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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 < 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 < 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 < 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.

Supplemental Digital Content is available in the text., 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 χ2 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.

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.

Over the last decades, interest toward athlete’s heart has progressively increased, leading to improve the knowledge on exercise-induced heart modifications. Sport may act as a trigger for life-threatening arrhythmias in patients with structural or electrical abnormalities, hence requiring to improve the diagnostic capability to differentiate physiological from pathological remodeling. Pathological alterations are often subtle at the initial stages; therefore, the challenge is to promptly identify athletes at risk of sudden cardiac death during the pre-participation screening protocols. Advanced imaging modalities such as coronary computed tomography angiography (CCTA) and cardiac magnetic resonance (CMR) can non-invasively depict coronary vessels and provide a deep morpho-functional and structural characterization of the myocardium, in order to rule out pathological life threatening alterations, which may overlap with athletes’ heart remodeling. The purpose of the present narrative review is to provide an overview of most frequent diagnostic challenges, defining the boundaries between athlete's heart remodeling and pathological structural alteration with a focus on the role and importance of CCTA and CMR.

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, Graphical Abstract ESPVR, slope of end-systolic pressure–volume relationship (i.e. the slope of the curve connecting the end-systolic points of the pressure–volume loops recorded during the transient occlusion of inferior vena cava); GLS, global longitudinal strain; GMWI, global myocardial work index; LV, left ventricular; VO2/kg, peak oxygen uptake.

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

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.

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 (ED) 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. 127 +/- 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. (C) 2021 Elsevier B.V. All rights reserved.

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/m2) but significantly lower compared to DCM (132 ml/m2; 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

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.

Routine vigorous exercise can lead to electrical, structural, and functional adaptations that can enhance exercise performance. There are several factors that determine the type and magnitude of exercise-induced cardiac remodeling (EICR) in trained athletes. In some athletes with pronounced cardiac remodeling, there can be an overlap in morphologic features with mild forms of cardiomyopathy creating gray zone scenarios whereby distinguishing health from disease can be difficult. An integrated clinical approach that factors athlete-specific characteristics (sex, size, sport, ethnicity, and training history) and findings from multimodality imaging are essential to help make this distinction.

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.

Repairing the fish heart Although humans show minimal regenerative capability, zebrafish can regenerate their hearts through a mechanism whereby heart muscle cells (cardiomyocytes) revert to a less mature state and then proliferate to replace the damaged tissue. Ogawa et al. show that Krüppel-like factor 1 (Klf1/Eklf), a transcription factor well known for its role in red blood cell development, is an essential factor for heart regeneration in zebrafish. Klf1 is specifically expressed in cardiomyocytes after injury, and its activation is sufficient to stimulate new cardiomyocyte production without injury. This potent effect is achieved through reprogramming of gene networks regulating cardiomyocyte differentiation and mitochondrial metabolism. Science , this issue p. 201

The relationship between structural and electrical remodeling in the heart, particularly after long-standing endurance training, remains unclear. Signal-averaged electrocardiogram (SAECG) may provide a more sensitive method to evaluate cardiac remodeling than a 12-lead electrocardiogram (ECG). Accurate measures of electrical function (SAECG filtered QRS duration (fQRSd) and late potentials (LP) and left-ventricular (LV) mass (cardiac magnetic resonance, CMR) can allow an assessment of structural remodeling and QRS prolongation. Endurance athletes (45-65 yr old,10 yr of endurance sport), screened to exclude cardiac disease, had standardized 12-lead ECG, SAECG, resting echocardiogram (ECHO), and CMR performed. SAECG fQRSd was correlated with QRS duration on the 12-lead ECG, and ECHO and CMR-derived LV mass. Participants (

High-intensity endurance exercise elicits acute cardiac imbalances that may be an important stimulus for adaptive cardiac remodeling. This study highlights that following a bout of high-intensity exercise that is typical of routine day-to-day cycling training, exercise-induced autonomic, biochemical, and functional cardiac imbalances are attenuated in middle-aged relative to young well-trained cyclists. These findings suggest that aging may alter exercise-induced stress stimulus response that initiates cardiac remodeling in Athlete’s Heart.

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.

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.

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.

