The relationship between exercise training and overall cardiovascular health is well defined, with associated reductions in incidence of cardiovascular disease and comorbidities such as hypertension, diabetes mellitus, cholesterol profile, body weight, and even some forms of cancer. In this regard, an exercise prescription is an effective tool to decrease all-cause mortality and improve overall health. As providers, properly educating patients on the type, amount, and intensity of exercise is important to ensure patients meet recommended exercise metrics to experience these health benefits. This review provides a concise, but comprehensive overview of the structural and functional aspects of exercise-induced cardiac remodeling, current recommended guidelines for exercise with supporting data, as well as the impact exercise has on various cardiovascular outcomes.

Endurance sports disciplines largely differ in terms of specific training and event modalities, likely resulting in diverse morpho-functional cardiac changes. Our study aims to assess elite athletes engaged in different endurance disciplines and describe cardiac remodelling in each. We enrolled 282 Olympic athletes (58.5% males, mean age 26.7 ± 4.7) practising long-distance running (57, 20.2%), triathlon (18, 6.4%), canoeing/rowing (76, 26.9%), cycling (65, 23%), long-distance swimming (21, 7.4%), cross-country skiing & biathlon (45, 16%). athletes underwent ECG, echocardiogram and exercise stress-test. Eccentric LV hypertrophy (EH) was present in 73.8% of athletes, without gender differences (p = 0.847), varying greatly among disciplines (p = 0.0005). Triathlon (94.4%) and cycling (87.7%) showed the highest prevalence. The largest LV volumes were observed in triathlon-athletes and cyclists (LVEDVi: males, p = 0.009, females, p = 0.002). The lowest LV dimensions were found in rowing/canoeing (males: p < 0.0001; females: p < 0.0001). Long-distance runners and swimmer presented intermediate extent of LV remodelling. Positive correlation between hours of training and LVMi (p = 0.0004) and LVEDVi (p = 0.048) was observed among cyclists. Indeed, cyclists with the highest EH (i.e., lowest LVMi\LVEDVi ratio) achieved the highest workload at exercise stress-test (p = 0.045) and better athletic achievements. Among endurance athletes, cyclists and triathletes present the most marked extent of LV EH, while canoeists and rowers the lowest degree, with major increase in LV mass. Intra-group analysis showed an association between eccentric hypertrophy and superior exercise capacity and higher athletic performances that may be related to an increased stroke volume and cardiac output, which improve cardiovascular efficiency during endurance exercise. These findings could be useful both for clinicians in identifying potential health issues in athletes and for coaches when assessing athletes' training status.

Participating in lifelong endurance sports is associated with an increased risk of atrial fibrillation (AF), potentially mediated through the process of left atrial (LA) remodeling which includes the progression of atrial fibrosis. This cross-sectional cohort study aimed to investigate LA remodeling including the presence and localization of LA fibrosis in lifelong endurance athletes. 42 master endurance athletes (76% male, age 54 ± 9 years), participating in Ironman races, (ultra) marathons and the Cape Epic Mountain Bike races, underwent clinical assessment with questionnaires, physical examination, and cardiac MRI (CMR). LA function, volumes, and left ventricular volumes were assessed. The extent of LA fibrosis, both global and regional, was derived from post-processed 3D late gadolinium-enhanced images using ADAS 3D. The median LA fibrotic burden as assessed by LGE-CMR was 2.5% (interquartile range, 1.1 to 7.6%). Fibrosis was heterogeneously distributed across the LA wall, with the highest burden observed along the left aspect of the posterior wall. There were no significant associations between LA fibrotic burden and atrial volume or functional parameters. Similarly, no associations were observed between fibrotic burden and sports level or training duration. LA fibrotic burden was significantly higher in participants who competed in long-distance mountain bike races versus participants who did not (7.3% [4.1-9.5] vs. 2.0% [0.5-5.6], p = 0.03). This study demonstrates the limited amount of LA fibrosis in lifelong master endurance athletes, with uneven distribution along the LA wall, most notably around the posterior side of the left inferior pulmonary vein. Participants engaged in long-distance mountain bike races exhibited significantly higher LA fibrotic burden, underscoring the potential impact of specific sports disciplines on LA remodeling, which may play a role in AF development.

High-intensity resistance training induces structural and functional adaptations in skeletal muscle, yet its impact on cardiac remodeling remains debated. This study aimed to investigate the longitudinal biventricular cardiac response to a 20-week high-intensity resistance training program in previously untrained, healthy males and examine the association between muscle strength gains and cardiac remodeling.

Twenty-seven male volunteers (aged 18-40 years) participated in a high-intensity resistance training program for 20 weeks. Assessments at baseline, 12 weeks, and 20 weeks included resting blood pressure, electrocardiogram (ECG), three-dimensional transthoracic echocardiography (3DTTE), cardiopulmonary exercise testing ([Formula: see text]O2peak), isokinetic dynamometry for muscle strength, and actimetry recordings. Time effects were analyzed using one-way repeated measures ANOVA (P < 0.05).

Twenty-two participants completed the study. Resistance training led to significant reductions in arterial systolic and diastolic blood pressure and heart rate. After 20 weeks of training, 3DTTE showed a significant increase in left ventricular (LV) mass (120.1 ± 15.4 g vs. 133.7 ± 16.3 g, p < 0.001), without inducing LV hypertrophy. Balanced increases were observed in LV end-diastolic volume (146.4 ± 18.9 ml vs. 157.9 ± 19.6 ml, p < 0.001) and right ventricular (RV) end-diastolic volume (119 ± 19.4 ml vs. 129.2 ± 21.6 ml, p < 0.001). LV and RV systolic and diastolic function remained unchanged. There were no changes in [Formula: see text]O2peak or daily activity levels. Maximal muscle strength in the quadriceps, hamstrings, triceps, and biceps was significantly correlated with LV and RV end-diastolic volumes and LV mass (p ≤ 0.001).

The resistance training program resulted in significant and rapid muscle strength gains and reduced blood pressure. Cardiac adaptations, including moderate biventricular dilatation, were observed without changes in cardiac function or [Formula: see text]O2peak and were associated with muscle strength gains. Our study highlights that intensive resistance training in novice male resistance trainers induces an adaptive cardiac response, reflecting a physiological adaptation linked to enhanced muscle performance.

