Middle-aged Endurance Athletes Research Articles

Atrial fibrillation in middle-aged athletes: Impact on left atrial, ventricular and exercise performance.

High volume endurance training may increase the risk of paroxysmal atrial fibrillation (AF) in middle-aged athletes. Limited data are available describing the cardiovascular phenotype of middle-aged endurance athletes, or the impact of AF on atrial function and exercise performance performed in sinus rhythm. The purpose of this study was to characterize LA phasic function at rest and during exercise in athletes with paroxysmal AF, and to determine its impact on exercise performance. Fifteen endurance trained males (EA) (56 ± 5 years) without AF and 14 endurance trained males with paroxysmal AF (EA-AF) (55 ± 8 years) underwent echocardiography during cycle-ergometry at light and moderate intensities. Resting LA maximal volumes were similar between EA and EA-AF (30 ± 4 vs. 29 ± 8 ml/m2, p = 0.50), and there were no differences in atrial electromechanical delay (AEMD). During moderate intensity exercise, EA-AF had reduced LA conduit (30 ± 6 vs. 40 ± 5 ml/m2, p = 0.002) LA booster volumes (17 ± 5 vs. 21 ± 4 ml/m2, p = 0.021), and reduced LV stroke volumes (100 ± 12 vs. 117 ± 16 ml, p = 0.007). These results demonstrate that exercise testing in athletes with AF unmasks evidence of adverse functional cardiac remodelling that may contribute to impaired exercise performance. It is unclear whether these functional alterations are the consequence of AF. Reductions in LA conduit volume, LA booster volume, and LV stroke volume during exercise may be helpful in clinical management and distinguishing pathologic from physiologic remodelling.

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 >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 >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 >3 hours after training. As compared to >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

The effect of chronic exercise training and acute exercise on power spectral analysis of heart rate variability.

Moderate to vigorous physical activity performed regularly is cardioprotective and reduces all-cause mortality, concomitant with increased resting heart rate variability (HRV). However, there are contradictory reports regarding the effects of chronic and acute exercise on nocturnal HRV in those performing exercise well-beyond physical activity guidelines. Therefore, the purpose of this study was to compare the power spectral analysis components of HRV in middle-aged endurance athletes (EA) and recreationally active individuals (REC) and explore acute exercise effects in EA. A total of 119 EA (52, 49-57 years) and 32 REC (56, 52-60 years) were recruited to complete 24h Holter monitoring (GE SEER 1000) in the absence of exercise. Fifty one EA (52, 49-57 years) then underwent 24h Holter monitoring following an intense bout of endurance exercise. Power spectral HRV analysis was completed hourly and averaged to quantify morning (1000-1200h), evening (1900-2100h), and nocturnal (0200-0400h) HRV. EA had greater very low frequency (VLF) and low frequency (LF) (both p< 0.001) compared to REC. LF/high frequency (HF) was greater in EA at 0200-0400h (p=0.04). Among all participants, the change in HR and HF from 1000-1200 to 0200-0400h was negatively correlated (r=-0.47, p< 0.001). Following acute exercise in EA, only nocturnal HRV was assessed. VLF (p< 0.001) and HF (p=0.008) decreased, while LF/HF increased (p=0.02). These results suggest that in EA, both long-term and acute exercises increase nocturnal sympathovagal activity through an increase in LF and decrease in HF, respectively. Further work is required to understand the mechanism underlying reduced nocturnal HRV in middle-aged EA and the long-term health implications.

