Aim Athletes frequently report palpitations during exercise, yet reliable electrocardiographic (ECG) rhythm monitoring during exercise remains a challenge in sports cardiology. This study compared the signal quality and user experience of multiple wearable ECG devices during exercise and prolonged ambulatory monitoring in endurance athletes. Methods and results Fifteen healthy recreational cyclists underwent a supervised three-hour cycling session followed by seven days of ambulatory monitoring using three wearable ECG devices: a single-lead ECG patch (SLP), single-lead ECG chest-strap (SLCS), and a multi-lead ECG patch (MLP). During exercise, the SLCS achieved the highest percentage of interpretable ECG recordings (100.0% [99.69–100.0]), significantly outperforming the SLP (98.1% [92.1–100.0]; p = 0.021) and the MLP (77.07% [30.09–97.86]; p = 0.009). Over 7 days, the SLP provided the longest total recording time (10,080 ± 0 min), while the SLCS captured the greatest proportion of time during exercise (33 ± 27% vs. <10% for other devices). Patch-based systems were preferred by participants for comfort and sleep but were associated with more frequent skin irritation. The SLCS was perceived as superior for fit during exercise but less comfortable for daily use. Conclusion The SLCS provides superior signal quality during exercise but is less likely to be worn during periods of rest and daily activities. Patch-based ECG devices are less reliable during exercise but allow continuous 24-hour recording. Wearable ECG device selection should therefore be individualized with SLCS preferred for exercise-associated symptoms and patch-based systems for continuous rhythm monitoring.

AIMS:To describe exercise haemodynamics across cardiac damage stages and evaluate the incremental prognostic impact of cardiac damage stage and exercise-induced pulmonary hypertension (exPHT) in patients with symptomatic moderate aortic stenosis (AS) and asymptomatic severe AS. METHODS AND RESULTS:A total of 436 consecutive patients with ≥ moderate AS (74 ± 10 years, 32% women, 56% severe AS) underwent cardiopulmonary exercise testing with echocardiography. The primary endpoint was heart failure (HF) death and HF hospitalizations. Cardiac damage stage was 0 in 93 patients, 1 (LV damage) in 135, 2 (LA/mitral damage) in 135, and 3-4 (pulmonary vasculature/tricuspid or RV damage) in 73. Higher stages were associated with worse exercise capacity and haemodynamics. Over a median follow-up of 37 months, 65 patients met the primary endpoint. After adjustment for age, AS severity, and aortic valve replacement, cardiac damage stage and exPHT were independently associated with HF outcomes [HR per stage increase 1.51 (1.26-1.82); P < 0.001; exPHT HR 2.36 (1.10-5.07); P = 0.03]. exPHT improved risk stratification in early-stage disease (stages 1-2), conferring an approximately five-fold higher risk of HF events in patients with exPHT [HR 4.45 (1.58-12.59); P < 0.01]. CONCLUSION:In patients with ≥ moderate AS and discordant symptoms, cardiac damage stage and exPHT independently refined HF risk stratification. ExPHT provides incremental prognostic value in early damage stages (1-2), representing over half of the cohort, supporting a stepwise approach of routine damage staging with selective with exPHT assessment with exercise echocardiography in this subgroup to guide more personalized management and potentially optimize AVR timing.

BACKGROUND AND AIMS:Prior studies on cardiac remodelling associated with exercise have relied on self-reported data of uncertain accuracy. In the present study, exercise duration and intensity were objectively quantified using heart rate (HR) monitors in athletes, and these metrics were correlated with cardiac magnetic resonance findings. METHODS:Young (16-23 years, n = 69) and middle-aged (45-70 years, n = 82) male endurance athletes with ≥80% of training sessions recorded via chest-worn HR monitors over 3 months were included. Training duration, session count, and intensity (classified into five HR zones and expressed as Edwards training impulse in arbitrary units) were analysed. Cardiac magnetic resonance measured indexed left/right ventricular volumes, ejection fraction, and left ventricular mass. RESULTS:Younger athletes trained more than older athletes [169 (127-209) vs 78 (49-114) hours; 23 129 (17 880-28 305) vs 12 620 (7168-17 607) arbitrary units; both P < .05] over a 3-month period. In all athletes, light-to-moderate-intensity training exceeded thresholds of >6 or >9 metabolic equivalent of tasks to describe intense activity. Training duration (r > .33, P < .05 for all) and Edwards training impulse (r > .29, P < .05 for all) correlated with cardiac dimensions, but the duration always outperformed intensity. Time spent in lower HR zones (1 and 2) correlated more with cardiac dimensions than higher-intensity training. Partial least squares analysis identified training duration in Zones 1&2 and 3 and age as key determinants of cardiac remodelling, whereas intensity was not a significant determinant of cardiac dimensions. CONCLUSIONS:Objective exercise quantification reveals new insights into cardiac remodelling, highlighting total exercise duration as a primary determinant of left/right ventricular volumes, independent of intensity. Traditional questionnaire-based methods may overlook these relationships.

