valuable modality that allows comprehensive initial evaluation of cardiac structures, function, and response to exercise. Several different echocardiographic techniques including M-Mode, 2D echo, Doppler, tissue Doppler, color tissue Doppler, and speckle tracking have been used in the evaluation of cardiac adaptation to exercise. The following discussion is a review of literature that has expanded our knowledge of the athlete's heart., (© 2021 Wiley Periodicals LLC.)

Athlete's heart (AH) is the result of morphological and functional cardiac modifications due to long-lasting athletic training. Athletes can develop very marked structural myocardial changes, which may simulate or cover unknown cardiomyopathies. The differential diagnosis between AH and cardiomyopathy is necessary to prevent the risk of catastrophic events, such as sudden cardiac death, but it can be a challenging task. The improvement of the imaging modalities and the introduction of the new technologies in cardiac magnetic resonance (CMR) and cardiac computed tomography (CCT) can allow overcoming this challenge. Therefore, the radiologist, specialized in cardiac imaging, could have a pivotal role in the differential diagnosis between structural adaptative changes observed in the AH and pathological anomalies of cardiomyopathies. In this review, we summarize the main CMR and CCT techniques to evaluate the cardiac morphology, function, and tissue characterization, and we analyze the imaging features of the AH and the key differences with the main cardiomyopathies.

Objectives: Distinguishing hypertrophic cardiomyopathy (HCM) from left ventricular hypertrophy (LVH) due to systematic training (athlete's heart, AH) from morphologic assessment remains challenging. The purpose of this study was to examine the role of T2 mapping and deformation imaging obtained by cardiovascular magnetic resonance (CMR) to discriminate AH from HCM with (HOCM) or without outflow tract obstruction (HNCM)., Methods: Thirty-three patients with HOCM, 9 with HNCM, 13 strength-trained athletes as well as individual age- and gender-matched controls received CMR. For T2 mapping, GRASE-derived multi-echo images were obtained and analyzed using dedicated software. Besides T2 mapping analyses, left ventricular (LV) dimensional and functional parameters were obtained including LV mass per body surface area (LVMi), interventricular septum thickness (IVS), and global longitudinal strain (GLS)., Results: While LVMi was not significantly different, IVS was thickened in HOCM patients compared to athlete's. Absolute values of GLS were significantly increased in patients with HOCM/HNCM compared to AH. Median T2 values were elevated compared to controls except in athlete's heart. ROC analysis revealed T2 values (AUC 0.78) and GLS (AUC 0.91) as good parameters to discriminate AH from overall HNCM/HOCM., Conclusion: Discrimination of pathologic from non-pathologic LVH has implications for risk assessment of competitive sports in athletes. Multiparametric CMR with parametric T2 mapping and deformation imaging may add information to distinguish AH from LVH due to HCM., Key Points: • Structural analyses using T2 mapping cardiovascular magnetic resonance imaging (CMR) may help to further distinguish myocardial diseases. • To differentiate pathologic from non-pathologic left ventricular hypertrophy, CMR including T2 mapping was obtained in patients with hypertrophic obstructive/non-obstructive cardiomyopathy (HOCM/HNCM) as well as in strength-trained athletes. • Elevated median T2 values in HOCM/HNCM compared with athlete's may add information to distinguish athlete's heart from pathologic left ventricular hypertrophy.