Determinants of high-risk coronary artery disease in ostensibly healthy male master endurance athletes

Abstract Background Healthy male master endurance athletes have a greater prevalence of high coronary calcium (CAC) scores compared to healthy sedentary counterparts, and some demonstrate high-risk plaque features. A number of theories have been postulated but reasons remain unclear. Concurrently atherosclerotic coronary artery disease (CAD) is the most common cause of sudden cardiac death in male master athletes drawing much public and scientific interest and making this an important public health issue. Purpose To examine the relationship of age, resting systolic blood pressure (SBP), exercise dose and sporting discipline with high-risk CAD markers in male master endurance athletes. Methods A prospective study undertaken over 19 months evaluated 214 male master (40–65 years) endurance athletes, free from known cardiovascular risk factors, symptoms or relevant health conditions. Clinical evaluation included cardiopulmonary exercise test, resting blood pressure (BP) and coronary computed tomogram angiography (CCTA). CCTA assessed CAC score, significant stenosis, (&amp;gt;50%) and plaque vulnerability markers. Exercise dose was defined by years of endurance exercise and average MET-hours/week (lifetime exercise volume multiplied by the metabolic equivalent scores). Resting BP was the average of 3 consecutive supine measures after at least 5 minutes rest. Results Athletes (mean age 51, SD 70.1) exercised for minimum 6 hours/week (median 8.5) for a median of 15 years (2–26). Almost half (60.2%) were multi-endurance athletes i.e. any combination swimming, cycling and running. The remainder were runners (22.4%) and cyclists (15.4%). Median Framingham risk score 3.2% (1.8–5.8). The mean resting BP was 129/80 mmHg and a quarter (26%) of athletes were hypertensive (≥140/90 mmHg) at rest. A CAC score &amp;gt;100 Agatston units (AU) was present in 16% of athletes. There was a total of 15 stenotic lesions in 11 (5%) athletes. 13% had plaque vulnerability markers. Logistic regression evaluated whether age, resting SBP, exercise dose measures and sporting discipline were predictive for a CAC score &amp;gt;100 AU, significant stenosis and plaque vulnerability markers (table 1). CAC score was associated with age, years of endurance exercise and resting SBP. A Stenosis &amp;gt;50% and plaque vulnerability markers were associated with resting SBP and cycling compared with all other sporting disciplines. Conclusion Despite correcting for age, higher exercise dose (years endurance exercise) is associated with CAC score &amp;gt;100 AU but does not predict significant stenosis or plaque vulnerability markers. Resting SBP and cycling strongly predict high-risk disease. Cycling enables a greater intensity of exercise compared with other endurance sports, which may be associated with prolonged rises in SBP. Resting SBP and cycling are important determinants for high-risk CAD in middle-aged male endurance athletes and should be considered when risk stratifying in pre-participation evaluation. Funding Acknowledgement Type of funding sources: Private company. Main funding source(s): British Heart Foundation Clinical Research Training Fellowship

Exaggerated Blood Pressure Responses To Exercise: Assessment Of Criteria In Middle-aged Male Endurance Athletes

Exaggerated Blood Pressure Responses To Exercise: Assessment Of Criteria In Middle-aged Male Endurance Athletes

A Novel Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) Biomarker—Anti-DSG2—Is Absent in Athletes With Right Ventricular Enlargement

BackgroundRight ventricular (RV) enlargement is common in endurance athletes. It is usually considered to be physiological, but it is possible that this remodelling is adverse, manifesting as a variant of arrhythmogenic right ventricular cardiomyopathy (ARVC), termed “exercise-induced ARVC.” A novel biomarker (anti-desmoglein-2 [anti-DSG2] antibody) has been shown to indicate ARVC with high sensitivity and specificity and may be an immune response to breakdown of RV desmosomes. It is not known if this antibody is present in endurance athletes with RV enlargement but without clinical ARVC. MethodsMiddle-aged, healthy endurance athletes with RV enlargement on cardiac magnetic resonance imaging had serum tested for the presence of the anti-DSG2 antibody. All athletes also underwent Holter monitoring, a signal-averaged electrocardiogram, and an exercise questionnaire. ResultsA total of 30 athletes (20 men, 10 women, average age 53 ± 6 years) were enrolled in this study with median RV end-diastolic volume indexes of 117.1 mL/m2 (men) and 103.5 mL/m2 (women). Athletes demonstrated other characteristics of endurance training, including depolarization abnormalities (abnormal signal-averaged electrocardiogram, 19 of 30) and incomplete right bundle branch block (8 of 30). No athlete met criteria for definite or probable ARVC. None of the athletes tested positive for anti-DSG2 antibody. ConclusionsAmong middle-aged endurance athletes with RV enlargement, the anti-DSG2 antibody, a suggested ARVC biomarker, is absent in all and is highly specific in this cohort (95% confidence interval, 88%-100%). Despite significant RV remodelling, these athletes did not express a previously characterized pathologic biomarker known to be sensitive for ARVC. Physiological exercise remodelling and pathologic ARVC remodelling are likely separate processes.