Background Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous disease characterized by exercise intolerance. Defining pathophysiologically distinct subgroups allows more personalized therapy, but efforts mainly relied on resting examinations. This study aimed to define HFpEF phenotypes based on exercise limitations using combined cardiopulmonary exercise testing with stress echocardiography. Methods A total of 913 patients with HFpEF were recruited from 4 third‐line centers and divided into derivation (n=623) and validation cohorts (n=290). Unsupervised graph‐based clustering of 61 cardiopulmonary exercise testing with stress echocardiography variables was used to identify HFpEF exercise phenotypes. Pathophysiological characteristics, exercise capacity, and clinical outcomes were compared between phenotypes. Results In the derivation cohort, cluster analysis identified 5 distinct HFpEF exercise phenotypes characterized by specific exercise responses: mild diastolic dysfunction (phenotype 1), impaired peripheral oxygen extraction (phenotype 2), right ventricular‐pulmonary artery uncoupling (phenotype 3), reduced left ventricular systolic reserve (phenotype 4), and chronotropic incompetence (phenotype 5). The composite outcome of all‐cause death and unplanned cardiovascular hospitalization differed significantly across phenotypes, with phenotypes 2 (hazard ratio [HR], 1.76 [95% CI, 1.07–2.91]), 4 (HR, 2.15 [95% CI, 1.27–3.65]), and 5 (HR, 2.19 [95% CI, 1.33–3.61]) showing higher rates of the primary combined outcome compared with phenotype 1. All phenotypes were replicated in the validation cohort. Conclusions Deep phenotyping of the exercise response in patients with HFpEF revealed 5 distinct phenogroups with marked differences in pathophysiology, exercise performance, and clinical outcomes. This subclassification may support more personalized therapeutic strategies and improve risk stratification in HFpEF.

Background Middle-aged male Masters athletes exhibit a higher burden of coronary atherosclerosis on coronary computed tomography angiography (CCTA) compared with healthy controls. Whether this is accompanied by differences in carotid atherosclerosis or aortic stiffness remains uncertain. We assessed carotid atherosclerosis and aortic stiffness across groups, association between carotid atherosclerosis and coronary disease, and the incremental value of carotid plaque beyond traditional risk factors. Methods In this cross-sectional analysis of the Master@Heart study, 549 low cardiovascular risk men (median age 55 [50–60] years), including lifelong athletes, late-onset athletes, and healthy controls, underwent vascular phenotyping. Carotid plaque was assessed by ultrasound, aortic stiffness by carotid–femoral pulse wave velocity (PWV), and coronary atherosclerosis by CCTA. Group differences were assessed using chi-square and Kruskal–Wallis tests. Association between carotid and coronary atherosclerosis was evaluated using regression models. Incremental discriminatory value was assessed using ROC curve analysis. Results Prevalence of ≥1 carotid plaque did not differ between lifelong athletes, late-onset athletes, and controls (29.5%vs. 33.2% vs. 27.9%; p = 0.54). Carotid stenosis ≥50% was rare (1.2%–2.7%) and similar across groups (p = 0.54). Median PWV did not differ between groups (p = 0.29). Carotid plaque was associated with coronary atherosclerosis on CCTA. However, adding carotid plaque to traditional risk factors did not improve discrimination of coronary atherosclerosis. Conclusion In middle-aged male Masters athletes, excess subclinical coronary atherosclerosis is observed without corresponding differences in carotid plaque or aortic stiffness. Although carotid plaque is associated with coronary atherosclerosis, it does not meaningfully improve risk discrimination beyond traditional risk factors.