BackgroundIntensive endurance exercise may induce a broad spectrum of right ventricular (RV) adaptation/remodelling patterns. Late gadolinium enhancement (LGE) has also been described in cardiovascular magnetic resonance (CMR) of some endurance athletes and its clinical meaning remains controversial. Our aim was to characterize the features of contrast CMR and the observed patterns of the LGE distribution in a cohort of highly trained endurance athletes.MethodsNinety-three highly trained endurance athletes (> 12 h training/week at least during the last 5 years; 36 ± 6 years old; 53% male) and 72 age and gender-matched controls underwent a resting contrast CMR. In a subgroup of 28 athletes, T1 mapping was also performed.ResultsHigh endurance training load was associated with larger bi-ventricular and bi-atrial sizes and a slight reduction of biventricular ejection fraction, as compared to controls in both genders (p p ConclusionsHighly trained endurance athletes showed a ten-fold increase in the prevalence of focal LGE as compared to control subjects, always confined to the hinge points. Additionally, those athletes with focal LGE demonstrated globally higher myocardial ECV values. This matrix remodelling and potential presence of myocardial fibrosis may be another feature of the athlete’s heart, of which the clinical and prognostic significance remains to be determined.

Left ventricular (LV) structural remodeling following athletic training has been evidenced through training-specific changes in wall thickness and geometry. Whether the LV response to changes in hemodynamic load also adapts in a training-specific manner is unknown. Using echocardiography, we examined LV responses of endurance-trained (

The purpose of this prospective study was to analyze the relationship between ventricular morphology and parameters of cardiac function in two different athletic groups and controls, using feature tracking cardiac magnetic resonance (FT-CMR). Twenty-three professional soccer players (22 ± 4 years), 19 competitive triathletes (28 ± 6 years) and 16 controls (26 ± 3 years) were included in the study. CMR was performed using a 1.5 T scanner. Cardiac chamber volumes, mass and biventricular global myocardial strain were obtained and compared. In comparison to the control subjects, athletes were characterized by a higher cardiac volume (p p p p p 2, p p p p r = 0.47, p r = − 0.28, p

Imaging techniques have allowed knowing the structural adaptative changes observed in the hearts of highly trained athletes. Athletes can develop very marked structural changes and the need may rise for a differential diagnosis with real cardiomyopathy. In this chapter, authors review the physiologic and morphologic features associated with athletic training and the keys to differentiate normal adaptive athlete's heart from mild or initial expression forms of left-heart side cardiomyopathies such as hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and left ventricle non-compaction (LVNC).

The success of systematic early age talent development has led to the professionalisation of youth sports academies used by clubs and governing bodies alike, and sports physicians are nowadays commonly confronted with paediatric cardiological problems. Medical cardiac care of the paediatric athlete is however in its infancy, and the international guidelines that are present for adult athletes, are not yet available. Similarly, reference data for ECG and echocardiography are incomplete. The aim of this article is to provide and introduction to the cardiac care of the paediatric athlete to facilitate healthy and above all, safe talent development, but also provide guidance on how to distinguish adaptive, beneficial cardiovascular remodelling from underlying pathology of congenital or inherited cardiovascular disease. Differences in presentation, diagnosis and treatment between childhood and adult athletes are highlighted and can educate the reader in the emerging field of paediatric sports cardiology.

Objectives The imaging features of dilated cardiomyopathy (DCM) overlap with physiological exercise-induced cardiac remodeling in active and otherwise healthy individuals. Distinguishing the two conditions is challenging. This study examined the diagnostic and prognostic roles of exercise stress imaging in asymptomatic patients with suspected DCM. Methods Exercise stress cardiovascular magnetic resonance (CMR) was performed in 60 asymptomatic patients with suspected DCM (dilated left ventricle and/or impaired systolic function on CMR), who also underwent DNA sequencing for DCM-causing genetic variants. Confirmed DCM was defined as genotype- and phenotype-positive (G+P+). Another 100 healthy subjects were recruited to establish normal exercise capacities (peak exercise cardiac index; PeakCI). The primary outcome was a composite of all-cause mortality, cardiac decompensation and ventricular arrhythmic events. Results No patients with confirmed G+P+ DCM had PeakCI exceeding the 35th percentile specific for age and sex. Applying this threshold in G-P+ patients, those with PeakCI below 35th percentile had characteristics similar to confirmed DCM while patients with higher PeakCI were younger, more active and higher longitudinal strain. Adverse cardiovascular events occurred only in patients with low exercise capacity (P = 0.004). Conclusions In individuals with suspected DCM, exercise stress CMR demonstrates diagnostic and prognostic potential in distinguishing between pathological DCM and physiological exercise-induced cardiac remodeling.

