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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

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.

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.

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.

Sudden cardiac death among top athletes is very rare, however, it is 2-4 times more frequent than in the age-matched control population. In the present study, the electrophysiological consequences of long-term exercise training were investigated on Ca

Aims Physiological cardiac adaptation in athletes is influenced by multiple factors. This study aimed to investigate the impact of sex, age, body size, sports type and training volume on cardiac adaptation in healthy athletes with cardiac magnetic resonance imaging. Methods A total of 327 athletes (242 male) were studied (adults ≥18 years old; adolescents 14–18 years old). Left and right ventricular ejection fractions, end-diastolic volume, end-systolic volume, stroke volumes and masses were measured. Left ventricular end-diastolic volume/left ventricular mass, right ventricular end-diastolic volume/right ventricular mass and derived right/left ventricular ratios were determined to study balanced ventricular adaptation. Athletes were categorised as skill, power, mixed and endurance athletes. Results Male athletes had higher left and right ventricular volumes and masses in both adult ( n = 215 (145 male); 24 ± 5 years old) and adolescent ( n = 112 (97 male); 16 ± 1 years old) groups compared with women (all P Conclusion There are significant sex differences in the physiological adaptation of adult and adolescent athlete’s heart; and male sex, higher training volume and endurance sports are major determinants of sports adaptation in adults.

In the last few years, multiple echocardiographic nomograms have been published. However, normal values calculated in the general population are not applicable to athletes, whose hearts may be enlarged and hypercontractile. Accordingly, athletes require specific nomograms. Our aim is to provide a critical review of echocardiographic nomograms on two-dimensional (2D) measures for athletes. We performed a systematic search in the National Library of Medicine for Medical Subject Headings and free text terms including echocardiography, athletes, normal values and nomograms. The search was refined by adding the keywords heart, sport, elite, master, children and young. Twenty-eight studies were selected for the final analysis. Our research revealed that currently available ranges of normality for athletes reported by different authors are quite consistent, with limited exceptions (e.g. atria, aorta). Numerical and methodological limitations, however, emerged. Numerical limitations included a limited sample size (e.g.

The heart is the primary pump that circulates blood through the entire cardiovascular system, serving many important functions in the body. Exercise training provides favorable anatomical and physiological changes that reduce the risk of heart disease and failure. Compared with pathological cardiac hypertrophy, exercise-induced physiological cardiac hypertrophy leads to an improvement in heart function. Exercise-induced cardiac remodeling is associated with gene regulatory mechanisms and cellular signaling pathways underlying cellular, molecular, and metabolic adaptations. Exercise training also promotes mitochondrial biogenesis and oxidative capacity leading to a decrease in cardiovascular disease. In this review, we summarized the exercise-induced adaptation in cardiac structure and function to understand cellular and molecular signaling pathways and mechanisms in preclinical and clinical trials.

Right ventricular (RV) function has proven to be a prognostic factor in heart failure with reduced and preserved ejection fraction and in pulmonary hypertension. RV function is also a cornerstone in the management of novel clinical issues, such as mechanical circulatory support devices or grown-up congenital heart disease patients. Despite the notable amount of circumferentially oriented myofibers in the subepicardial layer of the RV myocardium, the non-longitudinal motion directions are often neglected in the everyday assessment of RV function by echocardiography. However, the complex RV contraction pattern incorporates different motion components along three anatomically relevant axes: longitudinal shortening with traction of the tricuspid annulus towards the apex, radial motion of free wall often referred as the "bellows effect", and anteroposterior shortening of the chamber by stretching the free wall over the septum. Advanced echocardiographic techniques, such as speckle-tracking and 3D echocardiography allow an in-depth characterization of RV mechanical pattern, providing better understanding of RV systolic and diastolic function. In our current review, we summarize the existing knowledge regarding RV mechanical adaptation to pressure- and/or volume-overloaded states and also other physiologic or pathologic conditions.