BACKGROUND AND AIMS:In patients with unexplained dyspnea, heart failure with preserved ejection fraction (HFpEF) is a frequent cause. Diagnostic scores estimate HFpEF probability, but their prognostic role and clinical applicability in this population remain uncertain. This study evaluated the association of HFpEF scores with structural remodeling, functional limitation, and clinical outcomes. METHODS:This multicenter cohort study included 2,535 patients with unexplained dyspnea who underwent combined cardiopulmonary exercise testing and echocardiography. HFpEF probability was assessed using H₂FPEF, HFA-PEFF, and HFpEF-ABA scores, with patients stratified into risk categories. RESULTS:Higher scores correlated with adverse ventricular and atrial remodeling, impaired exercise capacity, and higher pulmonary pressures, both at rest and during exercise. Intermediate and high-risk categories for HFA-PEFF, H₂FPEF, and HFpEF-ABA scores showed significantly elevated hazard ratios versus the low-risk group: HFA-PEFF (HR 2.62 95%CI 1.56-4.40, p<0.001 and 5.49 95%CI 2.82-10.67, p=0.005), H₂FPEF (HR 2.74 95%CI 1.35-5.89, p<0.001 and 6.21 95%CI 2.86-13.5, p<0.001), and HFpEF-ABA (HR 1.28 95%CI 0.57-2.86, p=0.549 and 2.50 95%CI 1.02-6.14, p=0.046), all p<0.001. Event rates increased stepwise across score categories, reaching 10 per 100 patient-years in the high-score groups. Score performance differed, particularly in the elderly, women, and those with atrial fibrillation. Incorporating echocardiographic parameters, particularly resting pulmonary pressure, improved HFpEF-ABA prognostic accuracy. In the NT-proBNP subgroup, functional criteria and NT-proBNP remained independent predictors for outcome. CONCLUSIONS:HFpEF diagnostic scores reflect the structural and functional disease burden as well as clinical risk in unexplained dyspnea. These scores are complementary and may enhance risk stratification.

BACKGROUND:Secondary or functional mitral regurgitation (FMR) of atrial origin is prevalent in heart failure with preserved ejection fraction (HFpEF) and portends a worse clinical course. Unlike ventricular FMR, it lacks evidence-based treatment and is often overlooked. Sacubitril-valsartan may provide benefit in this HFpEF phenotype. OBJECTIVE:To assess the impact of sacubitril-valsartan on exercise hemodynamics in patients with HFpEF and atrial FMR. METHODS:This multicenter, prospective, randomized, open-label trial with blinded endpoint assessment enrolls patients with stable HFpEF and at least moderate FMR documented within 1 year prior to enrollment. Participants are randomly assigned to sacubitril-valsartan plus standard medical therapy or to standard therapy alone, consisting of a mineralocorticoid receptor antagonist and a sodium-glucose cotransporter-2 inhibitor. Cardiopulmonary exercise testing with echocardiography is performed at baseline and after 6 months, with interval 24-hour home blood pressure monitoring to ensure blood pressure control in both arms. The primary endpoint is the change in exercise-induced pulmonary hypertension, assessed by the change in the mean pulmonary arterial pressure to cardiac output slope. This slope reflects total pulmonary resistance driven by both pre- and postcapillary factors, capturing key HFpEF features, including myocardial properties, vascular remodeling and the overall impact of (dynamic) atrial FMR. Secondary endpoints include changes in FMR severity, peak oxygen consumption, natriuretic peptide levels, left atrial size and function, and patient-reported outcomes. Prespecified adverse events include hypotension, renal failure, hyperkalemia, and angioedema. CONCLUSION:The PRAISE-MR (Sacubitril-Valsartan in Heart Failure with Preserved Ejection Fraction and Secondary Mitral Valve Regurgitation) trial will evaluate whether sacubitril-valsartan, an angiotensin receptor neprilysin inhibitor, is beneficial in patients with HFpEF and atrial FMR.