ClinicalTrials.gov ID: NCT04187170.

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.

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.

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 < 0.001). 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.

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.

The use of a fixed theoretical-proportional-factor (TPF15) is one of the indirect highest-oxygen-consumptions (HOC) assessment methods, but it may not accurately reflect the physiological differences across various sports (cycling-triathlon-running-football-multisport). The aim of this study is to evaluate the variability of TPF across different sports, proposing a series of sport-specific new TPF values for more accurate HOC estimation.

A sample of 340 adults (26.01 ± 7.18 years) performed a maximal-incremental-test using sport-specific-ergometers. HOC was considered for cycling V ˙ O 2peak , whereas for the other investigated sports it was consideredV ˙ O 2max . HOC was directly measured using a gas-analyzer, and TPF values were calculated using heart rate (HR): the ratio of HRmax/HRrest multiplied for the measured values of HOC. A one-way ANOVA was used to measure differences and Bland-Altman plots were constructed to compare predicted and actual V ˙ O 2max /V ˙ O 2peak .

Actual HOC was significantly greater than those predicted by the fixed TPF15 (P < 0.001). Sport-specific new TPF values ranged from 16.55 in multisport to 20.15 in cycling, consistently exceeding the old fixed TPF15, and predicting therefore better HOC. The new TPF exhibited a closer agreement with the directly measuredV ˙ O 2max /V ˙ O 2peak  compared to the TPF15. Furthermore, the new TPF reduced the typical-measurement-error (14.94-17.78%) compared to TPF15 (15.63-24.13%).

This study suggests that new TPF values predictV ˙ O 2max /V ˙ O 2peak  with higher accuracy compared to the traditional method. The use of HRmax and HRrest values allows to customize training programs for different athletes. Future research should focus on validating these findings across larger populations of athletes.

Background and Objectives: Regular exercise is known to induce cardiovascular adaptations collectively referred to as "athlete's heart". While previous research has explored the morphological and functional cardiac adaptations in athletes, the relationship between vitamin D (25-hydroxyvitamin D [25(OH)D]) levels and echocardiographic parameters remains underexplored. This study aims to assess the association between 25(OH)D levels and structural and functional cardiac parameters using electrocardiographic (ECG) and echocardiographic evaluations in athletes. Materials and Methods: This case-control study included 93 male athletes, categorized into professional (n = 68) and recreational (n = 25) groups. Professional athletes were further divided into football (n = 19), weightlifting (n = 22), and running (n = 27) subgroups. Serum 25(OH)D levels were measured using high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS). Standard 12-lead ECG and transthoracic echocardiography were performed to assess cardiac structure and function. Data were analyzed using statistical tests that were appropriate for normal and non-normal distributions, with a significance level set at p < 0.05. Results: Athletes exhibited higher left ventricular interventricular septum (IVS) thickness and left ventricular posterior wall thickness (LVPWd) compared to the control group. Significant differences in diastolic function parameters, including early (E) and late (A) diastolic filling velocities and the E/A ratio, were observed among athlete subgroups. The weightlifting group showed lower end-systolic diameter (ESD) values than the football group. However, no statistically significant relationship was found between 25(OH)D levels and echocardiographic diastolic parameters. While more than half of the athletes had insufficient 25(OH)D levels (<30 ng/mL), their average values were higher than those reported in previous studies. Conclusions: This study demonstrates that 25(OH)D levels do not significantly influence echocardiographic diastolic parameters in athletes. However, notable differences in structural and functional cardiac findings were observed among different sports disciplines. These findings contribute to the understanding of cardiac adaptations in athletes and suggest that 25(OH)D may not play a crucial role in diastolic function. Further research is needed to explore the long-term effects of vitamin D on athletic cardiac performance.

The cardiac morphology of elite athletes is related to sports disciplines and race; however, no studies have examined the effects of sports discipline on East Asian athletes. Therefore, this study aimed to assess left ventricular (LV) remodeling using transthoracic echocardiography in elite Japanese athletes and establish standard values for the indicators of the cardiac morphology of elite athletes in East Asia, considering the influence of body size.

We retrospectively evaluated 1,363 elite Japanese athletes who underwent electrocardiography and transthoracic echocardiography between January 2011 and December 2021. The athletes were assigned to four sports discipline categories (skill, power, mixed, and endurance). We evaluated the differences in LV volume and mass between the groups for each sex.

The LV end-diastolic volume (LVEDV) and LV mass indexed to the body surface area (BSA) in the endurance group (LVEDV/BSA: 72.3 ± 11.4 mL/m2 in males and 68.7 ± 11.0 mL/m2 in females, LV mass/BSA: 121.1 ± 19.1 g/m2 in males and 106.5 ± 18.0 g/m2 in females) were significantly larger than those of any other groups. Both values were affected by sex, BSA, and endurance sport type, whereas only LV mass was affected by age.

Cardiac remodeling is proportional to the sport type, with a significantly greater effect in athletes playing endurance sports. The remodeling is particularly evident in the left ventricle; however, the corresponding remodeling is also observed in other heart chambers. Cardiac remodeling in elite Japanese athletes is similar to that observed in elite athletes of other races, except for the changes in LV wall thickness.

The complex phenomenon of the athlete's heart (AH) describes the chronic physiological structural and functional adaptation secondary to repeated exposure of an acute exercise stimulus.

This narrative review is based on published evidence.

Highly trained athletic individuals frequently display cardiac parameters which are suggestive of an AH and can exceed the traditional 'normal' limits.

The physiological processes underpinning the extent of cardiac adaption and how this is closely linked to exercise type, but also sex, ethnicity, and body size.

Since its seminal description by Morganroth and colleagues in 1975, our understanding of the AH has evolved in tandem with improvements in cardiac imaging techniques alongside the exploration of more diverse athletic populations. This narrative review aims to provide a balanced discussion of the multi-factorial nature of structure and function of the AH with specific reference to the unique physiological exercise stimuli.

Despite great interest in cardiac adaptations across a broad spectrum of athletic populations, future research designs should consider the use of new and novel imaging techniques to enhance our understanding of the acute cardiovascular responses which ultimately mediates such adaptations, especially in athletic populations underrepresented in the literature.