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.

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.

We conducted a meta‐analysis to synthesize the best available evidence comparing cardiac biventricular structure and function using cardiac magnetic resonance imaging (CMR) and transthoracic echocardiography (TTE) in elite female athletes and healthy controls (HC). Chronic exposure to exercise may induce cardiac chamber enlargement as a means to augment stroke volume, a condition known as the “athlete's heart.” These changes have not been clearly characterized in female athletes. Multiple databases were searched from inception to June 18, 2019. Outcomes of interest included left ventricular (LV) and right ventricular (RV) dimensional, volumetric, mass, and functional assessments in female athletes. Most values were indexed to body surface area. The final search yielded 22 studies, including 1000 female athletes from endurance, strength, and mixed athletic disciplines. CMR‐derived LV end‐diastolic volume (LVEDV) and RV end‐diastolic volume (RVEDV) were greater in endurance athletes (EA) versus HC (17.0% and 18.5%, respectively; both p, This article focuses on the morphological and physiological effects of endurance‐based exercise on the female heart. Much literature has been described in males, but this data features data that mirrors that of men and particularly focuses on left and right ventricular function using established and advanced imaging modalities.

Hypertrophic cardiomyopathy is one of the main causes of sudden cardiac death in young athletes. Differentiating between this pathological condition and ‘athlete's heart’ can be quite challenging, warranting a thorough clinical and imaging assessment. Clinicians often rely on detraining-induced attenuation of electrocardiographic and echocardiographic findings as a means of distinguishing between pathological and physiological cardiac remodeling. This report describes detraining-related regression of left ventricular hypertrophy in a young soccer player with a diagnosis of hypertrophic cardiomyopathy. It challenges the dogma that regression of electrocardiographic abnormalities and left ventricular hypertrophy is exclusive to physiological remodeling and questions the impact of exercise training in the phenotypic expression and progression of hypertrophic cardiomyopathy. Resumo: A miocardiopatia hipertrófica é uma das principais causas de morte súbita de origem cardíaca em jovens atletas. Distinguir entre esta patologia e o “coração de atleta” pode ser difícil, exigindo uma avaliação clínica e imagiológica exaustiva. Frequentemente recorre-se à atenuação dos achados eletrocardiográficos e ecocardiográficos induzidos pela pausa desportiva como forma de distinguir entre remodelagem fisiológica e patológica. Neste caso clínico descrevemos a regressão da hipertrofia ventricular esquerda induzida pela pausa desportiva num jovem futebolista com o diagnóstico de miocardiopatia hipertrófica. Este caso põe em causa o dogma de que a regressão das alterações eletrocardiográficas e a da hipertrofia ventricular esquerda é exclusiva da remodelação fisiológica e, simultaneamente, levanta dúvidas sobre a influência do treino físico na evolução e expressão fenotípica da miocardiopatia hipertrófica.

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 yrs.) men (111) and women (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/m3. 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.

Long-term exercise induces physiological cardiac adaptation, a condition referred to as athlete’s heart. Exercise tolerance is known to be associated with decreased cardiac passive stiffness. Passive stiffness of the heart muscle is determined by the giant elastic protein titin. The adult cardiac muscle contains two titin isoforms: the more compliant N2BA and the stiffer N2B. Titin-based passive stiffness may be controlled by altering the expression of the different isoforms or via post-translational modifications such as phosphorylation. Currently, there is very limited knowledge about titin’s role in cardiac adaptation during long-term exercise. Our aim was to determine the N2BA/N2B ratio and post-translational phosphorylation of titin in the left ventricle and to correlate the changes with the structure and transverse stiffness of cardiac sarcomeres in a rat model of an athlete’s heart. The athlete’s heart was induced by a 12-week-long swim-based training. In the exercised myocardium the N2BA/N2B ratio was significantly increased, Ser11878 of the PEVK domain was hypophosphorlyated, and the sarcomeric transverse elastic modulus was reduced. Thus, the reduced passive stiffness in the athlete’s heart is likely caused by a shift towards the expression of the longer cardiac titin isoform and a phosphorylation-induced softening of the PEVK domain which is manifested in a mechanical rearrangement locally, within the cardiac sarcomere.

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.