Hinge point fibrosis in athletes is not associated with structural, functional or electrical consequences: a comparison between young and middle-aged elite endurance athletes

Abstract Background The health benefits of extensive endurance training have been debated due to the report of myocardial fibrosis (MF), arrhythmias and temporary post-race cardiac impairment in middle-aged and veteran athletes. The extent of these changes is unknown in elite young athletes. Purpose To assess the prevalence of MF and its structural, functional and electrical impact in highly trained young endurance athletes (YA, 15–23 years) as compared to middle-aged athletes (MA, 30–50 years). We hypothesised that MF would be more frequent in MA and associated with more structural, functional and electrical abnormalities. Methods We prospectively assessed 197 YA and 34 MA. All had ECG, maximal oxygen consumption (VO2max) testing, cardiac magnetic resonance imaging (CMR), echocardiography and 24h-holter. Indexed left ventricular and right ventricular end diastolic volume (LVEDVi, RVEDVi), ejection fraction (LVEF, RVEF), left ventricular mass (LVMi), and MF defined as delayed gadolinium enhancement were assessed by CMR. LV and RV free wall strain (LVSL, RVfwSL) were assessed by 2D speckle tracking echocardiography. Ventricular premature beats (VPB) and non-sustained ventricular tachycardia (nsVT) were assessed by 24h-holter. Results YA and MA (18±2 vs 38±5 years [p&amp;lt;0.01]; 78% vs 80% male [p=0.99]) with an elite level of fitness (VO2max 61±8 vs 54±10 mL/min/kg [p&amp;lt;0.01]; % predicted VO2max 150±20 vs 158±30 [p=0.02]) had a large variance in LV and RV remodelling (Figure 1). MF was seen in 28 athletes (12.5%) and more prevalent in MA than in YA (23.5 vs 10.5%, p=0.048). MF was limited to the hinge points in all 8 MA with MF and 17 YA. 3 YA had LV lateral wall subepicardial MF. 27 of 187 (14.4%) male athletes had MF compared to 1 of 50 (2%) female athletes (p=0.01). MF+ MA(A) and YA(B) as well as MF− MA(C) and YA(D) had similar structural remodelling (LVEDVi 110±14 vs 118±14 vs 113±19 vs 110±16 mL/m2; RVEDVi 120±14 vs 128±17 vs 117±19 vs 125±23mL/m2; LVMi 77±11 vs 83±14 vs 81±14 vs 77±15g/m2, p&amp;gt;0.05). LVEF, LVSL and RVSL were similar (59±3 vs 58±5 vs 61±6 vs 58±6%; −18.8±2 vs −18.8±2 vs −19.8±2 vs −19.3±2%; −26.3±2.4 vs −24.4±2.4; −26.3±3 vs −25.8±3.5% respectively, p&amp;gt;0.05). LVEF &amp;lt;50% was seen in 19 (8.2%) athletes (0 [0%] vs [5%] 1 vs 1 [3.8%] vs 17 [9.6%]; p=0.51). RVEF was higher in D compared to C without further differences between groups (54±4 vs 54±6 vs 53±6 vs 57±5, p=0.005). RVEF&amp;lt;45% was seen 21 (9.1%) athletes (0 [0%] vs 1 [5%] vs 0 [0%] vs 20 [11.3%]; p=0.14). Abnormal T-wave inversion was similar (12.5 vs 5 vs 7.4 vs 6.2%, p=0.93) as was the prevalence of &amp;gt;100VPB/24h (12.5 vs 5 vs 11.1 vs 5.1%, p=0.42). 2 athletes had nsVT, both in D. All had similar exercise capacity (% predicted VO2max 157±26 vs 152±15 vs 147±24 vs 158±32%; p=0.11). Conclusion Hinge-point fibrosis was more prevalent in MA, possibly due to repeated hemodynamic stress during exercise, but is not associated with structural, functional or electrical consequences. Figure 1. Cardiac remodelling in elite athletes Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Fonds voor Wetenschappelijk Onderzoek (FWO)

