Middle-aged Endurance Athletes Research Articles

Burden of ventricular arrhythmias at 12-lead 24-hour ambulatory ECG monitoring in middle-aged endurance athletes versus sedentary controls.

Whether prolonged and intense exercise increases the incidence of ventricular arrhythmias in middle-aged athletes remains to be established. Prospective, case-control. We studied 134 healthy competitive athletes >30 years old (median age 45 (39-51) years, 83% males) who had been engaged in 9 ± 2 h per week of endurance sports activity (running, cycling, triathlon) for 13 ± 4 consecutive years. One hundred and thirty-four age- and gender-matched individuals served as controls. Both groups underwent 12-lead 24-h ambulatory electrocardiogram monitoring, which included a training session in athletes. Ventricular arrhythmias were evaluated in terms of number, complexity (i.e. couplet, triplet or non-sustained ventricular tachycardia), exercise-inducibility and morphology. Thirty-five (26%) athletes and 31 (23%) controls showed >10 isolated premature ventricular beats or ≥1 complex ventricular arrhythmia ( p = 0.53). Athletes with ventricular arrhythmias were older (median 48 versus 43 years old, p = 0.03) but did not differ with regard to hours of training and years of activity compared with athletes without ventricular arrhythmias. Ten (7%) athletes and six (5%) controls showed >500 premature ventricular beats/24 h ( p = 0.30): the most common ventricular arrhythmia morphologies were infundibular (six athletes and five controls) and fascicular (two athletes and one control). The prevalence of ventricular arrhythmias at 24-hour ambulatory electrocardiogram monitoring did not differ between middle-aged athletes and sedentary controls and was unrelated to the amount and duration of exercise. These findings do not support the hypothesis that endurance sports activity increases the burden of ventricular arrhythmias. Among individuals with frequent premature ventricular beats, the predominant ectopic QRS morphologies were consistent with the idiopathic and benign nature of the arrhythmia.

Does High-Intensity Endurance Training Increase the Risk of Atrial Fibrillation? A Longitudinal Study of Left Atrial Structure and Function.

Exercise mitigates many cardiovascular risk factors associated with atrial fibrillation. Endurance training has been associated with atrial structural changes which can increase the risk for atrial fibrillation. The dose of exercise training required for these changes is uncertain. We sought to evaluate the impact of exercise on left atrial (LA) mechanical and electrical function in healthy, sedentary, middle-aged adults. Sixty-one adults (52±5 years) were randomized to either 10 months of high-intensity exercise training or yoga. At baseline and post-training, all participants underwent maximal exercise stress testing to assess cardiorespiratory fitness, P-wave signal-averaged electrocardiography for filtered P-wave duration and atrial late potentials (root mean square voltage of the last 20 ms), and echocardiography for LA volume, left ventricular end-diastolic volume, and mitral inflow for assessment of LA active emptying. Post-training data were compared with 14 healthy age-matched Masters athletes. LA volume, Vo2 max, and left ventricular end-diastolic volume increased in the exercise group (15%, 17%, and 16%, respectively) with no change in control (P<0.0001). LA active emptying decreased post-exercise versus controls (5%; P=0.03). No significant changes in filtered P-wave duration or root mean square voltage of the last 20 ms occurred after exercise training. LA and left ventricular volumes remained below Masters athletes. The athletes had longer filtered P-wave duration but no difference in the frequency of atrial arrhythmia. Changes in LA structure, LA mechanical function, and left ventricular remodeling occurred after 10 months of exercise but without significant change in atrial electrical activity. A longer duration of training may be required to induce electrical changes thought to cause atrial fibrillation in middle-aged endurance athletes. URL: https://www.clinicaltrials.gov. Unique Identifier: NCT02039154.