AIMS:The prevalence of ventricular fibrosis and its association with ventricular arrhythmias (VAs) and reduced ventricular systolic function in endurance athletes remains unclear. METHODS AND RESULTS:We evaluated 296 young [median age 19 (17-22)] and 138 middle-aged [56 (50-60)] male endurance athletes, alongside 66 middle-aged non-athletic controls [54 (49-60)], all without known cardiac disease. Cardiac magnetic resonance imaging assessed myocardial fibrosis and biventricular function. Twenty-four-hour Holter monitoring was used to quantify VAs. Non-hinge-point fibrosis was more prevalent in middle-aged athletes compared with young athletes (20 vs. 3%, P < 0.001) and middle-aged controls (20 vs. 9%, P = 0.045), while hinge-point fibrosis did not differ. Reduced left ventricular ejection fraction and/or right ventricular ejection fraction was more frequent in middle-aged athletes than controls (23 vs. 8%, P = 0.009), but similar to young athletes (23 vs. 22%, P = 0.906). Middle-aged athletes had a higher prevalence of non-sustained ventricular tachycardia (8 vs. 2%, P = 0.006), >100 premature ventricular complexes/24 h (13 vs. 5%, P = 0.004), multifocal ventricular ectopy (11 vs. 4%, P = 0.003), and complex ventricular ectopy (25 vs. 10%, P < 0.001) compared with young athletes, with no significant differences compared with controls. Non-hinge-point fibrosis increased the odds of a higher burden of unifocal and multifocal ventricular ectopy, but not of reduced systolic function. CONCLUSION:Middle-aged athletes more frequently exhibit myocardial fibrosis than young athletes and middle-aged non-athletes. Non-hinge-point fibrosis is present in up to one-fifth of middle-aged athletes and predictive of a higher burden of both unifocal and multifocal ventricular ectopy. Reduced systolic function is more prevalent in athletes and not predicted by fibrosis. LAY SUMMARY:We studied young and middle-aged male endurance athletes and non-athletes using heart magnetic resonance imaging scans and 24 h heart rhythm monitoring to evaluate scarring of the heart muscle, pumping function, and abnormal heart rhythms.Scarring of the heart muscle is relatively common in middle-aged athletes, but rare in the young. About one in five middle-aged athletes showed a particular 'non-hinge-point' pattern of scar tissue, which was rare in young athletes and also less frequent in middle-aged non-athletic individuals.Non-hinge-point scar was linked with more frequent abnormal heart rhythms. Athletes with this pattern of scar more frequently had premature ventricular beats (extra beats originating from the heart's lower chambers).

BACKGROUND:Middle-aged and older endurance athletes have increased prevalence of coronary artery disease (CAD) on coronary computed tomography angiography compared with healthy controls, despite similarly low cardiovascular risk. Previous studies relied on self-reported data to quantify training load (TL), which poorly correlates with objective wearable-derived TL and may bias outcomes. The effect of objective TL on CAD risk remains unknown. METHODS:In this observational, cross-sectional analysis of the Master@Heart study, 222 men (median age, 54 [49-59] years) were included: 77 lifelong athletes, 98 late-onset athletes, and 47 controls. TL was assessed using objective wearable-derived training duration and intensity (12 consecutive months), as well as self-reported training measures. Coronary computed tomography angiography-derived CAD prevalence was compared across TL quartiles (Q) using a global unadjusted chi-square test and logistic regression, adjusted for cardiovascular risk factors and years of endurance exercise, to estimate odds ratios between Q4 and Q1. In addition, adjusted logistic regression models were fitted with continuous TL, using smoothing splines to capture potential nonlinear associations. RESULTS:Across quartiles of objective Edwards training impulse (training duration × heart rate-weighted intensity), unadjusted global differences were observed for ≥1 plaque (P<0.001), coronary artery calcification (CAC)>0 (P=0.002), and CAC>100 (P=0.012). Q4 participants had significantly higher adjusted odds of ≥1 plaque (odds ratio, 5.85; 95% CI, 2.33-14.71), CAC>0 (odds ratio, 5.03; 95% CI, 2.04-12.35), and CAC>100 (odds ratio, 3.50; 95% CI, 1.22-10.00) versus Q1. Similar associations were found for objective training duration, whereas no clear associations were observed for relative time spent in high-intensity zones. In continuous analyses, Edwards training impulse and objective training duration showed significant positive associations with ≥1 plaque and CAC>100 (P<0.05), whereas self-reported training duration was only significantly associated with CAC>100 (P<0.05). Metabolic equivalent of task-minutes per week based on self-reported TL was not associated with CAD (P>0.05). CONCLUSIONS:High training duration (hours/week), particularly when combined with cumulative high-intensity TL (Edwards training impulse), was independently associated with increased prevalence of subclinical CAD in middle-aged and older athletes and physically active controls. Exercise intensity alone, in the absence of high duration, was not clearly linked to CAD. These findings underscore the potential of objectively measured TL for understanding associations with subclinical CAD in endurance athletes. REGISTRATION:URL: https://www.clinicaltrials.gov; Unique identifier: NCT03711539.