Long-term endurance training is associated with structural, functional, and biochemical markers of cardiac dysfunction in highly trained athletes. Many studies have focused on structural changes in the right ventricle (RV) and few have examined functional adaptation of the right ventricle. This meta-analysis aims to compare the changes in right ventricular systolic function between endurance athletes and controls before and after exercise using speckle tracking echocardiography (STE).

A comprehensive search of relevant studies published before March 19, 2024 that examined RV systolic function using speckle tracking technology was conducted. Weighted mean differences (WMDs) and 95% confidence intervals (CIs) were used as pooled statistics. Meta regression was employed to identify sources of heterogeneity and publication bias was evaluated by Egger's test and funnel plots. Sensitivity analysis was performed by removing sources of significant change from the results of a single publication to evaluate the stability of the results.

Twenty studies were included with 1186 participants. A fixed effect meta-analysis revealed RV global longitudinal strain (GLS) WMD = 0.40, 95% CI (-0.08 ~ 0.89), p = 0.102 and free wall longitudinal strain (FWLS) WMD = 0.62, 95% CI (0.28 ~ 0.96), p < 0.001, random effect models of RV basal strain WMD = 2.94, 95% CI (2.00 ~ 3.88), p < 0.001 and RV apical strain WMD = -0.79, 95% CI (-1.95, 0.37), p = 0.245 between endurance athletes and controls. In addition, a random-effects meta-analysis revealed significant impairments in RV function when assessed by comparing RV GLS pre-endurance versus post endurance exercise WMD = 2.51, 95% CI (1.634 ~ 3.40), p < 0. 001.

The evidence obtained thus far suggests that reporting only global right ventricular strain data may obscure segment-specific adaptation changes, and the use of global and segmental strain analysis may help to identify potential functional changes in the right ventricle while differentiating between normal endurance athletes and non-active controls.

Concerns exist that long-term cardiac alterations occur after severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection, particularly in patients who were hospitalized in the acute phase or who remain symptomatic. This study investigates potential long-term functional and morphological alterations after SARS-CoV-2 infection.

The authors of this study investigated patients after SARS-CoV-2 infection by using a mobile 1.5T clinical magnetic resonance scanner for cardiac alterations. Cardiac function and dimensions were assessed using a highly efficient cardiac magnetic resonance protocol, which included cine sequences, global longitudinal and circumferential strain assessed by fast-Strain-ENCoded imaging, and T1 and T2 mapping. We assessed symptoms through a questionnaire. Patients were compared with a control group matched for age, gender, body mass index, and body surface area.

Median follow-up time was 395 (192-408) days. The final population included 183 participants (age 48.4 ± 14.3 years, 48.1% male (88/183)). During the acute phase of SARS-CoV-2 infection, 27 patients were hospital-admitted. Forty-two patients reported persistent symptoms (shortness of breath, chest pain, palpitations, or leg edema), and 63 reported impaired exercise tolerance. Left ventricular (LV) functional and morphological parameters were within the normal range. T1- and T2-relaxation times were also within the normal range, indicating that the presence of myocardial edema or fibrosis was unlikely. Persistently symptomatic patients showed a slightly reduced indexed LV stroke volume. Functional parameters remained normal in patients who were hospitalized for SARS-CoV-2, persistently symptomatic, or with ongoing impaired exercise tolerance.

Irrespective of ongoing symptoms or severity of prior illness, patients who have recovered from SARS-CoV-2 infection demonstrate normal functional and morphological cardiac parameters. Long-term cardiac changes due to SARS-CoV-2 infection appear to be rare.

Hypertrophic cardiomyopathy (HCM) is the most common hereditary cardiomyopathy. It is often caused by mutations of genes encoding for sarcomeric or sarcomere-associated proteins. Despite its clinical importance, divergent definitions are published by major cardiology societies. Some regard HCM as a specific genetic disease, whereas others define it as a broad 'spectrum of the thick heart'. The present narrative review aimed to assess both definitions from a pathoanatomical perspective. As a conjoint interdisciplinary and translational approach is needed to further increase knowledge and improve the understanding of HCM, the PubMed database was searched using several advanced search algorithms to explore the perspectives of the (forensic) pathologist, clinician, and basic researcher regarding the difference between the definitions of HCM. This discrepancy between definitions can impact critical data, such as prevalence and mortality rate, and complicate the understanding of the disease. For example, due to the different definitions, research findings regarding molecular changes from studies applying the narrow definition cannot be simply extended to the 'spectrum' of HCM.

The risk of cardiovascular disease increases significantly after menopause. We sought to assess the impact of different activity levels on cardiac structure and function in postmenopausal women. We grouped age-similar, postmenopausal women by self-reported physical activity levels over two decades. The study involved 34 women (age 61 ± 1 years; 11 ± 2 postmenopausal years; body mass index 23 ± 3 kg/m2) categorized into three activity tiers: sedentary (SED; ≤1 h exercise weekly; n = 9); moderately active (MOD; ≥2 ≤6 h low/moderate intensity exercise weekly; n = 11) and highly active (HIGH; >4 h of moderate/high intensity exercise weekly; n = 14). Maximum oxygen uptake (VO2max) differed significantly (p < 0.05) between the groups (24.9 ± 5.8; 30.5 ± 5.8; 38.4 ± 4.4 mL O2/kg/min; SED, MOD and HIGH respectively). Conversely, there were no differences (p > 0.05) in height, Total fat-free mass, body surface area or in echocardiographic measures of left ventricular (LV) morphology, systolic function, diastolic function and right ventricular function. Contrary to our hypothesis, these findings reveal that marked differences in activity level and VO2max are not reflected in measures of LV morphology or echocardiographic indicators of cardiac diastolic or systolic function in postmenopausal women of similar body size.