PROLONGED P WAVE DURATION IS NOT ASSOCIATED WITH SUBCLINICAL ATRIAL ARRHYTHMIAS IN MIDDLE-AGED ENDURANCE ATHLETES

PROLONGED P WAVE DURATION IS NOT ASSOCIATED WITH SUBCLINICAL ATRIAL ARRHYTHMIAS IN MIDDLE-AGED ENDURANCE ATHLETES

The ECG of athletes

There has been a long standing controversy on the role of a resting electrocardiogram (ECG) in the preparticipation examination of athletes, as well as in children and adolescents, in leisure time and competitive athletes. Besides other arguments, this was due to the limited validity, which led to false positive and false negative findings. Recent studies from different research groups yielded a significant improvement in establishing ECG criteria in athletes to discriminate normal from abnormal or pathological findings in athletes. This is additionally supported and improved by a software-based ECG device considering the new Seattle criteria. These new criteria from the Seattle conference reliably discriminate normal from abnormal findings. Frequent ECG findings in athletes, especially in those engaged in endurance sports are sinus bradycardia, atrioventricular (AV) block and signs of left ventricular hypertrophy. Abnormal findings are related to structural left ventricular alterations due to cardiomyopathy, mainly hypertrophic with or without outflow tract obstruction, arrhythmogenic right ventricular cardiomyopathy (ARVC) and dilated cardiomyopathy. The ECG findings suggestive of electrical conductance disorders are observed in channelopathies, Wolff-Parkinson-White (WPW) syndrome supraventricular arrhythmias or disturbances of cardiac conduction. The main diseases are long or short QT syndrome, Brugada syndrome and catecholaminergic polymorphic ventricular tachycardia. Atrial fibrillation, mostly paroxysmal, is also now more frequently observed especially in middle aged endurance athletes. Interpretation of ECG in young and older athletes requires in-depth knowledge in cardiology and sports medicine. The interpretation can only be carried out by considering medical history, clinical examination and ethnicity. Profound and long-term experience of athlete's ECG interpretation is required to protect athletes and to prevent cardiac emergencies.

Endurance sport and cardiovascular health

The cardiovascular benefits of exercise are established and individuals exercising regularly reduce their risk of adverse events from coronary artery disease by 50% and gain at least 3 additional years of life. When one considers the burgeoning epidemic of childhood obesity and its complications, exercise may be regarded as the most clinically and cost effective prescription dispensed by healthcare professionals. The intensity of exercise required to achieve these benefits is 6-8 METS which equates to walking briskly or jogging for 30 minutes daily. Competitive athlete, particularly those engaging in endurance events such as long distance running, cycling, rowing, canoeing, triathlon, marathon and iron man events partake in physical activity of a much higher intensity for as many as 20 hours per week. The requirement of a 5-6 fold increase in cardiac output is met by physiological structural and functional adaptations within the heart. Sinus bradycardia, large QRS complexes and a 15-20% increase in ventricular cavity size are the hall mark of the ‘athlete’s heart’ and are most pronounced in large male endurance athletes. Up to 50% of male endurance athletes show ventricular dimensions exceeding predicted upper limits for the general population. Such alterations are considered benign and reverse after a period of detraining. The potential hazards of intensive exercise are occasionally highlighted by the sudden cardiac death of an individual during or immediately after exercise, however, such catastrophes are extremely rare, largely striking young athletes harboring inherited or congenital arrhythmogenic substrates. Despite the emotive visibility afforded by these deaths in the media, the positive reputation of exercise remains unscathed by the fact that exercise is regarded as a mere trigger for arrhythmia in a small proportion of predisposed individuals but never directly incriminated in the pathogenesis of the fatal substrate. The past 2 decades has witnessed an extraordinarily engaging athletic milieu where humanly possible achievements seem infinite. In parallel there have been multiple reports of increased serum concentrations of biomarkers of cardiac damage and transient cardiac dysfunction after intensive endurance exercise. The mechanisms for these observations is uncertain but raise the possibility that repeated bouts of intensive endurance exercise may culminate in adverse cardiac remodeling and arrhythmogenic substrates in a small minority of endurance athletes. Perhaps the most persuasive evidence for this concern is the 5-fold increase in the prevalence of atrial fibrillation in middle aged endurance athletes compared with the relatively sedentary population of the same age.

Masked hypertension and cardiac remodeling in middle-aged endurance athletes.

Extensive endurance training and arterial hypertension are established risk factors for atrial fibrillation. We aimed to assess the proportion of masked hypertension in endurance athletes and the impact on cardiac remodeling, mechanics, and supraventricular tachycardias (SVT). Male participants of a 10-mile race were recruited and included if office blood pressure was normal (<140/90 mmHg). Athletes were stratified into a masked hypertension and normotension group by ambulatory blood pressure. Primary endpoint was diastolic function, expressed as peak early diastolic mitral annulus velocity (E'). Left ventricular global strain, left ventricular mass/volume ratio, left atrial volume index, signal-averaged P-wave duration (SAPWD), and SVT during 24-h Holter monitoring were recorded. From 108 runners recruited, 87 were included in the final analysis. Thirty-three (38%) had masked hypertension. The mean age was 42 ± 8 years. Groups did not differ with respect to age, body composition, cumulative training hours, and 10-mile race time. Athletes with masked hypertension had a lower E' and a higher left ventricular mass/volume ratio. Left ventricular global strain, left atrial volume index, SAPWD, and SVT showed no significant differences between the groups. In multiple linear regression analysis, masked hypertension was independently associated with E' (beta = -0.270, P = 0.004) and left ventricular mass/volume ratio (beta = 0.206, P = 0.049). Cumulative training hours was the only independent predictor for left atrial volume index (beta = 0.474, P < 0.001) and SAPWD (beta = 0.481, P < 0.001). In our study, a relevant proportion of middle-aged athletes had masked hypertension, associated with a lower diastolic function and a higher left ventricular mass/volume ratio, but unrelated to left ventricular systolic function, atrial remodeling, or SVT.