AIMS:Previous studies have not examined the role of non-electrical myocardial disease substrates in determining the optimal atrio-ventricular delay (AVD) settings. We conducted virtual patient simulations to evaluate whether myocardial disease substrates influence the acute response to AVD optimization at rest and during exercise. METHODS AND RESULTS:The CircAdapt cardiovascular model was used to simulate various left ventricular (LV) remodelling found in cardiac resynchronization therapy candidates. We simulated electrical dyssynchrony, LV dilatation with preserved and reduced contractility, and increased LV passive stiffness. We simulated cardiac resynchronization following biventricular (BiVP) and non-selective LBB pacing (nsLBBP). The paced-AVD ranged from 220 to 40 ms. Cardiac output and heart rate were increased to simulate different levels of exercise. The optimal AVD was the one leading to the highest stroke volume (SV) and the lowest mean left atrial pressure (mLAP). At rest, in simulations with healthy myocardium the gain in SV by AVD optimization was larger compared to those with reduced contractility and stiff myocardium. However, mLAP was comparably decreased by AVD optimization in both healthy and diseased myocardium. During exercise, the optimal AVD shifted to shorter values, and mLAP was more sensitive to AVD, particularly in the presence of hypo-contractile and stiff myocardium. CONCLUSION:Simulations show that hypocontractility and stiffness reduce the effect of AVD optimization on SV but enhance its benefit in lowering mLAP. Notably, virtual patients with stiff ventricles experience greater benefits from AVD optimization during exercise compared to resting conditions. Furthermore, nsLBBP provides more favourable improvements in mLAP than BiVP.

Abstract Background Exercise-induced pulmonary hypertension, characterized by mean pulmonary artery pressure over cardiac output slope (mPAP/CO slope) > 3mmHg/L/min is associated with worse outcome in greater than moderate primary mitral regurgitation (PMR). However, the prognostic value of right ventricle to pulmonary artery coupling (RVPAc) is unknown. Purpose Assess the prognostic value of RVPAc; determine the additional value of exercise over rest RVPAc and compare these findings to the mPAP/CO slope. Methods The single center study included consecutive patients with greater than moderate PMR, no/discordant symptoms, left ventricular ejection fraction >60% and absence of concomitant valvular disease greater than moderate or permanent atrial fibrillation (AF) referred to simultaneous CPET and exercise echocardiography (CPET-echo). A thorough echocardiographic assessment of right ventricle (RV) systolic function and RVPAc (TAPSE/sPAP, ratio of tricuspid annular plane systolic excursion over systolic pulmonary artery pressure) was performed using a dedicated RV window. mPAP and CO were obtained by Doppler echocardiography. Primary outcome was the composite of cardiovascular mortality, unplanned cardiovascular hospitalization and new AF episodes. Results A total of 159 consecutive patients (64±11 years, 59% men) were included. The event-free survival rate was 84% at 1 year and 78% at 2 years. Patients who fulfilled the primary combined endpoint had significantly larger left atrium indexed volumes (LAVi), lower left atrial strain and strain rate at rest and strain at intermediate exercise, lower absolute and normalized peak oxygen uptake (VO2peak), and a significantly higher mPAP/CO slope. They had significantly lower TAPSE, RV free wall S’ and TAPSE/sPAP. Sequentially adding intermediate or high exercise TAPSE/sPAP and percent-predicted VO2peak to the baseline predictive model (age, LAVi, mitral regurgitation grade and TAPSE/sPAP at rest) significantly improved the area under the curve (AUC) of the baseline logistic regression model (AUC: 0.71 vs. 0.80 and 0.71 vs. 0.81, p<0.05, respectively), with LAVi and TAPSE/sPAP at intermediate or high exercise remaining as significant independent variables (although coupling assessment at high exercise technically less feasible). Replacing exercise TAPSE/sPAP with mPAP/CO yields models with comparable accuracy (Figure 1). Exercise TAPSE/sPAP <0,6 was related to a higher event rate (Figure 2) Conclusion Decreased rest or exercise TAPSE/sPAP are single point measures of RVPAc, associated with adverse outcome in patients with greater than moderate PMR and no or discordant symptoms. Exercise TAPSE/sPAP has independent additional value over rest TAPSE/sPAP in predicting adverse events, with a similar accuracy as mPAP/CO slope. Exercise TAPSE/sPAP represents a potential alternative to mPAP/CO slope in this population, being readily available and simpler to adopt in clinical practice.