Cardiac remodelling is often most profound in male athletes and in athletes with the greatest volumes of endurance training and is characterized by chamber enlargement and a mild-to-modest hypertrophy. The diastolic filling of the left ventricle (LV) is a complex process including the early recoil of the contracted LV, the active relaxation of the myocardium, the compliance of the myocardium, the filling pressures, and heart rate. Echocardiography is the cornerstone for the clinical assessment of LV diastolic function. LV diastolic function is usually enhanced in elite endurance athletes characterized by improved early filling of the ventricle, while it is preserved or enhanced in other athletes associated with the type of training being performed. This allows for the high performance of any endurance athlete. Typical findings when using resting echocardiography for the assessment of LV diastolic function in endurance athletes include a dilated LV with normal or mildly reduced LV ejection fraction (EF), significantly enlarged left atrium (LA) beyond the commonly used cut-off of 34 mL/m2, and a significantly elevated E/A ratio. The early-diastolic mitral annular velocity and the E-wave peak velocity are usually normal. Importantly, interpretation of the echocardiographic indices of LV diastolic function should always consider the clinical context and other parameters of systolic and diastolic functions. In the absence of an underlying pathology, single measurements outside the expected range for similar athletes will often not represent the pathology.

Cardiac phenotypic plasticity, the remodelling of heart structure and function, is a response to any sustained (or repeated) stimulus or stressor that results in a change in heart performance. Cardiac plasticity can be either adaptive (beneficial) or maladaptive (pathological), depending on the nature and intensity of the stimulus. Here, we draw on articles published in this Special Issue of Journal of Experimental Biology, and from the broader comparative physiology literature, to highlight the core components that enable cardiac plasticity, including structural remodelling, excitation-contraction coupling remodelling and metabolic rewiring. We discuss when and how these changes occur, with a focus on the underlying molecular mechanisms, from the regulation of gene transcription by epigenetic processes to post-translational modifications of cardiac proteins. Looking to the future, we anticipate that the growing use of -omics technologies in integration with traditional comparative physiology approaches will allow researchers to continue to uncover the vast scope for plasticity in cardiac function across animals.

Non-specific myocardial fibrosis (NSMF) is a heterogeneous entity. We aimed to evaluate young athletes with and without NSMF to establish potentially clinically significance.

We analysed data from 328 young athletes. We identified 61 with NSMF and compared them with 75 matched controls. Athletes with NSMF were divided into Group 1 (n = 28) with 'minor' fibrosis and Group 2 (n = 33) with non-insertion point fibrosis, defined as 'major'. Athletes were followed-up for adverse events. Finally, we tested various machine learning (ML) algorithms to create a prediction model for 'major' fibrosis. We created 4 different classifiers.

Athletes of black ethnicity were more likely to have a subepicardial pattern (OR: 5.0, p = 0.004). Athletes with 'major' fibrosis demonstrated a higher prevalence of lateral T-wave inversion (TWI) ( < 0.001) and ventricular arrhythmias (VEs > 500/24 h, p = 0.046; non-sustained VT, p = 0.043). Athletes with 'minor' fibrosis demonstrated higher right ventricular volumes (p = 0.013), maximum Watts (p = 0.022) and maximum VO2 (p = 0.005). Lateral TWI (p = 0.026) and VO2 < 44 mL/min/Kg (p = 0.040) remained the only significant predictors for 'major' fibrosis. During follow up, athletes with 'major' fibrosis were 9.1 times more likely to exhibit adverse events (OR 13.4, p = 0.041). All ML models outperformed the benchmark method in predicting significant MF, best accuracy achieved by the random forest classifier (90%).

Lateral TWI and reduced exercise performance are associated with higher burden of fibrosis. Fibrosis was associated with increased ventricular arrhythmia and adverse events. A comprehensive assessment can help develop a ML-based model for significant fibrosis, which could also guide clinical practice and appropriate CMR referrals.

Background: The foot racing disciplines include sprints, middle distances, and long distances, which vary in terms of intensities, duration of training, and metabolic demands. The aim of our study was to evaluate the differences in morpho-functional parameters describing cardiac remodeling in a large cohort of Olympic athletes practicing the different track subspecialties. Methods: We evaluated 140 track and field (52.1% males, mean age 26.3 ± 4.3 years) Olympic athletes divided into four groups according to the distance performed: Group A (46, 32.9%): 100 and 200 mt; Group B (34, 24.3%): 400 mt; Group C (25, 17.9%): 800, 1500, and 3000 mt; Group D (35, 24.9%): 5000, 10,000 mt, and marathon distance. The athletes underwent a pre-participation screening, which included transthoracic echocardiography and exercise stress testing. Results: In Group A and in Group B, most athletes presented normal cardiac geometry (41/46, 89.1% in Group A and 31/34, 91.2% in Group B, p < 0.0001). Instead, in Groups C and D, more than half presented eccentric cardiac remodeling (13\25, 52% in Group C and 23\35, 65.7% in Group D). No significant differences were found between subspecialties in LVEF (p = 0.587), diastolic function (p = 0.431), and training hours/week (p = 0.078). Conclusions: In conclusion, the presence and extent of cardiac remodeling vary according to the distance of the discipline practiced, with the largest dimensional increase in both left and right ventricles and atria in mid- and long-distance runners and the lowest in sprinters.

Exercise-induced hypertension (EIH) is thought to be associated with increased cardiovascular (CV) risks. However, no previous studies have investigated the effects of EIH on CV systems in marathon runners without CV risk factors using both 24-hr ambulatory blood pressure (BP) monitoring and exercise stress echocardiography (ESE). This study firstly described differences in CV adaptations according to EIH assessed by both exams. Marathon runners between 35 and 64 years of age without CV risk factors were eligible. All the participants underwent both 24-hr ambulatory BP monitoring and ESE. EIH was defined as a maximal exercise systolic BP≥210 mmHg. The EIH group (n=19) had shorter training history and higher exercise intensity compared to the non-EIH group (n=23). The average systolic BP was higher in the EIH group than in the non-EIH group. Left cardiac chamber size and left ventricular mass (LVM) were also higher in the EIH group compared to the non-EIH group. Maximal BP during ESE was positively correlated with both parameters. Exaggerated BP response during exercise needs to be monitored for pre-emptive measurements before it results in progressive cardiovascular maladaptation.

