Exercise-induced Cardiac Remodeling Research Articles

Association between FT3 Levels and Exercise-Induced Cardiac Remodeling in Elite Athletes.

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.

Association between FT3 Levels and Exercise-Induced Cardiac Remodeling in Elite Athletes

Association between FT3 Levels and Exercise-Induced Cardiac Remodeling in Elite Athletes

Reduced Ejection Fraction in Elite Endurance Athletes: Clinical and Genetic Overlap With Dilated Cardiomyopathy.

Exercise-induced cardiac remodeling can be profound, resulting in clinical overlap with dilated cardiomyopathy, yet the significance of reduced ejection fraction (EF) in athletes is unclear. The aim is to assess the prevalence, clinical consequences, and genetic predisposition of reduced EF in athletes. Young endurance athletes were recruited from elite training programs and underwent comprehensive cardiac phenotyping and genetic testing. Those with reduced EF using cardiac magnetic resonance imaging (defined as left ventricular EF <50%, or right ventricular EF <45%, or both) were compared with athletes with normal EF. A validated polygenic risk score for indexed left ventricular end-systolic volume (LVESVi-PRS), previously associated with dilated cardiomyopathy, was assessed. Clinical events were recorded over a mean of 4.4 years. Of the 281 elite endurance athletes (22±8 years, 79.7% male) undergoing comprehensive assessment, 44 of 281 (15.7%) had reduced left ventricular EF (N=12; 4.3%), right ventricular EF (N=14; 5.0%), or both (N=18; 6.4%). Reduced EF was associated with a higher burden of ventricular premature beats (13.6% versus 3.8% with >100 ventricular premature beats/24 h; P=0.008) and lower left ventricular global longitudinal strain (-17%±2% versus -19%±2%; P<0.001). Athletes with reduced EF had a higher mean LVESVi-PRS (0.57±0.13 versus 0.51±0.14; P=0.009) with athletes in the top decile of LVESVi-PRS having an 11-fold increase in the likelihood of reduced EF compared with those in the bottom decile (P=0.034). Male sex and higher LVESVi-PRS were the only significant predictors of reduced EF in a multivariate analysis that included age and fitness. During follow-up, no athletes developed symptomatic heart failure or arrhythmias. Two athletes died, 1 from trauma and 1 from sudden cardiac death, the latter having a reduced right ventricular EF and a LVESVi-PRS >95%. Reduced EF occurs in approximately 1 in 6 elite endurance athletes and is related to genetic predisposition in addition to exercise training. Genetic and imaging markers may help identify endurance athletes in whom scrutiny about long-term clinical outcomes may be appropriate. URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=374976&isReview=true; Unique identifier: ACTRN12618000716268.

Team Approach: Diagnosis, Management, and Prevention of Sudden Cardiac Arrest in the Athlete.

» Sudden cardiac events during sports competition are rare but tragic occurrences that require a timely, comprehensive response by well-prepared athletic trainers and medical providers. This sequence should prioritize prompt emergency medical system activation, immediate initiation of cardiopulmonary resuscitation (CPR), automated early defibrillation (AED), and comprehensive advanced life support efforts.» Exercise-induced cardiac remodeling, referred to as the "athlete's heart," refers to a host of adaptive changes that increase cardiac chamber size and wall thickness to allow for greater pressures and volumes during exercise. This remodeling phenotype may overlap with other inherited cardiomyopathies and cardiac abnormalities, which can complicate clinical care. The long-term implications of this electrical and structural remodeling on cardiac function are unknown.» Although the best screening strategies to optimize primary prevention of sudden cardiac arrest is an evolving topic, the effectiveness of CPR and early defibrillation use in treating out-of-hospital sudden cardiac arrest has been well-established, despite their reported underuse.

Temporal relationship between training and episodes of atrial fibrillation in endurance athletes