Left ventricular hypertrophy (LVH) is an adaptive response to physiological or pathological stimuli, and distinguishing between the two has obvious clinical implications. However, asymmetric septal hypertrophy and preserved cardiac function are noted in early stages in both cases. We characterized the early anatomic and functional changes in a mouse model of physiological and pathological stress using serial echocardiography-based morphometry and tissue velocity imaging. Weight-matched CF-1 male mice were separated into Controls ( n = 10), treadmill Exercise 1 h daily for 5 days/wk ( n = 7), and transverse aortic constriction (TAC, n = 7). Hypertrophy was noted first in the left ventricle basal septum compared with other segments in Exercise (0.84 ± 0.02 vs. 0.79 ± 0.03 mm, P = 0.03) and TAC (0.86 ± 0.05 vs. 0.77 ± 0.04 mm, P = 0.02) at 4 and 3 wk, respectively. At 8 wk, eccentric LVH was noted in Exercise and concentric LVH in TAC. Septal E/E′ ratio increased in TAC (32.6 ± 3.7 vs. 37 ± 6.2, P = 0.002) compared with the Controls and Exercise (32.3 ± 5.2 vs. 32.8 ± 3.8 and 31.2 ± 4.9 vs. 28.2 ± 5.0, respectively, nonsignificant for both). Septal s′ decreased in TAC (21 ± 3.6 vs. 17 ± 4.2 mm/s, P = 0.04) but increased in Exercise (19.6 ± 4.1 vs. 29.2 ± 2.3 mm/s, P = 0.001) and was unchanged in Controls (20.1 ± 4.2 vs. 20.9 ± 5.1 mm/s, nonsignificant). With similar asymmetric septal hypertrophy and normal global function during the first 4–8 wk of pathological and physiological stress, there is an early marginal increase with subsequent decrease in systolic tissue velocity in pathological but early and progressive increase in physiological hypertrophy. Tissue velocities may help adjudicate between these two states when there are no overt anatomic or functional differences. NEW & NOTEWORTHY Pathological and physiological stress-induced ventricular hypertrophy have different clinical connotations but present with asymmetric septal hypertrophy and normal global function in their early stages. We observed a marginal but statistically significant decrease in systolic tissue velocity in pathological but progressive increase in velocity in physiological hypertrophy. Tissue velocity imaging could be an important tool in the management of asymmetric septal hypertrophy by adjudicating between these two etiologies when there are no overt anatomic or functional differences.

Background Although exercise-induced cardiac hypertrophy has been intensively investigated, its development and regression dynamics have not been comprehensively described. In the current study, we aimed to characterize the effects of regular exercise training and detraining on left ventricular (LV) morphology and function. Methods Rats were divided into exercised (n = 12) and control (n = 12) groups. Exercised rats swam 200 min/day for 12 weeks. After completion of the training protocol, rats remained sedentary for 8 weeks (detraining period). Echocardiographic follow-up was performed regularly to obtain LV long- and short-axis recordings for speckle-tracking echocardiography analysis. Global longitudinal and circumferential strain and systolic strain rate were measured. LV pressure-volume analysis was performed using additional groups of rats to obtain haemodynamic data. Results Echocardiographic examinations showed the development of LV hypertrophy in the exercised group. These differences disappeared during the detraining period. Strain and strain rate values were all increased after the training period, whereas supernormal values rapidly reversed to the control level after training cessation. Load-independent haemodynamic indices, e.g., preload recruitable stroke work, confirmed the exercise-induced systolic improvement and complete regression after detraining. Conclusions and translational aspect Our results provide the first comprehensive data to describe the development and regression dynamics of morphological and functional aspects of physiological hypertrophy in detail. Speckle-tracking echocardiography has been proven to be feasible to follow-up changes induced by exercise training and detraining and might provide an early possibility to differentiate between physiological and pathological conditions.