Background: Differentiation between exercise induced adaptive myocardial hypertrophy (athlete's heart) and hypertrophic cardiomyopathy (HCM) is currently based on echocardiographic and cardiac magnetic resonance (CMR) criteria, but these may be insufficient in patients with subtle phenotype expression. This study aimed to assess whether left ventricular (LV) fractal pattern could permit to differentiate athlete's heart from HCM., Methods: We recruited retrospectively 61 elite marathon runners, 67 patients with HCM, and 33 healthy subjects. A CMR study was performed in all subjects and the LV trabeculae fractal dimension (FD) was measured in end-diastolic frames of each short-axis cine sequence. For group comparison, the ratio of maximal myocardial wall thickness (mMWT)/indexed LV end-diastolic volume (LVED) was determined., Results: As compared with athletes, patients with HCM had significantly (p < 0.001) greater FD in the LV basal (1.30 ± 0.07 vs. 1.23 ± 0.05) and apical (1.38 ± 0.06 vs. 1.30 ± 0.07) regions and in the whole heart (1.34 ± 0.05 vs. 1.27 ± 0.05). FD increased with age, left atrial area and indexed left ventricular mass (p < 0.05 for all) and correlated negatively with LV and RV end-diastolic volumes (p < 0.05 each). The addition of whole heart FD to the ratio of maximal myocardial wall thickness/indexed LVEDV lead to an improvement in the ability to discriminate HCM with a net reclassification index (NRI) of 71%., Conclusions: The FD regional distribution of the LV trabeculae differentiates patients with athlete's heart from patients with HCM. The addition of whole heart FD to the mMWT/indexed LVEDV ratio improves the predictive capacity of the model to differentiate both entities., Competing Interests: Declaration of Competing Interest The authors report no conflicts of interest., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Cardiac regeneration requires dedifferentiation and proliferation of mature cardiomyocytes, but the mechanisms underlying this plasticity remain unclear. Here, we identify a potent cardiomyogenic role for Krüppel-like factor 1 (Klf1/Eklf), which is induced in adult zebrafish myocardium upon injury. Myocardial inhibition of Klf1 function does not affect heart development, but it severely impairs regeneration. Transient Klf1 activation is sufficient to expand mature myocardium in uninjured hearts. Klf1 directs epigenetic reprogramming of the cardiac transcription factor network, permitting coordinated cardiomyocyte dedifferentiation and proliferation. Myocardial expansion is supported by Klf1-induced rewiring of mitochondrial metabolism from oxidative respiration to anabolic pathways. Our findings establish Klf1 as a core transcriptional regulator of cardiomyocyte renewal in adult zebrafish hearts., (Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Acute exhaustive endurance exercise can differentially impact the right ventricle (RV) versus the left ventricle (LV). However, the hemodynamic basis for these differences and its impact on postexercise recovery remain unclear. Therefore, we assessed cardiac structure and function along with hemodynamic properties of mice subjected to single bouts (216 ± 8 min) of exhaustive swimming (ES). One-hour after ES, LVs displayed mild diastolic impairment compared with that in sedentary (SED) mice. Following dobutamine administration to assess functional reserve, diastolic and systolic function were slightly impaired. Twenty-four hours after ES, LV function was largely indistinguishable from that in SED. By contrast, 1-h post swim, RVs showed pronounced impairment of diastolic and systolic function with and without dobutamine, which persisted 24 h later. The degree of RV impairment correlated with the time-to-exhaustion. To identify hemodynamic factors mediating chamber-specific responses to ES, LV pressure was recorded during swimming. Swimming initiated immediate increases in heart rates (HRs), systolic pressure, dP/d t max and -dP/d t min , which remained stable for ∼45 min. LV end-diastolic pressures (LVEDP) increased to ≥45 mmHg during the first 10 min and subsequently declined. After 45 min, HR and -dP/d t min declined, which correlated with gradual elevations in LVEDP (to ∼45 mmHg) as mice approached exhaustion. All parameters rapidly normalized postexercise. Consistent with human studies, our findings demonstrate a disproportionate negative impact of acute exhaustive exercise on RVs that persisted for at least 24 h. We speculate that the differential effects of exhaustive exercise on the ventricles arise from a ∼2-fold greater hemodynamic load in the RV than in LV originating from profound elevations in LVEDPs as mice approach exhaustion. NEW & NOTEWORTHY Acute exhaustive exercise differentially impacts the right ventricle (RV) versus left ventricle (LV), yet the underlying hemodynamic basis remains unclear. Using pressure-volume analyses and pressure-telemetry implantation in mice, we confirmed a marked disproportionate and persistent negative impact of exhaustive exercise on the RV. These differences in responses of the ventricles to exhaustive exercise are of clinical relevance, reflecting ∼2-fold greater hemodynamic RV loads versus LVs arising from massive (∼45 mmHg) increases in LV end-diastolic pressures at exhaustion.

Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease caused by mutations of desmosomal genes in about 50% of patients. Affected patients may have defective non-desmosomal genes. The ACM phenotype may occur in other genetic cardiomyopathies, cardio-cutaneous syndromes or neuromuscular disorders. A sizeable proportion of patients have non-genetic diseases with clinical features resembling ACM (phenocopies). The identification of biventricular and left-dominant phenotypic variants has made differential diagnosis more difficult because of the broader spectrum of phenocopies which requires a detailed clinical study with appropriate evaluation of most prominent and discriminatory disease features. Conditions that enter into differential diagnosis of ACM include heart muscle diseases affecting the right ventricle, the left ventricle, or both. To confirm a conclusive diagnosis of ACM, these differential possibilities need to be reasonably excluded by an accurate and targeted clinical evaluation. This article reviews the clinical and imaging features of major phenocopies of ACM and provides indications for differential diagnosis. The recent etiologic classification of Arrhythmogenic Cardiomyopathies, whose common denominator is the distinctive phenotype characterized by a hypokinetic and non-dilated ventricle with a large amount of myocardial fibrosis underlying its propensity to generate ventricular arrhythmias is also addressed.