OBJECTIVE:Atrial fibrillation (AF) is a common comorbidity in patients with heart failure with preserved ejection fraction (HFpEF) that contributes to increased morbidity and mortality. We sought to evaluate the impact of AF on key HFpEF features, including exercise tolerance (peak oxygen uptake, VO2peak) hemodynamic responses, and peripheral oxygen extraction (a-vO2diff). METHODS:Patients referred to a multidsciplinary clinic for evaluation of unexplained dyspnea and diagnosed with HFpEF after a comprehensive clinical and hemodynamic evaluation were stratified on the basis of whether they were in persistent/permanent AF (AFPersist; n = 86), paroxysmal AF (AFParox; n = 328), or sinus rhythm (SR; n = 274). Cardiopulmonary exercise testing with simultaneous echocardiography was applied to assess the VO2peak, a-vO2diff, and exercise hemodynamics. Groups were compared using analysis of covariance with adjustment for age, sex, body mass index, and the presence of hypertension and diabetes. RESULTS:Compared with patients in SR or with AFParox, patients with HFpEF and AFPersist had a lower VO2peak (1.3-2.4 mL/kg/min lower, P < .001). This coincided with lower peak exercise cardiac output (CO, 0.6-1.2 L/min lower), secondary to a lesser stroke volume (14-17 mL lower, P < .001), and a smaller left ventricular end-diastolic volume (15-18 mL lower, P < .001) that tended to decrease during exercise. In contrast, there was no impact of AF status on peak exercise a-vO2diff, mean pulmonary artery pressure or the mean pulmonary artery pressure/CO slope. CONCLUSIONS:Patients with HFpEF and AFPersist have a lower VO2peak secondary to decreased CO, SV, and reduced end-diastolic volume reserve. Rhythm control strategies may therefore be pivotal in optimizing exercise performance and clinical outcomes in patients with HFpEF and AF.

Background The impact of pulmonary vein isolation (PVI) using pulsed field ablation (PFA) on left atrial (LA) function remains incompletely understood. Objective To compare the effects of PVI performed with PFA vs radiofrequency ablation (RFA) on LA mechanical function in patients with paroxysmal atrial fibrillation (PAF), using serial echocardiographic strain analysis. Methods In this prospective, single-center study, patients undergoing a first-time PVI for PAF with either RFA or PFA were included. All participants underwent transthoracic echocardiography with 2-dimensional speckle tracking analysis at 3 time points: at baseline (immediately before ablation), in the acute phase (immediately after ablation), and in the chronic phase (3 months post-ablation). LA reservoir strain (LASr) and LA contraction strain (LASct) were assessed as primary parameters of LA mechanical function. Results A total of 59 patients were analyzed (RFA: 28; PFA: 31). In the PFA group, LASr and LASct decreased significantly in the acute phase (LASr: 26.5 ± 5.8% to 22.9 ± 6.6%, P = .010; LASct: 12.2 ± 3.6% to 8.6 ± 3.1%, P < .001). At 3-month follow-up, LASr had recovered to baseline levels (25.8 ± 7.9%, P = .531), while LASct remained significantly reduced (10.9 ± 4.3%, P = .031). In contrast, no significant changes in LASr or LASct were observed in the RFA group at any time point. Conclusion PVI using PFA is associated with acute LA stunning, with persistent impairment in contractile function at 3 months despite recovery of reservoir function. These findings suggest subtle, lasting alterations in atrial mechanics not observed with RFA.