Data about the functional adaptation of the right ventricle (RV) to intense exercise are limited. Our aim was to characterize the RV mechanical pattern in top-level athletes using three-dimensional echocardiography. A total of 60 elite water polo athletes (19 ± 4 yr, 17 ± 6 h of training/wk, 50% women and 50% men) and 40 healthy sedentary control subjects were enrolled. We measured the RV end-diastolic volume index (RVEDVi) and ejection fraction (RVEF) using dedicated software. Furthermore, we determined RV global longitudinal (RV GLS) and circumferential strain (RV GCS) and the relative contribution of longitudinal ejection fraction (LEF) and radial ejection fraction (REF) to RVEF using the ReVISION method. Athletes also underwent cardiopulmonary exercise testing [O2 consumption (V̇o2)/kg]. Athletes had significantly higher RVEDVi compared with control subjects (athletes vs. control subjects, 88 ± 11 vs. 65 ± 10 ml/m2, P < 0.001); however, they also demonstrated lower RVEF (56 ± 4% vs. 61 ± 5%, P < 0.001). RV GLS was comparable between the two groups (−22 ± 5% vs. −23 ± 5%, P = 0.24), whereas RV GCS was significantly lower in athletes (−21 ± 4% vs. −26 ± 7%, P < 0.001). Athletes had higher LEF and lower REF contribution to RVEF (LEF/RVEF: 0.50 ± 0.07 vs. 0.42 ± 0.07, P < 0.001; REF/RVEF: 0.33 ± 0.08 vs. 0.45 ± 0.08, P < 0.001). Moreover, the pattern of RV functional shift correlated with V̇o2/kg (LEF/RVEF: r = 0.30, P < 0.05; REF/RVEF: r = −0.27, P < 0.05). RV mechanical adaptation to long-term intense exercise implies a functional shift; the relative contribution of longitudinal motion to global function was increased, whereas the radial shortening was significantly decreased, in athletes. Moreover, this functional pattern correlates with aerobic exercise performance, representing a potential new resting marker of an athlete’s heart. NEW & NOTEWORTHY Intensive regular physical exercise results in significant changes of right ventricular morphology and function. By separate quantification of the right ventricular longitudinal and radial function, a relative dominance of longitudinal motion and a decrease in radial motion can be observed compared with sedentary controls. Moreover, this contraction pattern correlates with cardiopulmonary fitness. According to these results, this functional shift of the right ventricle may represent a novel marker of an athlete’s heart.

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.

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 (caPI3KTg+). 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 caPI3KTg+ mice. Cardiac Akt and FoxO1 protein expressions were significantly reduced in hearts of caPI3KTg+ 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.

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

Contains fulltext : 249141.pdf (Publisher’s version ) (Closed access) 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 p0.05). 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. 01 februari 2022

Background: Most of our knowledge on training-induced cardiac remodeling is derived from men, with the paucity of data from women representing an important gap in knowledge. The aim of the study was to define the electrocardiographic and morphological features of female athlete’s heart, with special attention to differences related to sex and sport. Methods: Seven hundred twenty Olympic athletes (360 females and 360 age- and sport-matched males, mean age: 23±5 years) were evaluated by clinical, resting, and exercise electrocardiography and echocardiography. Results: Anterior T-wave inversion was more common in females than males ( P P P P Conclusions: Sex significantly affects cardiac remodeling in athletes, with females presenting a different electrical and structural remodeling. Women maintain a normal LV geometry, with relative larger increase of cavity dimensions compared with men. Type of sport has a relevant impact, with endurance athletes exhibiting the greatest degree of RV and LV dimensional remodeling. The present study confirms the need for a sex-based approach for interpreting the complex features of athlete’s heart in women.

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.

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The Authors’ reply We are grateful to Dr Stuart1 for his interest in our paper.2 We agree entirely that our dilated cardiomyopathy (DCM) cohort were indeed highly selected. Most individuals with DCM do not have the capacity to exercise intensively and would not fit in the differential diagnosis of an athlete’s heart with borderline or mildly reduced left ventricular (LV) ejection fraction. For the purposes of this study, we sought to identify individuals with a mild form of DCM who were motivated to and could exercise intensively for a prolonged …

Rationale:Cardiac CITED4 is induced by exercise and is sufficient to cause physiological hypertrophy and mitigate adverse ventricular remodeling after ischemic injury. However, the role of endogenous CITED4 in response to physiological or pathological stress is unknown.Objective:To investigate the role of CITED4 in murine models of exercise and pressure overload.Methods and Results:We generated cardiomyocyte-specific CITED4 knockout mice (C4KO) and subjected them to an intensive swim exercise protocol as well as transverse aortic constriction (TAC). Echocardiography, western blotting, qPCR, immunohistochemistry, immunofluorescence, and transcriptional profiling for mRNA and miRNA expression were performed. Cellular crosstalk was investigated in vitro. CITED4 deletion in cardiomyocytes did not affect baseline cardiac size or function in young adult mice. C4KO mice developed modest cardiac dysfunction and dilation in response to exercise. After TAC, C4KOs developed severe heart failure with left ventricular dilation, impaired cardiomyocyte growth accompanied by reduced mammalian target of rapamycin (mTOR) activity and maladaptive cardiac remodeling with increased apoptosis, autophagy, and impaired mitochondrial signaling. Interstitial fibrosis was markedly increased in C4KO hearts after TAC. RNAseq revealed induction of a pro-fibrotic miRNA network. miR30d was decreased in C4KO hearts after TAC and mediated crosstalk between cardiomyocytes and fibroblasts to modulate fibrosis. miR30d inhibition was sufficient to increase cardiac dysfunction and fibrosis after TAC.Conclusions:CITED4 protects against pathological cardiac remodeling by regulating mTOR activity and a network of miRNAs mediating cardiomyocyte to fibroblast crosstalk. Our findings highlight the importance of CITED4 in response to both physiological and pathological stimuli.