Abstract Background Prolonged endurance training promotes exercise-induced cardiac remodeling and atrial fibrillation (AF), the most common arrhythmia among middle-aged endurance athletes. However, there is a lack of data on the impact of training sessions on the recurrence of AF episodes and current guidelines do not provide specific training recommendations for athletes diagnosed with AF. Both sympathetic stimulation during exercise and parasympathetic activity after exercise are possible mechanisms for recurrent episodes of AF. Purpose To assess the temporal relationship of training sessions with recurrent AF episodes among endurance athletes with paroxysmal AF. Methods The Effects of Detraining in Endurance Athletes with Atrial Fibrillation Trial is an international multicenter randomized controlled trial that includes athletes engaged in regular endurance sports ≥five hours per week, diagnosed with paroxysmal AF. AF episodes lasting ≥30 seconds were registered using wireless insertable cardiac monitors (ICM) and reviewed by an experienced cardiologist. Training sessions were registered using sports watches. We analyzed AF episodes and training data for the period from ICM implantation to randomization, and report event rates and rate ratios with 95% confidence intervals (CIs) for recurrent AF episodes during or within 3 hours after training sessions, compared to &amp;gt;3 hours after training. Results Eighteen athletes (1 female, 17 male) with a median age of 55 years (range 44-74) were included. The combined duration of monitoring was 845 days/20,280 hours (median 38.5, range 12-97 days). The athletes performed a total of 619 hours of training during 559 training sessions. In total, 66 AF episodes (median 1, range 0-15) were registered, of which 37 (56%) occurred within 24 hours after the start of a training sessions. Ten AF episodes (15%) occurred during a training session, 12 (18%) occurred within 3 hours after a training session and 44 (67%) occurred &amp;gt;3 hours after training. Figure 1 shows recurrent AF episodes during training (red bars) and within 24 hours from the start of a training session (blue bars) and smoothed density estimates. The event rate per 24 hours was 0.39 for AF during training, 0.17 the first 3 hours after training and 0.06 &amp;gt;3 hours after training. As compared to &amp;gt;3 hours after training, the rate ratio was 6.6 (95% CI 3.8 to 11.6) for recurrent AF episodes during training sessions and 3.9 (95% CI 2.2 to 6.9) for AF episodes during or within 3 hours after training. Conclusion Among middle-aged endurance athletes with paroxysmal AF, the rate of recurrent AF episodes was highest during and within 3 hours after training sessions. The impact of training and the pathophysiology of exercise-induced AF should be investigated further, with the aim of developing preventive strategies specific to athletic populations.Figure 1

Assessment of Pulmonary Arteries Hemodynamics and Its Relationship With Cardiac Remodeling and Myocardial Fibrosis in Athletes With Four-Dimensional Flow MRI.

Exercise-induced cardiac remodeling (CR) and myocardial fibrosis (MF) can increase cardiovascular risk in athletes. Early detection of pulmonary arterial hemodynamics parameters among athletes may be beneficial in optimizing the frequency of clinical follow-ups. To analyze the hemodynamics of pulmonary arteries and its relationship with CR and MF in athletes using four-dimensional (4D) flow MRI. Prospective. One hundred twenty-one athletes (median age, 24 years; mean exercise per week 10 hours, for mean of 5 years) and twenty-onesedentary healthy controls (median age, 25 years; exercise per week <3 hours, irregular pattern). True fast imaging with steady state free precession, time-resolved 3D Cartesian phase-contrast, and phase sensitive inversion recovery late gadolinium enhancement sequences at 3.0 T. CR was defined as any cardiac parameters exceeding the 99th percentile upper reference limits, encompassing ventricular function, bi-atrium and bi-ventricle diameters, and ventricular wall thickness. MF was visually evaluated by three independent radiologists. 4D flow parameters were assessed in the main, right, and left pulmonary arteries (MPA, RPA, and LPA, respectively) and compared between different groups. Four machine learning (ML) models were developed to differentiate between athletes with and without CR and/or MF. Univariate analysis was used to compare groups. Area under the receiver operating characteristic curve (AUC) was used to assess the performance of the ML models. Athletes had significantly higher WSSmax in the MPA, RPA, and LPA than controls. Athletes with CR and/or MF (N = 30) had significantly lower RPmax from MPA to RPA than those without (N = 91). Among the ML models, the gradient boosting machine model had the highest performance, with an AUC of 0.90. The pulmonary arterial hemodynamics parameters could differentiate CR and/or MF in athletes, which may be potential to assist in optimizing frequency of follow-up. 1 TECHNICAL EFFICACY: Stage 2.