A 3-Week, Low-Carbohydrate, High-Fat Diet Improves Multiple Serum Inflammatory Markers in Endurance-Trained Males.

Waldman, HS, Heatherly, AJ, Killen, LG, Hollingsworth, A, Koh, Y, and O'Neal, EK. A three-week, low-carbohydrate, high-fat diet improves multiple serum inflammatory markers in endurance-trained males. J Strength Cond Res 36(9): 2502-2508, 2022-This study examined the effects of a low-carbohydrate, high-fat diet (LCHF) on inflammatory marker responses in middle-aged endurance athletes. Eight male runners maintained their habitual mixed diet (HMD) in the first phase of the study before switching to a noncalorically restricted LCHF diet (∼70% of kcals from fat; carbohydrate <50 g) for 3 weeks. Subjects completed a 50-minute fixed pace treadmill running protocol in a hot environment, followed by a 5-km outdoor time trial. Fasting serum samples were collected immediately after exercise and heat stress restriction, and again 24 hours after the exercise/heat stressor. Thirty inflammation markers were assessed using the multiplex flow immunoassay technique. Seven markers (BAFF/TNFSF-13, sCD30/TNFRSF8, sCD163, Chitinase3-like1, gp130SIL-6Rβ, sTNFR-1, and sTNFR-2) reached statistical significance ( p < 0.05) favoring LCHF before exercise, and sCD30/TNFRSF8 favored ( p < 0.05) LCHF before (HMD = 459 ± 111; LCHF = 296 ± 100) and after (HMD = 385 ± 104; LCHF = 285 ± 104 pg·ml -1 ) exercise. Although the current dietary intervention was short in duration, LCHF seems to offer some protection against multiple chronic inflammation markers for physically active men between ages 30 and 50 years.

Middle-aged endurance athletes exhibit lower cerebrovascular impedance than sedentary peers.

Because elevated hemodynamic pulsatility could be mechanical stress against the brain, the dampening function of central and cerebral arteries is crucial. Regular endurance exercise training favorably restores the deteriorated dampening function of the aorta and carotid arteries in older populations, yet its effect on cerebrovascular dampening function remains unknown. To address this question, we compared cerebrovascular impedance, a frequency-domain relationship of the cerebral pressure and flow, in 21 middle-aged masters athletes who have been engaged in endurance training and races for >10 yr (MA, 53 ± 4 yr) with sedentary 21 age-matched (MS, 53 ± 5 yr) and 21 young (YS, 29 ± 6 yr) individuals. Using transfer function analysis, cerebrovascular impedance was computed from the simultaneously recorded carotid artery pressure (CAP, via applanation tonometry) and middle cerebral artery blood flow velocity (CBFV, via transcranial Doppler). In the frequency range of 0.78-3.12 Hz, coherence between pulsatile changes in CAP and CBFV was higher than 0.90 in all groups. All subjects exhibited the highest impedance modulus in the range of the first harmonic oscillations (0.78-1.56 Hz) mainly originating from cardiac ejection. Impedance modulus in this range was significantly lower in the MA than MS groups (0.88 ± 0.24 vs. 1.15 ± 0.29 mmHg·s/cm, P = 0.011) and equivalent to the YS (0.92 ± 0.30 mmHg·s/cm). Among middle-aged subjects, higher impedance modulus was correlated with lower mean CBFV (r = -0.776, P < 0.001) and cerebral cortical perfusion evaluated by MRI (r = -0.371, P = 0.015). These results suggest that middle-aged endurance athletes exhibited the significantly lower modulus of cerebrovascular impedance, which is associated with higher CBFV and cerebral cortical perfusion.NEW & NOTEWORTHY Impedance modulus in the range of first harmonic oscillations (0.78-1.56 Hz), which reflects heart rate at rest, was lower in middle-aged endurance athletes than in age-matched sedentary peers and was similar to young individuals. Prolonged endurance training is associated with the improved cerebrovascular dampening function in middle-aged adults. Lower cerebrovascular impedance modulus may contribute to maintaining brain perfusion in midlife.