Exercise-induced cardiac remodeling is well-described in male athletes but incompletely understood in females. This study aimed to examine sex-differences in cardiac structure, function and fibrosis relative to fitness, and to determine reference ranges for ‘normal’ chamber size in a large cohort of healthy male and female highly trained endurance athletes. This multi-centre international study utilised cardiac magnetic resonance imaging and cardiopulmonary exercise testing (VO2peak) to assess sex-specific relationships between measures of biventricular chamber size, function, fibrosis and VO2peak. Of the 364 endurance athletes included, 36.5% were female. Compared to males, female athletes achieved lower VO2peak (50.7 [40.2-57.0] vs 59.0 [41.0–65.0]mL/kg/min, p<0.001), had smaller absolute and BSA-indexed left and right end-diastolic volumes (LVEDV and RVEDV, respectively) but similar volumes when indexed to fat-free mass. Both sexes showed a strong association between LVEDV and VO2peak (r=0.60-0.66) and a similar co-efficient describing the linear relationship between VO2peak and LVEDV (Figure 1, Females: VO2peak[mL/min] = 12.1*LVEDV+963.9; Males: VO2peak = 15.3*LVEDV+806.8, p=0.100) and BSA-indexed LVEDV (Females: VO2peak[mL/kg/min] = 0.37*LVEDV/BSA+12.5; Males: VO2peak = 0.51*LVEDV/BSA-1.2, p=0.059). There was no difference between right ventricular (RV) measures and VO2peak, however males had a 3.8 times higher odds of reduced RV ejection fraction. Prevalent myocardial scar was similar for both female (14.2%) and male (19.9%) athletes (Figure 2, p=0.180). Female and male athletes demonstrate similar cardiac remodeling relative to fitness and no sex difference in myocardial scar. The female athlete’s heart can show profound adaptation and previous assertions that female hearts have lesser capacity for remodeling should be reappraised.Figure 1.Ventricular Size and FitnessFigure 2.Myocardial Fibrosis by Sex

BACKGROUND:A greater prevalence of arrhythmias has been described in endurance athletes, but it remains unclear whether this risk persists after detraining. We aimed to evaluate the prevalence of arrhythmias and their relationship with cardiac remodeling in lifelong and retired master endurance athletes compared to non-athletic controls. METHODS:We performed a cross-sectional analysis of observational studies that used echocardiography and cardiac magnetic resonance to detail cardiac structure and function, and Holter monitors to identify atrial and ventricular arrhythmias in 185 endurance athletes and 81 non-athletic controls aged ≥40 years. Athletes were categorized as active lifelong (n = 144) or retired (n = 41) based on hours per week of high-intensity endurance exercise within 5 years of enrollment and validated by percentage of predicted maximal oxygen consumption (VO2max). Athletes with overt cardiomyopathies, channelopathies, pre-excitation, and/or myocardial infarction were excluded. RESULTS:Lifelong athletes (median age = 55 years (interquartile range (IQR): 46-62), 79% male) were significantly fitter than retired athletes (median age = 66 years (IQR: 58-71), 95% male) and controls (median age = 53 years (IQR: 48-60), 96% male), respectively (predicted VO2max: 131% ± 18% vs. 99% ± 14% vs. 98% ± 15%, p < 0.001). Compared to controls, athletes in our cohort had a higher prevalence of atrial fibrillation ((AF): 32% vs. 0%, p < 0.001) and non-sustained ventricular tachycardia ((NSVT): 9% vs. 1%, p = 0.007). There was no difference in prevalence of any arrhythmia between lifelong and retired athletes. Lifelong athletes had larger ventricular volumes than retired athletes, who had ventricular volumes similar to controls (left ventricular end-diastolic volume indexed to body surface area (LVEDVi): 101 ± 20 mL/m2vs. 86 ± 16 mL/m2vs. 94 ± 18 mL/m2, p < 0.001; right ventricular end-diastolic volume indexed to body surface area (RVEDVi): 117 ± 23 mL/m2vs. 101 ± 19 mL/m2vs. 100 ± 19 mL/m2, p < 0.001). Athletes had more scar (40% vs. 18%, p = 0.002) and larger left atria (median volume = 45 mL/m2 (IQR: 38-52) vs. 31 mL/m2 (IQR: 25-38), p < 0.001) than controls, with no difference in atrial volumes and non-ischaemic scar between the athlete groups. CONCLUSION:Master endurance athletes have a higher prevalence of AF and NSVT than non-athletic controls. Whereas ventricular remodeling tends to reverse with detraining, the propensity to arrhythmias persists regardless of whether they are actively exercising or retired.