Abstract 14247: Speckle Tracking Echocardiography for Assessment of Left Ventricular Remodeling in Soccer Athletes

Introduction: Speckle-tracking echocardiography (STE)-derived strain is a sensitive tool to detect early signs of exercise-induced cardiac remodeling in athletes, which may contribute to differentiate between physiological and pathological adaptation to sports. Objective: We aimed to assess the effect of regular athletic training on myocardial function assessed by STE in soccer players. Methods: We prospectively enrolled teenager soccer players who participate in regular training in a professional soccer team from Minas Gerais, Brazil. All asymptomatic athletes without known cardiovascular disease and with a structurally normal heart on transthoracic echocardiogram were included. Global longitudinal strain (GLS) by STE was performed in each athlete and measured offline using EchoPAC (GE) software. GLS was categorized according to absolute value |x| and GLS &lt;16% was considered decreased, 16% to 18% borderline and &gt;18% normal. Clinical, demographic and echocardiographic variables associated with reduced and borderline GLS were assessed by logistic regression. Results: The study population consisted of 352 male trained athletes with a mean age of 14 years (range 9 to 20), body mass index (BMI) of 20.4 ± 2.8 kg/m2, and left ventricular ejection fraction (LVEF) of 70 ± 6%. In the overall study population, the mean GLS value was -19.6 ± 2.2%, decreased in 13 athletes (3.7%) and borderline in 57 athletes (16.3%). In multivariable logistic regression analysis, BMI (odds ratio [OR] 1.38; 95% confidence interval [CI] 1.21 - 1.59; p&lt;0.001), LVEF (OR 0.94; 95% CI 0.91 - 0.98; p=0.004), left atrial volume (OR 0.89; 95% CI 0.83 - 0.95; p=0.001), E/e' ratio (OR 1.52; 95% CI 1.07 - 2.11; p=0.019) and E/A ratio (OR 0.37; 95% CI 0.18 - 0.78; p=0.009) were independently associated with reduced and borderline GLS. The model was well calibrated and with good discrimination, yielding a C-statistic of 0.78 (95% CI 0.72 - 0.85). Conclusions: This study provides sport-specific GLS values in the setting of normal LVEF in young athletes. Determinants of abnormal GLS include diastolic and systolic echocardiographic parameters related to exercise adaptation. Decreased myocardial deformation by STE may reflect a forthright relaxed cardiac state rather than underlying pathology.

Echocardiographic Evaluation of the Athlete's Heart: Focused Review and Update.

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

Normative Values for Sport-Specific Left Ventricular Dimensions and Exercise-Induced Cardiac Remodeling in Elite Spanish Male and Female Athletes

BackgroundThere is debate about the magnitude of geometrical remodeling [i.e., left ventricle (LV) cavity enlargement vs. wall thickening] in the heart of elite athletes, and no limits of normality have been yet established for different sports. We aimed to determine sex- and sport-specific normative values of LV dimensions in elite white adult athletes.MethodsThis was a single-center, retrospective study of Spanish elite athletes. Athletes were grouped by sport and its relative dynamic/static component (Mitchell’s classification). LV dimensions were measured with two-dimensional-guided M-mode echocardiography imaging to compute normative values. We also developed an online and app-based calculator (https://sites.google.com/lapolart.es/athlete-lv/welcome?authuser=0) to provide clinicians with sports- and Mitchell’s category-specific Z-scores for different LV dimensions.ResultsWe studied 3282 athletes (46 different sports, 37.8% women, mean age 23 ± 6 years). The majority (85.4%) showed normal cardiac geometry, particularly women (90.9%). Eccentric hypertrophy was relatively prevalent (13.4%), and concentric remodeling or hypertrophy was a rare finding (each < 0.8% of total). The proportion of normal cardiac geometry and eccentric hypertrophy decreased and increased, respectively, with the dynamic (in both sexes) or static component (in male athletes) of the sport irrespective of the other (static or dynamic) component. The 95th percentile values of LV dimensions did not exceed the following limits in any of the Mitchell categories: septal wall thickness, 12 mm (males) and 10 mm (females); LV posterior wall, 11 mm and 10 mm; and LV end-diastolic diameter, 64 mm and 57 mm.ConclusionsThe majority of elite athletes had normal LV geometry, and although some presented with LV eccentric hypertrophy, concentric remodeling or hypertrophy was very uncommon. The present study provides sport-specific normative values that can serve to identify those athletes for whom a detailed examination might be recommendable (i.e., those exceeding the 95th percentile for their sex and sport).