Heart rate variability and recovery following maximal exercise in endurance athletes and physically active individuals.

The purpose of this study was to determine potential adverse cardiac effects of chronic endurance training by comparing sympathovagal modulation via heart rate variability (HRV) and heart rate recovery (HRR) in middle-aged endurance athletes (EA) and physically active individuals (PA) following maximal exercise. Thirty-six (age, 53 ± 5 years) EA and 19 (age, 56 ± 5 years) PA were recruited to complete a 2-week exercise diary and graded exercise to exhaustion. Time domain and power spectral HRV analyses were completed on recorded R-R intervals. EA had a greater HRR slope following exercise (95% confidence interval, 0.0134-0.0138 vs. 0.0101-0.0104 beats/s; p < 0.001). While EA had greater HRR at 1-5 min after exercise (all p < 0.01), PA and EA did not differ when expressed as a percentage of baseline heart rate (130 ± 19 vs. 139 ± 19; p = 0.2). Root mean square of successive differences in R-R intervals (rest and immediately after exercise) were elevated in EA (p < 0.05). Low-frequency (LF) and high-frequency (HF) spectral components were nonsignificantly elevated after exercise (p = 0.045-0.147) in EA while LF/HF was not different (p = 0.529-0.986). This data suggests greater HRR in EA may arise in part due to a lower resting HR. While nonsignificant elevations in HF and LF in EA produces a LF/HF similar to PA, absolute spectral component modulation differed. These observations require further exploration. Novelty Acute effects of exercise on HRV in EA compared with a relevant control group, PA, are unknown. EA had greater HRR and nonsignificant elevations in LF and HF compared with PA, yet LF/HF was not different. Future work should explore the implications of this observation.

Cerebrovascular Impedance in Middle-aged Endurance Athletes

Cerebrovascular Impedance in Middle-aged Endurance Athletes

Cardiac Remodeling in Middle-Aged Endurance Athletes and Recreationally Active Individuals: Challenges in Defining the “Athlete's Heart”

Chronic endurance exercise is known to elicit cardiac morphologic and functional adaptations collectively known as the “athlete's heart.” 1 Paterick T.E. Gordon T. Spiegel D. Echocardiography: profiling of the athlete's heart. J Am Soc Echocardiogr. 2014; 27: 940-948 Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar Yet the extent to which exercise burden and other phenotypic factors dictate the extent of cardiac remodeling remains understudied. While there are significant data in younger, elite athletes, reference values for cardiac morphology in long-standing, middle-aged endurance athletes (EAs) performing high-volume exercise, particularly when compared with recreationally active adults (RECs) who perform recommended levels of physical activity, remain limited. We therefore evaluated cardiac structure and training-related factors associated with cardiac remodeling. We hypothesized that middle-aged EAs would have greater cardiac remodeling than RECs. We further hypothesized that a higher peak rate of oxygen consumption ( V ˙ O2peak) and greater weekly exercise hours would predict a larger left ventricular (LV) volume.

Burden of premature atrial beats in middle-aged endurance athletes with and without lone atrial fibrillation versus sedentary controls.