Athlete's heart (AH) represents the heart's remarkable ability to adapt structurally and functionally to prolonged and intensive athletic training. Characterized by increased left ventricular (LV) wall thickness, enlarged cardiac chambers, and augmented cardiac mass, AH typically maintains or enhances systolic and diastolic functions. Despite the positive health implications, these adaptations can obscure the difference between benign physiological changes and early manifestations of cardiac pathologies such as dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and arrhythmogenic cardiomyopathy (ACM). This article reviews the imaging characteristics of AH across various modalities, emphasizing echocardiography, cardiac magnetic resonance (CMR), and cardiac computed tomography as primary tools for evaluating cardiac function and distinguishing physiological adaptations from pathological conditions. The findings highlight the need for precise diagnostic criteria and advanced imaging techniques to ensure accurate differentiation, preventing misdiagnosis and its associated risks, such as sudden cardiac death (SCD). Understanding these adaptations and employing the appropriate imaging methods are crucial for athletes' effective management and health optimization.

Intensive training efforts are associated with hemodynamic changes accompanied by increases in cardiac output and stroke volume related to higher peak oxygen consumption and better athletic performance during exercise. These hemodynamic changes induce an enlargement of cardiac chambers, but also of the atria and may result in an athletes' heart (AH). Data from large studies about atrial enlargement in AH are sparse.

Competitive athletes aged ≥18 years, who presented for pre-participation screening 04/2020-10/2021 were included in this study and stratified for AH (defined as physiologically increased heart volume >13.0 in males and >12.0 mL/kg in females).

Overall, 646 athletes aged ≥18 years (median age 24.0 [20.0/31.0] years; 206 [31.9%] females) were included in our study 04/2020-10/2021; among these, 118 (18.3%) had an AH. The computed absolute heart volume was 969.4 (853.1/1083.0) mL in athletes with AH and 841.3 (707.4/966.3) mL in those without AH (p < 0.001). AH was associated with larger left ventricular mass (206.6 ± 39.0 vs. 182.7 ± 44.2 g, p < 0.001). LA area (15.4 [13.7/18.2] vs. 14.3 [12.0/16.3] cm2, p < 0.001) and RA area (15.8 [13.8/18.6] vs. 14.5 [12.3/17.0] cm2, p < 0.001) were enlarged in AH versus those athletes without AH. The logistic regressions confirmed an independent association of AH on LV mass (OR 1.05 [95% CI 1.04-1.06], p < 0.001). LA area (OR 1.29 [95% CI 1.19-1.39], p < 0.001) as well as RA area (OR 1.28 [95% CI 1.19-1.38], p < 0.001) were afflicted by AH.

An AH is accompanied by significant enlargement of the atria as well as increased cardiac muscle mass.

Transthoracic echocardiography (TTE) is routinely required during pre-participation screening in the presence of symptoms, family history of sudden cardiac death or cardiomyopathies <40-year-old, murmurs, abnormal ECG findings or in the follow-up of athletes with a history of cardiovascular disease (CVD). TTE is a cost-effective first-line imaging modality to evaluate the cardiac remodeling due to long-term, intense training, previously known as the athlete's heart, and to rule out the presence of conditions at risk of sudden cardiac death, including cardiomyopathies, coronary artery anomalies, congenital, aortic and heart valve diseases. Moreover, TTE is useful for distinguishing physiological cardiac adaptations during intense exercise from pathological behavior due to an underlying CVD. In this expert opinion statement endorsed by the Italian Society of Sports Cardiology, we discussed common clinical scenarios where a TTE is required and conditions falling in the grey zone between the athlete's heart and underlying cardiomyopathies or other CVD. In addition, we propose a minimum dataset that should be included in the report for the most common indications of TTE in sports cardiology clinical practice.

Previous studies demonstrated that variations of fT3, even within the euthyroid range, can influence cardiac function. Our aim was to investigate whether thyroid hormones, even within the euthyroid range, are associated with the magnitude of exercise-induced cardiac remodeling in Olympic athletes.

We evaluated 1342 Olympic athletes (mean age 25.6 ± 5.1) practicing different sporting disciplines (power, skills, endurance, and mixed). Athletes underwent blood testing (thyroid stimulating hormone, fT3, and fT4), echocardiography, and exercise-stress testing. Athletes taking thyroid hormones, affected by thyroiditis, or presenting TSH out of ranges were excluded.

The level of thyroid hormones varied according to the type of sporting discipline practiced: endurance athletes presented the lowest TSH (p < 0.0001), fT3 (p = 0.007), and fT4 (p < 0.0001) in comparison to the remaining ones. Resting heart rate (HR) was positively correlated to fT3 in athletes of different disciplines (power: p = 0.0002, R2 = 0.04; skill: p = 0.0009, R2 = 0.05; endurance: p = 0.007, R2 = 0.03; and mixed: p = 0.04, R2 = 0.01). The same results were seen for peak HR in the exercise-stress test in athletes engaged in power, skill, and endurance (respectively, p < 0.0001, R2 = 0.04; p = 0.01, R2 = 0.04; and p = 0.005, R2 = 0.02). Moreover, a positive correlation was observed with cardiac dimensions, i.e., interventricular septum (power: p < 0.0001, R2 = 0.11; skill: p = 0.02, R2 = 0.03; endurance: p = 0.002, R2 = 0.03; mixed: p < 0.0001, R2 = 0.04). Furthermore, fT3 was directly correlated with the left ventricle (LV) end-diastolic volume in skills (p = 0.04, R2 = 0.03), endurance (p = 0.04, R2 = 0.01), and mixed (p = 0.04, R2 = 0.01).

Thyroid hormones, even within the euthyroid range, are associated with cardiac adaptive response to exercise and may contribute to exercise-induced cardiac remodeling.