Right Heart Structure and Function in Lifelong Recreational Endurance Athletes with and without Paroxysmal Atrial Fibrillation

Healthy young athletes adapt to the increased demands of endurance exercise with symmetric cardiac remodeling. Male veteran endurance athletes have an increased risk for atrial fibrillation (AF), and some athletes seem susceptible to changes mimicking arrhythmogenic cardiomyopathy. Intense exercise puts a disproportionate hemodynamic load on the right-sided heart chambers. Despite this, data describing right heart structure and function in older veteran athletes are scarce. The aim of this study was to investigate structural and functional characteristics of the right heart in veteran athletes with and without AF to contribute to the understanding of exercise-induced cardiac remodeling in this group. Three hundred two male participants, of whom 151 were veteran skiers (62 with paroxysmal AF) and 151 were control subjects from the general population (62 with paroxysmal AF), underwent echocardiographic examinations in sinus rhythm to evaluate right atrial (RA) and right ventricular (RV) structure and function. While 87 of the participants had never exercised regularly, 50, 43, and 122 men had practiced regular endurance exercise for 1 to 20, 20 to 40, and >40years, respectively. RA volume and RV size increased with cumulative years of exercise (P<.001), with a disproportionate increase in RV size compared with left ventricular (LV) size, regardless of AF status (P<.001). RA and RV function assessed by strain remained similar despite lifelong exposure to endurance exercise. AF was associated with reduced RA strain irrespective of exposure to exercise (P<.001). RA and RV sizes and RV/LV ratio showed a dose-response relationship with cumulative years of endurance exercise, whereas RA and RV function did not, indicating that increasing RV/LV ratio may represent a physiologic adaptation to prolonged endurance exercise. AF was associated with reduced RA function, regardless of exposure to exercise, suggesting that RA functional parameters are more closely linked to AF than RA size in veteran athletes.

Cardiac effects of detraining in athletes: A narrative review.

Routine physical activity stimulates numerous morphologic and functional adaptations of the cardiac system, which are commonly referred to as exercise-induced cardiac remodeling (EICR). EICR has been well documented in elite and recreational athletes, but comparatively little is known about the "reverse" cardiac adaptations during detraining in an athletic population. To assess the morphologic and functional cardiac effects of detraining in athletes. Eligible studies were identified in PubMed from inception to May 2020. Studies were included if they assessed the cardiac effects of detraining periods in athletes. A total of 16 studies from the literature search were identified and included in this review. These studies included athletes from multiple different sporting disciplines and detraining periods ranged from 3 weeks to 13 years. Detraining periods led to significantly decreased right ventricular and left (LV) ventricular dimensions, LV mass, and LV wall thickness, but only limited changes in systolic and diastolic functional parameters were observed. From the limited data available in this population, cardiac atrophy has been observed with short periods of detraining (1-8 weeks) but often spares systolic and diastolic heart function. Supplemental exercise training during times of rehabilitation to combat cardiac regression has not been vigorously studied in athletes, so the ideal frequency, intensity, and modality of exercise needed to maintain EICR remains unclear.

Mechanisms of Exercise-Induced Cardiac Remodeling Differ Between Young and Aged Hearts.

Aging induces physiological and molecular changes in the heart that increase the risk for heart disease. Several of these changes are targetable by exercise. We hypothesize that the mechanisms by which exercise improves cardiac function in the aged heart differ from those in the young exercised heart.

Exercise-Generated β-Aminoisobutyric Acid (BAIBA) Reduces Cardiomyocyte Metabolic Stress and Apoptosis Caused by Mitochondrial Dysfunction Through the miR-208b/AMPK Pathway