The burden of premature atrial beats (PABs) at 24-h electrocardiographic (ECG) monitoring correlates with the risk of atrial fibrillation. It is unknown whether prolonged and intense exercise increases the burden of PABs, thus contributing to the higher prevalence of atrial fibrillation observed in middle-aged athletes. We compared the burden of PABs at 24-h ECG monitoring off therapy in 134 healthy middle-aged (30-60-year-old) competitive athletes who had practised 9 (7-11) h of endurance sports for 8 (4-15) consecutive years, 134 age- and gender-matched healthy sedentary individuals, and 66 middle-aged patients (20 athletes and 46 non-athletes) with 'lone' paroxysmal atrial fibrillation. More than 50 PABs/24 h or ≥1 run of ≥3 PABs were recorded in 23/134 (17%) healthy athletes and in 29/134 (22%) sedentary controls (p = 0.61). Healthy athletes with frequent or repetitive PABs were older (median 50 years vs. 43 years, p < 0.01) and had practised sport for a longer time (median 10 years vs. 6 years, p = 0.03). At multivariable analysis only age (odds ratio 1.11, 95% confidence interval 1.04-1.20, p < 0.01) remained an independent predictor of a higher burden of PABs. Also among patients with 'lone' paroxysmal atrial fibrillation, there was no difference in the prevalence of >50 PABs/24 h or ≥1 run of ≥3 PABs between athletes (40%) and controls (48%, p = 0.74). Middle-aged endurance athletes, with or without paroxysmal atrial fibrillation, did not show a higher burden of PABs at 24-h ECG monitoring than sedentary controls. Age, but not intensity and duration of sports activity, predicted a higher burden of PABs among healthy athletes.

PHYSIOLOGIC CARDIAC REMODELING IN MIDDLE-AGED ATHLETES IS INDEPENDENT OF ENDURANCE SPORT DISCIPLINE: A CARDIAC MAGNETIC RESONANCE STUDY

Physiologic cardiac remodelling has been characterized extensively in endurance trained athletes using both echocardiographic and cardiac magnetic resonance (CMR) imaging. Few data exist describing sport-specific CMR-derived values for middle-aged endurance athletes who perform sport-specific exercise that may differ in terms of exercise burden and extent of cardiac remodeling. This study sought to characterize cardiac structure and function by CMR in middle-aged endurance athletes (EA) by sporting discipline, and in comparison to recreationally-active adults (RA) who meet current physical activity recommendations. Healthy middle-aged EA (runners, cyclists, and triathletes) and RA control subjects with at a minimum of 10 years of regular physical activity and/or sport participation underwent exercise testing and a standardized cardiac magnetic resonance imaging (3.0 T MRI scanner). Participant demographics were not different between groups (Table 1), with the exception of a higher maximal exercise capacity in EA vs. RA. Atrial and ventricular volumes indexed to body surface area (BSA) were greater among all EA vs. RA groups despite no differences in LV and RV ejection fractions (Table 1). LV mass indexed to BSA and right atrial area were greater among all EA vs. RA groups. No differences in cardiac morphology and function data were observed between EA groups (runners vs. cyclists vs. triathletes). Middle-aged endurance athletes had physiological cardiac adaptations in both the atria and ventricles, characteristic of a long-standing endurance sport history and largely independent of sport modality. These CMR-derived data may provide reference ranges for physiologic remodeling in a cohort of middle-aged athletes.

DOES PHYSIOLOGIC CARDIAC REMODELING IN ENDURANCE ATHLETES ALTER REPOLARIZATION OR QT DYNAMICS?