Short-term periodized aerobic training does not attenuate strength capacity or jump performance in recreational endurance athletes

The purpose of this study was to investigate the effects of three different distributions of aerobic training on the isokinetic strength and vertical jump performance [SJ, CMJ and Abalakov (ABA)] in thirty middle-aged endurance athletes (38.7 ± 9.8 yrs; 174.7 ± 6.5 cm; 72.0 ± 9.8 kg). Three zones of training were required to quantify volume of training: Zone 1, low-intensity-training < VT1; Zone 2, threshold-training, between VT1 and VT2; and Zone 3, high-intensity-training > VT2. The INC group (n = 10) began training in the Zone 1 and then gradually built up training in Zone 2 and Zone 3, thereby increasing the intensity of aerobic activity over the 4-week training period. The CON group (n = 10) performed the same activity every week in Zones 1, 2 and 3. The FRE group followed a free distribution of endurance training loads (n = 10). The results showed significant decreases in peak torque knee extension 30° (p < 0.05) in CON group and significant decreases (p < 0.05) in ABA in FRE group. Results provide a physiological basis to support several performance studies that consistently indicate 5 d·wk(-1) endurance training does not impair strength development over the short term. In conclusion, variations in volume and intensity in training groups did not interfere with isokinetic strength and vertical jump performance.

Atrial fibrillation in endurance athletes

There is a growing population of veteran endurance athletes, regularly participating in training and competition. Although the graded benefit of exercise on cardiovascular health and mortality is well established, recent studies have raised concern that prolonged and strenuous endurance exercise may predispose to atrial and ventricular arrhythmias. Atrial fibrillation (AF) and atrial flutter are facilitated by atrial remodelling, atrial ectopy, and an imbalance of the autonomic nervous system. Endurance sports practice has an impact on all of these factors and may therefore act as a promoter of these arrhythmias. In an animal model, long-term intensive exercise training induced fibrosis in both atria and increased susceptibility to AF. While the prevalence of AF is low in young competitive athletes, it increases substantially in the aging athlete, which is possibly associated with an accumulation of lifetime training hours and participation in competitions. A recent meta-analysis revealed a 5-fold increased risk of AF in middle-aged endurance athletes with a striking male predominance. Beside physical activity, height and absolute left atrial size are independent risk factors for lone AF and the stature of men per se may explain part of their higher risk of AF. Furthermore, for a comparable amount of training volume and performance, male non-elite athletes exhibit a higher blood pressure at rest and peak exercise, a more concentric type of left ventricular remodelling, and an altered diastolic function, possibly contributing to a more pronounced atrial remodelling. The sports cardiologist should be aware of the distinctive features of AF in athletes. Therapeutic recommendations should be given in close cooperation with an electrophysiologist. Reduction of training volume is often not desired and drug therapy not well tolerated. An early ablation strategy may be appropriate for some athletes with an impaired physical performance, especially when continuation of competitive activity is intended. This review focuses on the prevalence, risk factors, and mechanisms of AF in endurance athletes, and possible therapeutic options.

Blood pressure reduction following prolonged exercise in young and middle-aged endurance athletes

Previous studies examining the relationship between exercise dose and post-exercise hypotension (PEH) have employed a limited range of exercise duration and subject age. We extended the dose-response curve by studying two intensities of prolonged exercise that may produce a greater magnitude of PEH and reveal age differences in the exercise dose-response relationship for PEH. Two groups of healthy recreational endurance athletes were studied: Young (n = 17; age 28 ± 1.1 years) and middle-aged participants (n = 18; 52 ± 0.90 years). They performed on separate occasions, 120 min of prolonged exercise (running) at moderate (60% VO2max) and high intensities (80% VO2max). PEH after 1 hour of recovery was similar within each age group for either exercise intensity, but was significantly greater in the middle-aged group (moderate intensity, -12.3 ± 1.6 mmHg; high intensity, -15.1 ± 1.7 mmHg) compared with the young group (moderate intensity, -1.2 ± 1.7 mmHg; high intensity, -5.7 ± 2.5 mmHg; p < 0.05). Stepwise regression showed that baseline blood pressure but not age was significantly related to the degree of PEH. Thus, the greater PEH seen in the middle-aged group is attributed to their higher baseline blood pressure (124 ± 3.0/79 ± 2.0 mmHg) than the young group (111 ± 2.0/69 ± 1.8 mmHg). A reduced total peripheral resistance following exercise was the primary contributor to PEH across both age groups and exercise intensities. We conclude that prolonged exercise induces a significant PEH regardless of exercise intensity.