Background: According to the ESC guidelines, sport disciplines are classified in relation to the predominant component (skill, power, mixed and endurance), including a wide range of disciplines with different isometric/isotonic exercises and exercise-induced heart remodeling. The aim of our study was to evaluate differences in morpho-functional cardiac adaptations in power athletes, comparing judokas with weightlifters. Methods: We enrolled 55 Olympic athletes (38 judokas, 17 weightlifters), aged 24.5 ± 3.8 years, 25 (45.4%) of whom were males, and they underwent a pre-participation evaluation, including a physical examination, ECG, transthoracic echocardiogram, and exercise stress test. Results: The judokas presented significant differences in cardiac adaptations, with larger left ventricle (LV) end-diastolic and end-systolic volumes indexed (LVEDVi, p = 0.002 and LVESVi, p = 0.004) and higher LVMass values indexed (p = 0.033), but similar LV wall thicknesses (p = 0.093) and LV ejection fractions (p = 0.981). Also, the left atrium (LA) dimension (p = 0.0002) and volume indexed (p < 0.0001) were higher in the judokas, as were the larger right ventricle (RV) areas. Finally, the judokas showed higher VO2max (p = 0.012), O2 pulse (p = 0.007), VE/O2 LT1 (p = 0.041) and VE/O2 LT2 (p = 0.036) values, with a lower resting heart rate (p = 0.031) and higher exercise capacity (p = 0.011). Conclusions: The judokas showed substantial differences in cardiac morpho-functional adaptations from the weightlifters, and, accordingly, judo should be more properly considered not a pure strength sport but more similar to mixed disciplines of the ESC classification.

The effects of conditioning on cardiac function in young horses is still unknown. For this reason, this study evaluated the left ventricular (LV) function of young horses by echocardiography after six weeks of conditioning. Fourteen untrained young purebred Arabian horses were evaluated at rest and after a stress test (ST) before and after a six-week conditioning program. There was an increase in V4 (p < 0.001) after conditioning, as well as a reduction in both heart rate (HR) at rest and peak HR during the ST (p < 0.001). There was also a reduction in internal diameter, along with an increase in interventricular septal, free wall and mean thicknesses and LV mass (p < 0.05). After the ST, the conditioned animals showed higher values of velocity time integral, stroke volume, systolic and cardiac indices, ejection (ET) and deceleration times (DT), end-diastolic volume, time to onset of radial myocardial velocity during early diastole and time to peak of transmitral flow velocity, in addition to reduced pre-ejection period (PEP), PEP/ET ratio and mean velocity of circumferential fiber shortening (p < 0.05). The conditioning protocol promoted physiological adaptations that indicate an improvement in the animals' aerobic capacity associated with an enhanced left ventricular function.

Some individuals who go to fitness centers for various purposes perform resistance exercise (RE) alone, while others engage in combined exercise (CE) by including cardio exercises along with RE. Studying the effects of these two different training methods on left ventricular (LV) systolic and diastolic parameters and left atrial mechanical function is an important step toward understanding the effects of different types of exercise on cardiac function. This knowledge has significant implications for public health, as it can inform the development of targeted and effective exercise programs that prioritize cardiovascular health and reduce the risk of adverse outcomes. Therefore, the primary aim of this study is to comprehensively investigate the LV systolic and diastolic parameters of athletes who engage in RE and CE using ECHO, to contribute to the growing body of literature on the cardiovascular effects of different types of exercise. Forty-two amateur athletes aged between 17 and 52 were included in our study. The participants consisted of the RE (n = 26) group who did only resistance exercise during the weekly exercise period, and the CE group (n = 16) who also did cardio exercise with resistance exercises. After determining sports age (year), weekly exercise frequency (day), and training volume (min) in addition to demographic information of RE and CE groups, left ventricular systolic and diastolic parameters and left atrial functions were determined by ECHO. Findings from our study revealed that parameters including the left ventricular end-diastolic diameter (LVEDD) (p = .008), left ventricular end-diastolic volume (LVEDV) (p = .020), stroke volume index (SV-I) (p = .048), conduit volume (CV-I) (p = .001), and aortic strain (AS) (p = .017) were notably higher in the RE group compared to the CE group. Also left atrial active emptying volüme (LAAEV) of CE was higher than the RE group (p = .031). In conclusion, the cardiac parameters of the RE group showed more athlete's heart characteristics than the CE group. These results may help to optimize the cardiovascular benefits of exercise routines while minimizing the potential risks associated with improper training.

To evaluate the morphology of the "athlete's heart", left ventricular (LV) wall thickness (WT) and end-diastolic internal diameter (LVIDd) at rest were addressed in publications on skiers, rowers, swimmers, cyclists, runners, weightlifters (n = 927), and untrained controls (n = 173) and related to the acute and maximal cardiovascular response to their respective disciplines. Dimensions of the heart at rest and functional variables established during the various sport disciplines were scaled to body weight for comparison among athletes independent of body mass. The two measures of LV were related (r = 0.8; P = 0.04) across athletic disciplines. With allometric scaling to body weight, LVIDd was similar between weightlifters and controls but 7%-15% larger in the other athletic groups, while WT was 9%-24% enlarged in all athletes. The LVIDd was related to stroke volume, oxygen pulse, maximal oxygen uptake, cardiac output, and blood volume (r =  ~ 0.9, P < 0.05), while there was no relationship between WT and these variables (P > 0.05). In conclusion, while cardiac enlargement is, in part, essential for the generation of the cardiac output and thus stroke volume needed for competitive endurance exercise, an enlarged WT seems important for the development of the wall tension required for establishing normal arterial pressure in the enlarged LVIDd.

Increased left atrial (LA) size and reduced LA function have been associated with heart failure and atrial fibrillation (AF) in at-risk populations. However, atrial remodeling has also been associated with exercise training and the relationship between fitness, LA size, and function has not been defined across the fitness spectrum. In a cross-sectional study of 559 ostensibly healthy participants, comprising 304 males (mean age, 46 ± 20 yr) and 255 females (mean age, 47 ± 15 yr), we sought to define the relationship between cardiorespiratory fitness (CRF), LA size, and function. We also aimed to interrogate sex differences in atrial factors influencing CRF. Echocardiographic measures included biplane measures of LA volumes indexed to body surface area (LAVi) and atrial deformation using two-dimensional speckle tracking. CRF was measured as peak oxygen consumption (V̇o2peak) during cardiopulmonary exercise testing (CPET). Using multivariable regression, age, sex, weight, and LAVi (P < 0.001 for all) predicted V̇o2peak (P < 0.001, R2 = 0.66 for combined model). After accounting for these variables, heart rate reserve added strength to the model (P < 0.001, R2 = 0.74) but LA strain parameters did not predict V̇o2peak. These findings add important nuance to the perception that LA size is a marker of cardiac pathology. LA size should be considered in the context of fitness, and it is likely that the adverse prognostic associations of increased LA size may be confined to those with LA enlargement and low fitness.NEW & NOTEWORTHY Left atrial (LA) structure better predicts cardiorespiratory fitness (CRF) than LA function. LA function adds little statistical value to predictive models of peak oxygen uptake (V̇o2peak) in healthy individuals, suggesting limited discriminatory for CRF once LA size is factored. In the wider population of ostensibly healthy individuals, the association between increased LA volume and higher CRF provides an important counter to the association between atrial enlargement and heart failure symptoms in those with cardiac pathology.