Increases in QT and QTc duration, and their alterations with changes in heart rate, are associated with dysrhythmias and increased sudden death rates in population studies. Long standing endurance sport is associated with reduced cardiac mortality. Endurance athletes are known to develop physiologic LV remodeling concomitant with increases in LV mass, which may be associated with QT prolongation. However, QT dynamics in middle-aged athletes has not been studied extensively. We sought to compare the QT interval at rest and during exercise in healthy middle-aged adults with and without a history of long-standing endurance exercise. Healthy participants on no medications, between 45-65 years old (>10 years of regular physical activity participation) were recruited, and underwent physical examination. Eligible participants, including 86 endurance athletes (EA) and 24 recreationally-active (RA) adults, had a resting baseline 12-lead ECG and a standardized graded exercise testing with a 12-lead ECG taken every 1-2 minutes during exercise until exhaustion. QT intervals were measured as the longest QT in anterior precordial lead or lead 2 by two investigators and discrepancies resolved by consensus; QT intervals were corrected for rate using Bazett’s formula (QTc=QT/√RR in sec). Seventy-five participants also had a resting cardiac magnetic resonance to evaluate cardiac structure and physiological remodeling related to exercise. Participant demographics and ECG characteristics are summarized in Table 1. The higher cardiorespiratory fitness (VO2max) and left-ventricular mass reflected normal physiological adaptation to endurance exercise training. While mean resting QT interval was longer in EA vs. RA, there was no difference when QT interval was corrected for heart rate (QTc). The QT and QTc slopes (linear relationship of QT vs. RR and QTc vs. RR during exercise) were not different between EA and RA. Among long-standing middle-aged athletes with normal physiologic remodeling, there is no difference in QT intervals in EA vs. RA when corrected for their lower resting heart rate. Despite physiologic LV remodelling, chronic endurance exercise training is associated with normal repolarization at rest and during exercise among middle-aged endurance athletes.

Prolonged P wave duration is associated with right atrial dimensions, but not atrial arrhythmias, in middle-aged endurance athletes

BackgroundAtrial arrhythmias occur at a higher than expected prevalence amongst endurance athletes. Few studies have examined both atrial structure and arrhythmias in middle-aged endurance athletes. We examined the relationship between P-wave duration, atrial dimensions, and the presence of atrial ectopy in long-standing, middle-aged endurance athletes. MethodsMiddle-aged athletes with a minimum of 10 years of competitive endurance sport history and no history of structural heart disease or clinical atrial arrhythmias, had 12-lead ECGs to assess P-wave duration, signal-averaged ECGs (SAECG) to assess filtered P-wave duration, a 24 h Holter monitor to assess atrial ectopy, and echocardiography and cardiac magnetic resonance imaging to assess atrial structural characteristics. ResultsAmongst endurance athletes (n = 104; mean age = 54 ± 5 years; 63% male), filtered P-wave duration on SAECG was correlated with P-wave duration on 12-lead ECG (r = 0.36, p, 0.0001), as well as with larger CMR-derived RA areas (r = 0.30, p = 0.01) and volumes (r = 0.24, p < 0.05). There was no correlation between filtered P-wave duration and any LA measures on imaging (p > 0.05). There was no correlation between the incidence of atrial ectopy (premature atrial contractions or atrial tachycardia) and any electrocardiographic or structural measures. ConclusionLonger filtered P-wave duration was associated with larger RA areas and volumes, without an increase in atrial ectopy.

Left ventricular hypertrophy in middle-aged endurance athletes: is it blood pressure related?

Both regular physical activity and hypertension may be related to increased myocardial thickness, but the interplay between these two factors in causing cardiac remodeling in athletes is still a matter of debate. The aim of this study was to analyze the relation between resting and peak exercise blood pressure (BP) and myocardial hypertrophy in healthy middle-aged amateur endurance athletes. The study included 30 male, long-term athletes (mean age 40.9±6.6 years) who underwent resting BP assessment, cardiopulmonary exercise testing with peak exercise BP measurement, and cardiac magnetic resonance. We found that interventricular septal diameter is increased in athletes with high-normal resting BP (n=11, 37%) - median 13 mm (interquartile range: 12-13.75 mm), but not in those with optimal or normal BP (n=19) - median 10 mm (10-11.75 mm), P=0.001. This finding is accompanied by significantly higher left and right ventricular mass index and larger left atrial area in the first group. These differences are even more pronounced in athletes in whom high-normal BP is accompanied by exaggerated blood pressure response (EBPR) to exercise, whereas isolated EBPR to exercise does not lead to hypertrophy or further left atrial enlargement. Prehypertension, isolated or combined with EBPR to exercise, affects cardiac remodeling in athletes. Identification of increased myocardial thickness in pure endurance middle-aged athletes should merit further investigation on masked hypertension.