ObjectiveTo explore the cardioprotective effects of exercise-derived β-aminoisobutyric (BAIBA) on cardiomyocyte apoptosis and energy metabolism in a rat model of heart failure (HF).MethodsIn male Sprague-Dawley rats (8-week-old), myocardial infarction (MI) was used to induce HF by ligating the left anterior descending branch of the coronary artery. In the Sham group, the coronary artery was threaded but not ligated. After HF development, Sham and HF rats were exercised 60 min daily, 5 days/week on a treadmill for 8 weeks (50–60% maximal intensity) and exercise-induced cardiac remodeling after MI were assessed using echocardiography, hematoxylin and eosin (H&E), Masson's Trichrome, and TUNEL staining for the detection of apoptosis-associated factors in cardiac tissue. High-throughput sequencing and mass spectrometry were used to measure BAIBA production and to explore its cardioprotective effects and molecular actions. To further characterize the cardioprotective effects of BAIBA, an in vitro model of apoptosis was generated by applying H2O2 to H9C2 cells to induce mitochondrial dysfunction. In addition, cells were transfected with either a miR-208b analog or a miR-208b inhibitor. Apoptosis-related proteins were detected by Western Blotting (WB). ATP production was also assessed by luminometry. After administration of BAIBA and Compound C, the expression of proteins related to apoptosis, mitochondrial function, lipid uptake, and β-oxidative were determined. Changes in the levels of reactive oxygen species (ROS) were assessed by fluorescence microscopy. In addition, alterations in membrane potential (δψm) were obtained by confocal microscopy.ResultsRats with HF after MI are accompanied by mitochondrial dysfunction, metabolic stress and apoptosis. Reduced expression of apoptosis-related proteins was observed, together with increased ATP production and reduced mitochondrial dysfunction in the exercised compared with the Sham (non-exercised) HF group. Importantly, exercise increased the production of BAIBA, irrespective of the presence of HF. To assess whether BAIBA had similar effects to exercise in ameliorating HF-induced adverse cardiac remodeling, rats were treated with 75 mg/kg/ day of BAIBA and we found BAIBA had a similar cardioprotective effect. Transcriptomic analyses found that the expression of miR-208b was increased after BAIBA administration, and subsequent transfection with an miR-208b analog ameliorated both the expression of apoptosis-related proteins and energy metabolism in H2O2-treated H9C2 cells. In combining transcriptomic with metabolomic analyses, we identified AMPK as a downstream target for BAIBA in attenuating metabolic stress in HF. Further cell experiments confirmed that BAIBA increased AMPK phosphorylation and had a cardioprotective effect on downstream fatty acid uptake, oxidative efficiency, and mitochondrial function, which was prevented by the AMPK inhibitor Compound C.ConclusionExercise-generated BAIBA can reduce cardiomyocyte metabolic stress and apoptosis induced by mitochondrial dysfunction through the miR-208b/AMPK pathway.

Exercise and the Female Heart

Female participation in sport has increased sharply during the last few decades, and for the third straight Olympic Games, there were more women than men on the US roster for the 2020 Tokyo Games. Given this, an understanding of the differences between men and women with respect to exercise-induced cardiac remodeling is critical for those caring for female athletes. Recent studies have provided insight into female-specific cardiac remodeling and have enhanced our understanding on the upper limits of cardiac remodeling in female athletes and how these adaptations compare with sedentary females, male athletes, and cardiomyopathies. Female athletes display fewer signs of adaptive remodeling on ECG compared with male athletes. Structurally, male athletes have larger absolute cardiac dimensions, but female athletes have similar or larger chamber size when adjusted for body size. Female athletes have a lower incidence of sudden cardiac arrest or death compared with male athletes in the early competitive years (high school, college, and professional) and in the masters athlete years. In addition, female athletes are less likely to have coronary disease and atrial fibrillation compared with male athletes. Data on longevity indicate that female athletes live longer than their sedentary counterparts. Unlike men, there has been no convincing association of extreme exercise and cardiovascular disease in longer-term endurance female athletes. The underlying mechanisms of these sex-based differences are not very well understood, and future studies are warranted to better understand the mechanisms of cardiac adaptation in female athletes.

Prevalence Of Thoracic Aorta Dilation In A Military Population

Introduction: Exercise-induced cardiac remodeling is a complex structural and functional physiologic adaptation to various forms of exercise. We evaluated a unique population comprising active duty military members (age >= 40) to determine the prevalence of thoracic aorta dilation.

Aging Athlete's Heart: An Echocardiographic Evaluation of Competitive Sprint- versus Endurance-Trained Master Athletes

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. In this observational cross-sectional study, echocardiographic examinations were conducted in 143 sprint-trained (age range, 36-83years) and 114 endurance-trained (age range, 38-85years) 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. 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. 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 towardconcentric 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.

Ventricular late potentials measured by signal-averaged electrocardiogram in young professional soccer players