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

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.

There is still debate on the range of normal physiologic changes of the right ventricle or ventricular (RV) function in athletes. Genetic links to arrhythmogenic cardiomyopathy (ACM) are well-established. There is no current consensus on the importance of extensive exercise and exercise-induced injury to the RV. During the intensive exercise of endurance sports, the cardiac structures adapt to athletic load over time. Some athletes develop RV cardiomyopathy possibly caused by genetic predisposition, whilst others develop arrhythmias from the RV. Endurance sports lead to increased volume and pressure load in both ventricles and increased myocardial mass. The extent of volume increase and changes in myocardial structure contribute to impairment of RV function and pose a challenge in cardiovascular sports medicine. Genetic predisposition to ACM may play an important role in the risk of sudden cardiac death of athletes. In this review, we discuss and evaluate existing results and opinions. Intensive training in competitive dynamic/power and endurance sports leads to specific RV adaptation, but physiological adaptation without genetic predisposition does not necessarily lead to severe complications in endurance sports. Discriminating between physiological adaptation and pathological form of ACM or RV impairment provoked by reinforced exercise presents a challenge to clinical sports cardiologists.

Background Left atrial ( LA ) size and cardiorespiratory fitness ( CRF ) are predictors of future cardiovascular events in high‐risk populations. LA dilatation is a diagnostic criterion for left ventricular diastolic dysfunction. However, LA is dilated in endurance athletes with high CRF , but little is known about the association between CRF and LA size in healthy, free‐living individuals. We hypothesized that in a healthy population, LA size was associated with CRF and leisure‐time physical activity, but not with echocardiographic indexes of left ventricular diastolic dysfunction. Methods and Results In this cross‐sectional study from HUNT (Nord‐Trøndelag Health Study), 107 men and 138 women, aged 20 to 82 years, without hypertension, cardiovascular, pulmonary, or malignant disease participated. LA volume was assessed by echocardiography and indexed to body surface area LAVI (left atrial volume index). CRF was measured as peak oxygen uptake ( VO 2peak ) using ergospirometry, and percent of age‐ and‐sex‐predicted VO 2peak was calculated. Indexes of left ventricular diastolic dysfunction were assessed in accordance with latest recommendations. LAVI was >34 mL/m 2 in 39% of participants, and LAVI was positively associated with VO 2peak and percentage of age‐ and‐sex‐predicted VO 2peak (β (95% CI) 0.18 (0.09‐0.28) and 0.10 (0.05‐0.15)), respectively) weighted minutes of physical activity per week (β [95% CI ], 0.01 [0.003–0.015]). LAVI was not associated with other indexes of left ventricular diastolic dysfunction. There was an effect modification between age and VO 2peak /percentage of age‐ and‐sex‐predicted VO 2peak showing higher LAVI with advanced age and higher VO 2peak /percentage of age‐ and‐sex‐predicted VO 2peak as presented in prediction diagrams. Conclusions Interpretation of LAVI as a marker of diastolic dysfunction should be done in relation to age‐relative CRF . Studies on the prognostic value of LAVI in fit subpopulations are needed.