The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110α (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor that regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by 1 ) swim training or 2 ) cardiac-specific transgenic expression of constitutively active PI3K (caPI3K Tg+ ). Under basal conditions, male and female cKO mice displayed mild interstitial fibrosis compared with control (CON) littermates, but no other signs of cardiac pathology were present. In response to exercise training, female CON mice displayed an increase (∼21%) in heart weight normalized to tibia length vs. untrained mice. Exercise-induced hypertrophy was blunted in cKO mice. Exercise increased cardiac Akt phosphorylation and IGF1R expression but was comparable between genotypes. However, differences in Foxo3a, Hsp70, and autophagy markers were identified in hearts of exercised cKO mice. Deletion of FoxO1 did not reduce cardiac hypertrophy in male or female caPI3K Tg+ mice. Cardiac Akt and FoxO1 protein expressions were significantly reduced in hearts of caPI3K Tg+ mice, which may represent a negative feedback mechanism from chronic caPI3K, and negate any further effect of reducing FoxO1 in the cKO. In summary, FoxO1 contributes to exercise-induced hypertrophy. This has important implications when one is considering FoxO1 as a target for treating the diseased heart. NEW & NOTEWORTHY Regulators of exercise-induced physiological cardiac hypertrophy and protection are considered promising targets for the treatment of heart failure. Unlike pathological hypertrophy, the transcriptional regulation of physiological hypertrophy has remained largely elusive. To our knowledge, this is the first study to show that the transcription factor FoxO1 is a critical mediator of exercise-induced cardiac hypertrophy. Given that exercise-induced hypertrophy is protective, this finding has important implications when one is considering FoxO1 as a target for treating the diseased heart.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disease associated with a high risk of sudden cardiac death. Among other factors, physical exercise has been clearly identified as a strong determinant of phenotypic expression of the disease, arrhythmia risk, and disease progression. Because of this, current guidelines advise that individuals with ARVC should not participate in competitive or frequent high-intensity endurance exercise. Exercise-induced electrical and morphological para-physiological remodelling (the so-called 'athlete's heart') may mimic several of the classic features of ARVC. Therefore, the current International Task Force Criteria for disease diagnosis may not perform as well in athletes. Clear adjudication between the two conditions is often a real challenge, with false positives, that may lead to unnecessary treatments, and false negatives, which may leave patients unprotected, both of which are equally inacceptable. This review aims to summarize the molecular interactions caused by physical activity in inducing cardiac structural alterations, and the impact of sports on arrhythmia occurrence and other clinical consequences in patients with ARVC, and help the physicians in setting the two conditions apart., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.)

Athlete's heart results from physiological adaptations to the increased demands of exercise, and left atrial (LA) enlargement (LAE) is a fundamental component. However, LAE occurs in certain pathological conditions and it might represent a diagnostic challenge in athletes. LA volume index (LAVi) by echo is a convenient diagnostic tool for LAE identification. We hypothesized that accumulated lifetime training thousand hours (LTH) would have a main role in LAE. Therefore, our aim was to assess the association between LTH, LAVi and LAE in athletes. Young and middle-aged males with different training levels were included and grouped as recreational (REa, n = 30), competitive (COa, n = 169) and elite (ELa, n = 80) athletes for LTH calculation and echo assessment. LA dimensions resulted greater in ELa when compared to other groups (p < 0.001). LAVi correlated stronger with LTH than with age (p < 0.001). Polynomial regression analysis showed a non-linear, almost triphasic, effect of cumulative training on LA size (p < 0.02). Multivariate logistic regression, including LTH, age, body surface area, systolic blood pressure and other explanatory variables to predict LAE, showed LTH as the sole significant factor [OR 1.45 (CI 1.1-1.92), p < 0.008]. ROC analysis found an optimal cut off point of 3.6 LTH for LAE identification (AUC = 0.84, p < 0.001. RR = 5.65, p < 0.001). We conclude that LAE associates with LTH more than with other clinical parameters, and with less impact at higher amounts of LTH. Lifetime training greater than 3600 hours increases the probability of finding LAE in athletes. Future research should provide more insights and implications of these findings.