We examined the longitudinal associations of sedentary time (ST), light physical activity (LPA), and moderate-to-vigorous PA (MVPA) from childhood with carotid-femoral pulse wave velocity (cfPWV), a measure of arterial stiffness and carotid intima-media thickness (cIMT).

We studied 1339 children, aged 11 years from Avon Longitudinal Study of Parents and Children, UK, followed up for 13 years. Accelerometer-based ST, LPA, and MVPA were assessed at ages 11, 15, and 24 years clinic visits. cfPWV and cIMT were measured with Vicorder and ultrasound, respectively, at ages 17 and 24 years.

Among 1339 [56.4% female] participants, mean ST increased from ages 11 through 24 years, while mean LPA and MVPA decreased. Persistently high ST tertile from childhood was associated with increased cfPWV progression, effect estimate 0.047 m/s; [(95% CI 0.005 to 0.090); p = 0.030], but not cIMT progression. Persistently high LPA tertile category was associated with decreased cfPWV progression in males -0.022 m/s; [(-0.028 to -0.017); p < 0.001] and females -0.027 m/s; [(-0.044 to -0.010); p < 0.001]. Cumulative LPA exposure decreased the odds of progressively worsening cfPWV [Odds ratio 0.994 (0.994-0.995); p < 0.0001] and cIMT. Persistent exposure to ≥60 min/day of MVPA was paradoxically associated with increased cfPWV progression in males 0.053 m/s; [(0.030 to 0.077); p < 0.001] and females 0.012 m/s; [(0.002 to 0.022); p = 0.016]. Persistent exposure to ≥60 min/day of MVPA was inversely associated with cIMT progression in females -0.017 mm; [(-0.026 to -0.009); p < 0.001].

LPA >3 h/day from childhood may attenuate progressively worsening vascular damage associated with increased ST in youth.

Sudden cardiac death (SCD) is rare among athletes. However, hypertrophic cardiomyopathy is the leading cause of SCD among those <35 years of age. Meanwhile, coronary artery disease (CAD) is the primary SCD cause among those ≥35 years of age. CAD-induced plaque ruptures are believed to be a significant cause of cardiovascular diseases in middle-aged individuals who participate in extreme long-distance running activities such as marathons. A total of 1970 articles related to EIH were identified using search terms. Out of these, 1946 studies were excluded for reasons such as arterial hypertension, exercise-induced pulmonary hypertension, the absence of exercise stress testing (EST), and a lack of relevance to EIH. The study analyzed 24 studies related to both long-distance runners with exercise-induced hypertension (EIH) and the general public. Among these, 11 studies were quasi-experimentally designed studies used in randomized controlled trials (RCTs) on long-distance runners with EIH. Additionally, 12 studies utilized cohort designs, and one study with a quasi-experimental design was conducted among the general population. Recent studies suggest that an imbalance between oxygen demand and supply due to ventricular hypertrophy may be the actual cause of cardiovascular disease, regardless of CAD. Exercising excessively over an extended period can reduce endothelial function and increase arterial stiffness, which in turn increases afterload and leads to an excessive increase in blood pressure during exercise. Exercise-induced hypertension (EIH), which increases the morbidity rate of resting hypertension and is a risk factor for cardio-cerebro-vascular diseases, is more prevalent in middle-aged long-distance runners than in runners from other age groups, and it increases the prevalence of critical arrhythmias, such as atrial fibrillation or ventricular arrhythmias. EIH is associated with angiotensin II activity, and angiotensin II receptor blockers show promising effects in middle-aged runners. Further, guidelines for preventing excessive participation in races and restricting exercise intensity and frequency would be useful. This review identifies EIH as a potential risk factor for cardiovascular diseases and describes how EIH induces SCD.

Few training studies have assessed the impact of different modes of exercise on changes in cardiac function. This study investigated changes in left ventricular (LV) systolic and diastolic function following endurance (END) and resistance (RES) training in healthy participants. Sixty-four individuals participated in a randomized crossover design trial, involving 12 wk of END and RES training, separated by a 12-wk washout. Echocardiograms assessed systolic function [ejection fraction (EF) and global longitudinal strain (GLS)], diastolic function [mitral valve early velocity (E), tissue Doppler velocity (e'), their ratio (E/e')], and left atrial volume indexed to body surface area (LA ESVi). LV mass (LVM) increased with both RES (Δ5.3 ± 11.9, P = 0.001) and END (Δ7.5 ± 13.9, P < 0.001). Once adjusted for lean body mass (LVMi), changes remained significant following END. E/e' improved following END (Δ-0.35 ± 0.98, P = 0.011) not RES (Δ0.35 ± 1.11, P =0.157; P = 0.001 between modes). LA ESVi increased with END (Δ2.0 ± 6.1, P = 0.019) but not RES (Δ1.7 ± 5.7, P = 0.113). EF and GLS were not impacted significantly by either mode of training. Adaptation in LVM and LA volumes, as well as diastolic function, was exercise mode specific. Twelve weeks of intensive END increased LVM, LA volumes, and increased diastolic function. Following RES, LVM increased, although this was attenuated after accounting for changes in lean body mass. There were no changes in systolic function following either mode of exercise training.NEW & NOTEWORTHY Different types of exercise training induce distinct physiological adaptations however few exercise training studies have assessed the impact of different modes of exercise on cardiac function. This study investigated changes in left ventricular systolic and diastolic function following exercise training. Participants completed both endurance and resistance training separated by a 12-wk washout period so each participant is their own control. We present adaptations in cardiac structure and diastolic function are exercise mode specific.