Invasive Coronary Physiological Assessment in Symptomatic Middle-Aged Endurance Athletes

Abstract Despite the health benefits of routine exercise, coronary artery disease (CAD) is common among older competitive athletes and is an important cause of sudden cardiac death. Athletes with suspected or confirmed CAD routinely undergo conventional coronary angiography involving the performance of invasive coronary physiological assessment using the fractional flow reserve (FFR) or the instantaneous-wave free ratio (iFR). Data defining the role of invasive coronary physiological assessment, while robust in general clinical populations, are untested among older competitive athletes with [...]

Pulmonary hemodynamic and right ventricular responses to brief and prolonged exercise in middle-aged endurance athletes.

Right ventricular (RV) function is closely coupled to pulmonary arterial (PA) hemodynamics and is believed to decline with prolonged exercise. A linear pressure-flow relationship is thought to exist between PA pressures and increasing exercise intensity in athletes, yet a paucity of directly measured pulmonary hemodynamic data exists supporting this contention. We sought to describe the PA pressure, PA wedge pressure (PAWP), and RV functional responses to brief and prolonged exercise in endurance-trained athletes. Twenty-one healthy athletes (54 ± 5 yr) underwent right heart catheterization to assess pulmonary hemodynamics during graded, submaximal exercise. Measurements were made at rest and during three stages of steady-state, semiupright cycle ergometry at heart rates of 100 beats/min (EX1), 130 beats/min (EX2), and 150 beats/min (EX3). Five athletes completed an additional 34 min at 130 beats/min for a total exercise time of 60 min [prolonged exercise (PLG)]. PA pressures and PAWP increased significantly at EX1 without a further rise at EX2, EX3, or PLG. PAWP adjusted for absolute work rate demonstrated a significant decline as exercise intensity increased from EX1 to EX2. The resistance compliance time constant decreased at EX1 without further changes at EX2, EX3, and prolonged exercise. RV function did not decline during PLG. After an initial rise in PA pressure and PAWP during early, nonsteady-state exercise, values remained constant despite increases in exercise intensity and duration. These data indicate that in healthy, middle-aged endurance-trained athletes, the PA and pulmonary venous/left atrial compartments rapidly accommodate high conduit flows produced during intensive and prolonged exercise while maintaining RV function. NEW & NOTEWORTHY The right ventricular (RV)-pulmonary arterial (PA) circulatory unit has not been well studied during prolonged exercise, and this study provides an ecological approach that reflects a typical bout of endurance training integrating a transition from rest to exercise with successive increases in intensity, progressing to steady-state, sustained exercise. We demonstrated a remarkably constant response of the PA and PA wedge pressure during incremental, steady-state exercise and that no changes occur in pulmonary pressures throughout prolonged exercise, concomitant to a preservation of RV performance.

Competitive Endurance Activities of Middle-aged Athletes as a Risk Factor for Atrial Fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia in athletes. Epidemiological studies have documented a greater prevalence of AF in athletes engaged in long-term endurance sports. Several mechanisms were proposed to underlie the association between exercise and AF, but the exact pathophysiology remains unclear. The studies up to now have been concentrated on the competitive middle-aged endurance athletes, but there is no evidence of AF prevalence among highly active noncompetitive athletes of the same age. Endurance athletes who do not compete might be at a lower risk for AF than their competitive peers. This hypothesis is theoretically examined, and the current evidence summarized in this article.