Background and objectivesAthlete’s heart is characterized by structural cardiac changes, including enlargement and hypertrophy. However, exercise-induced cardiac electrical remodeling is not well known in Asian athletes. We sought to evaluate the association between vigorous exercise and the development of abnormal late potential on signal-averaged electrocardiogram (SAECG).MethodWe analyzed 48 Korean professional soccer players and 71 healthy sedentary controls who underwent SAECG and transthoracic echocardiography at Kyung Hee University Hospital. An SAECG was considered abnormal (positive for ventricular late potential) when any one of the three following criteria was met: filtered QRS duration > 114 ms, root-mean-square voltage in the terminal 40 ms < 20 uV, or a voltage < 40 uV for more than 38 ms.ResultsFragmented QRS was more commonly found in athletes (1.4% vs. 10.4%). Athletes demonstrated significantly higher proportion of filtered QRS duration > 114 ms (7.0% vs. 22.9%, P = 0.013) and lower terminal QRS root-mean-square voltage < 20 uV (5.6% vs. 20.8%, P = 0.012). Ventricular late potential on SAECG was significantly more frequent in athletes (15.5% vs. 35.4%, P = 0.012). Regarding echocardiographic parameters, the athletes had larger cardiac chamber size; however, these differences became non-significant after adjustment for body surface area, except left ventricular mass index (65.7 ± 12.7 g/m2 vs. 84.7 ± 17.7 g/m2, P < 0.001).ConclusionAbnormal SAECG findings were significantly more common in athletes than in controls. Further study is needed to determine the clinical impact of these abnormal SAECGs in athletes and cardiac outcomes in the long term.

Gender Difference of Cardiac Remodeling in University Athletes: Results from 2015 Gwangju Summer Universiade.

Background and ObjectivesThere is little data about cardiac geometry in highly trained young athletes, especially female specific changes. We investigated gender difference on exercise induced cardiac remodeling (EICR) in highly trained university athletes.MethodsA total of 1,185 university athletes divided into 2 groups; female (n=497, 22.0±2.3 years) vs. male (n=688, 22.6±2.4 years). Remodeling of the left ventricle (LV), left atrium (LA), right ventricle (RV), and any cardiac chamber were compared.ResultsLV, LA, RV, and any remodeling was found in 156 (13.2%), 206 (17.4%), 82 (6.9%), and 379 athletes (31.9%), respectively. LV, LA, and any remodeling were more common in male than female athletes (n=53, 12.1% vs. n=103, 15.5%, p=0.065), (n=65, 13.1% vs. n=141, 20.5%, p<0.001), (n=144, 30.0% vs. n=235, 34.2%, p=0.058), respectively, whereas RV remodeling was significantly more common in female than male athletes (n=56, 11.3% vs. n=26, 3.8%, p<0.001). Interestingly, the development of LV, LA, and RV remodeling were not overlapped in many of athletes, suggesting different mechanism of EICR according to cardiac chamber. Various predictors including sports type, heart rate, muscle mass, fat mass, body surface area, and training time were differently involved in cardiac remodeling, and there were gender differences of these predictors for cardiac remodeling.ConclusionsEICR was common in both sex and was independently developed among cardiac chambers in highly trained university athletes. LV and LA remodeling were common in males, whereas RV remodeling was significantly more common in females demonstrating gender difference in EICR. The present study also demonstrated gender difference in the predictors of EICR.

Exercise-induced cardiac remodeling during adolescence.

Exercise-induced cardiac remodeling during adolescence.

Identification of Potentially Relevant Genes for Excessive Exercise-Induced Pathological Cardiac Hypertrophy in Zebrafish

Exercise-induced cardiac remodeling has aroused public concern for some time, as sudden cardiac death is known to occur in athletes; however, little is known about the underlying mechanism of exercise-induced cardiac injury. In the present study, we established an excessive exercise-induced pathologic cardiac hypertrophy model in zebrafish with increased myocardial fibrosis, myofibril disassembly, mitochondrial degradation, upregulated expression of the pathological hypertrophy marker genes in the heart, contractile impairment, and cardiopulmonary function impairment. High-throughput RNA-seq analysis revealed that the differentially expressed genes were enriched in the regulation of autophagy, protein folding, and degradation, myofibril development, angiogenesis, metabolic reprogramming, and insulin and FoxO signaling pathways. FOXO proteins may be the core mediator of the regulatory network needed to promote the pathological response. Further, PPI network analysis showed that pik3c3, gapdh, fbox32, fzr1, ubox5, lmo7a, kctd7, fbxo9, lonrf1l, fbxl4, nhpb2l1b, nhp2, fbl, hsp90aa1.1, snrpd3l, dhx15, mrto4, ruvbl1, hspa8b, and faub are the hub genes that correlate with the pathogenesis of pathological cardiac hypertrophy. The underlying regulatory pathways and cardiac pressure-responsive molecules identified in the present study will provide valuable insights for the supervision and clinical treatment of pathological cardiac hypertrophy induced by excessive exercise.