Cardiac adaptations to exercise on an elite level have been well studied. Strain analysis by speckle tracking echocardiography has emerged as a tool for sports cardiologists to assess the nature of hypertrophy in athletes' hearts. In prior studies, strain values generally did not change in physiological adaptations to exercise but were reduced in pathological hypertrophy. However, research in this field has focused almost solely on male athletes. Purpose of the present study is to investigate strain values in the hearts of female elite athletes in football and volleyball. In this cross-sectional study echocardiography was performed on 19 female elite football-players, 16 female elite volleyball-players and 16 physically inactive controls. Conventional echocardiographic data was documented as well as left ventricular longitudinal, radial and circumferential strain values gained by speckle tracking echocardiography. The hearts of the female athletes had a thicker septal wall, a larger overall mass and larger atria than the hearts in the control group. Global longitudinal, radial and circumferential strain values did not differ between the athletes and controls or between sporting disciplines. No correlation between septal wall thickness and global strain values could be documented. Cardiac adaptations to elite level exercise in female volleyball and football players do not influence global strain values. This has been documented for male athletes of several disciplines. The present study adds to the very limited control-group comparisons of left ventricular strain values in elite female athletes. The findings indicate that global strain values can be used when assessing the cardiac health in female athletes.

Over the past few years, the approach to the 'arrhythmic patient' has profoundly changed. An early clinical presentation of arrhythmia is often accompanied by non-specific symptoms and followed by inconclusive electrocardiographic findings. In this scenario, cardiac magnetic resonance (CMR) has been established as a clinical tool of fundamental importance for a correct prognostic stratification of the arrhythmic patient. This technique provides a high-spatial-resolution tomographic evaluation of the heart, which allows studying accurately the ventricular volumes, identifying even segmental kinetic anomalies and properly detecting diffuse or focal tissue alterations through an excellent tissue characterization, while depicting different patterns of fibrosis distribution, myocardial edema or fatty substitution. Through these capabilities, CMR has a pivotal role for the adequate management of the arrhythmic patient, allowing the identification of those phenotypic manifestations characteristic of structural heart diseases. Therefore, CMR provides valuable information to reclassify the patient within the wide spectrum of potentially arrhythmogenic heart diseases, the definition of which remains the major determinants for both an adequate treatment and a poor prognosis. The purpose of this review study was to focus on the role of CMR in the evaluation of the main cardiac clinical entities associated with arrhythmogenic phenomena and to present a brief debate on the main pathophysiological mechanisms involved in the arrhythmogenesis process.

Intense exercise-induced right ventricular remodeling is a potential adaptation of cardiac function and structure. The features of the remodeling may overlap with those of a very early form of arrhythmogenic right ventricular cardiomyopathy (ARVC): at this early stage, it could be difficult to discriminate ARVC, from exercise-induced cardiac adaptation that may develop in normal individuals. The purpose of this paper is to discuss which exercise-induced remodeling may be a pathological or a physiological finding. A complete evaluation may be required to identify the pathological features of ARVC that would include potential risk of sudden cardiac death during sport or, to avoid the false diagnosis of ARVC. The most recent expert assessment of arrhythmogenic cardiomyopathy focuses on endurance athletes presenting with clinical features indistinguishable from ARVC.

Exercise training induces morphological and functional cardiovascular adaptation known as the “athlete’s heart” with changes including dilatation, hypertrophy, and increased stroke volume. These changes may overlap with pathological appearances. Distinguishing athletic cardiac remodelling from cardiomyopathy is important and is a frequent medical dilemma. Cardiac magnetic resonance (CMR) has a role in clinical care as it can refine discrimination of health from a disease where ECG and echocardiography alone have left or generated uncertainty. CMR can more precisely assess cardiac structure and function as well as characterise the myocardium detecting key changes including myocardial scar and diffuse fibrosis. In this review, we will review the role of CMR in sports cardiology.

Arrhythmogenic right-ventricular cardiomyopathy (ARVC) is a genetically determined heart disease characterized by progressive myocyte death and substitution by fibrofatty tissue. Life-threatening ventricular arrhythmias may occur during the course of the disease and are distinctively triggered by sports activity: for this reason, ARVC is one of the leading causes of sudden death in the athlete. Early identification of affected athletes by preparticipation screening in the pre-symptomatic phase is essential, but differential diagnosis with the athlete's heart may be challenging. Variants with predominant involvement of the left ventricle are difficult to diagnose unless cardiac magnetic resonance is performed. Athletes with overt ARVC or asymptomatic carriers of pathological gene mutations, including those with an implantable cardioverter defibrillator, should refrain from competitive sports, while a moderate-intensity recreational physical activity appears safe.