The significant morbidity and premature mortality of type 2 diabetes mellitus (T2DM) is largely associated with its cardiovascular consequences. Focus has long been on the arterial atheromatosis of DM giving rise to early stroke and myocardial infarctions, whereas less attention has been given to its non-ischemic cardiovascular consequences. Irrespective of ischemic changes, T2DM is associated with heart failure (HF) most commonly with preserved ejection fraction (HFpEF). Largely due to increasing population ages, hypertension, obesity and T2DM, HFpEF is becoming the most prevalent form of heart failure. Unfortunately, randomized controlled trials of HFpEF have largely been futile, and it now seems logical to address the important different phenotypes of HFpEF to understand their underlying pathophysiology. In the early phases, HFpEF is associated with a significantly impaired ability to increase cardiac output with exercise. The lowered cardiac output with exercise results from both cardiac and peripheral causes. T2DM is associated with left ventricular (LV) diastolic dysfunction based on LV hypertrophy with myocardial disperse fibrosis and significantly impaired ability for myocardial blood flow increments with exercise. T2DM is also associated with impaired ability for skeletal muscle vasodilation during exercise, and as is the case in the myocardium, such changes may be related to vascular rarefaction. The present review discusses the underlying phenotypical changes of the heart and peripheral vascular system and their importance for an adequate increase in cardiac output. Since many of the described cardiovascular changes with T2DM must be considered difficult to change if fully developed, it is suggested that patients with T2DM are early evaluated with respect to their cardiovascular compromise.

Increased physical activity (PA) may mitigate the negative cardiovascular health effects of sedentary behavior in adolescents. However, the relationship of PA and sedentary time from childhood with cardiac function in adolescence remains underexplored. Therefore, we investigated the associations of cumulative sedentary time and PA from childhood to adolescence with cardiac function in adolescence.

Participants were 153 adolescents (69 girls) who were aged 6 to 8 years at baseline, 8 to 10 years at 2-year follow-up, and 15 to 17 years at 8-year follow-up. Cumulative sedentary time and PA exposure between baseline and 2-year follow-up and between baseline and 8-year follow-up were measured using a combined accelerometer and heart rate monitor. Cardiac function was assessed using impedance cardiography at 8-year follow-up. The data were analyzed using linear regression analyses adjusted for age and sex. Cumulative moderate to vigorous PA (standardized regression coefficient [β]=-0.323 [95% CI, -0.527 to -0.119]) and vigorous PA (β=-0.295 [95% CI, -0.508 to -0.083]) from baseline to 8-year follow-up were inversely associated with cardiac work at 8-year follow-up. Conversely, cumulative sedentary time had a positive association (β=0.245 [95% CI, 0.092-0.398]). Cumulative vigorous PA from baseline to 8-year follow-up was inversely associated with cardiac work index at 8-year follow-up (β=-0.218 [95% CI, -0.436 to 0.000]).

Higher levels of sedentary time and lower levels of PA during childhood were associated with higher cardiac work in adolescence, highlighting the importance of increasing PA and reducing sedentary time from childhood.

Detraining refers to a loss of training adaptations resulting from reductions in training stimulus due to illness, injury, or active recovery breaks in a training cycle and is associated with a reduction in left ventricular mass (LVM). The purpose of this study was to conduct a systematic review and meta-analysis to determine the influence of detraining on LVM in endurance-trained, healthy individuals.

Using electronic databases (e.g. EMBASE and MEDLINE), a literature search was performed looking for prospective detraining studies in humans. Inclusion criteria were adults, endurance-trained individuals with no known chronic disease, detraining intervention >1 week, and pre- and post-detraining LVM reported. A pooled statistic for random effects was used to assess changes in LVM with detraining. Fifteen investigations (19 analyses) with a total of 196 participants (ages 18-55 years, 15% female) met inclusion criteria, with detraining ranging between 1.4 and 15 weeks. The meta-analysis revealed a significant reduction in LVM with detraining (standardized mean difference = -0.586; 95% confidence interval = -0.817, -0.355; P < 0.001). Independently, length of detraining was not correlated with the change in LVM. However, a meta-regression model revealed length of the detraining, when training status was accounted for, was associated with the reduction of LVM (Q = 15.20, df = 3, P = 0.0017). Highly trained/elite athletes had greater reductions in LVM compared with recreational and newly trained individuals (P < 0.01). Limitations included relatively few female participants and inconsistent reporting of intervention details.

In summary, LVM is reduced following detraining of one week or more. Further research may provide a greater understanding of the effects of sex, age, and type of detraining on changes in LVM in endurance-trained individuals.

To investigate the association between leisure time physical activity (LTPA) and MRI-based diastolic function and the mediating role of metabolic health.

This cross-sectional analysis comprised 901 participants (46% women, mean age (SD): 56 (6) years (The Netherlands, 2008-2012)). LTPA was assessed via questionnaire, quantified in metabolic equivalent of tasks (METs)-minutes per week and participants underwent abdominal and cardiovascular MRI. Confirmatory factor analysis was used to construct the metabolic load factor. Piecewise structural equation model with adjustments for confounders was used to determine associations between LTPA and diastolic function and the mediating effect of metabolic load.

Significant differences in mitral early/late peak filling rate (E/A) ratio per SD of LTPA (men=1999, women=1870 MET-min/week) of 0.18, (95% CI= 0.03 to 0.33, p=0.021) were observed in men, but not in women: -0.01 (-0.01 to 0.34, p=0.058). Difference in deceleration time of mitral early filling (E-DT) was 0.13 (0.01 to 0.24, p=0.030) in men and 0.17 (0.05 to 0.28, p=0.005) in women. Metabolic load, including MRI-based visceral and subcutaneous adipose tissue, fasting glucose, high-density lipoprotein cholesterol and triglycerides, mediated these associations as follows: E/A-ratio of 0.030 (0.000 to 0.067, 19% mediated, p=0.047) in men but not in women: 0.058 (0.027 to 0.089, p<0.001) and E-DT not in men 0.004 (-0.012 to 0.021, p=0.602) but did in women 0.044 (0.013 to 0.057, 27% mediated, p=0.006).

A larger amount of LTPA was associated with improved diastolic function where confirmatory factor analysis-based metabolic load partly mediated this effect. Future studies should assess whether improving indicators of metabolic load alongside LTPA will benefit healthy diastolic function even more.