Bradycardia In Athletes Research Articles

Wide Spectrum of Bradyarrhythmias and Supraventricular Tachyarrhythmias in Sportsmen: Run Forrest, Run?!

The intricate relationship between sports participation and cardiac arrhythmias is a key focus of cardiovascular research. Physical activity, integral to preventing atherosclerotic cardiovascular disease, induces structural, functional, and electrical changes in the heart, potentially triggering arrhythmias, particularly atrial fibrillation (AF). Despite the cardiovascular benefits, the optimal exercise amount remains unclear, revealing a J-shaped association between AF and exercise. Endurance athletes, particularly males, face elevated AF risks, influenced by age. Risk factors vary among sports modalities, with unique physiological responses in swim training potentially elevating AF risk. Clinical management of AF in athletes necessitates a delicate balance between rhythm control, rate control, and anticoagulation therapy. Sport-induced bradyarrhythmias, including sinus bradycardia and conduction disturbances, are prevalent among athletes. Managing bradycardia in athletes proves challenging due to its complex and not fully understood pathophysiology. Careful consideration is required, particularly in symptomatic cases, where pacemaker implantation may be necessary for sinus node dysfunction. Although pacing is recommended for specific atrioventricular (AV) blocks, milder forms often prevail without restricting sports participation. This review explores the nuanced relationship between exercise and tachy- and bradyarrhythmia in athletes, addressing the challenges clinicians face when optimizing patient care in this distinctive population.

BRADYCARDIA IN ATHLETES: DOES THE TYPE OF SPORT MAKE ANY DIFFERENCE? – A SYSTEMATIC REVIEW

ABSTRACT Bradycardia in athletes can range from moderate to severe, and the factors that contribute to slow heart rate are complex. Studies investigating the mechanisms associated with this condition are controversial, and may be linked to the form of exercise practiced. A systematic literature review was conducted to discuss bradycardia mechanisms in athletes who practice different forms of sport. The databases consulted were Pubmed (MEDLINE), Clinical Trials, Cochrane, Scopus, Web of Science, SciELO, Sport Discus and PEDro. The search included English language articles published up to January 2019, that evaluated athletes who practiced different forms of sport. One hundred and ninety-three articles were found, ten of which met the inclusion criteria, with 1549 male and female athletes who practiced diverse forms of sport. Resting heart rate and cardiac structure were studied in association with the form of sport practiced, through heart rate variability, electrocardiogram, echocardiogram and pharmacological blockade. The studies suggest that a slow resting heart rate cannot be explained by increased vagal modulation alone, but also includes changes in cardiac structure. According to the studies, different sports seem to produce different cardiac responses, and the bradycardia found in athletes can be explained by non-autonomic and autonomic mechanisms, depending on the type of effort or the form of sport practiced. However, the mechanism underlying the slow heart rate in each form of sport is still unclear. Level of evidence II; Prognostic studies - Investigating the effect of a patient characteristic on the outcome of disease.

P4423Extreme bradycardia in athletes is due to intrinsic changes within the heart

Abstract Background It is well known that athletes and in particular endurance athletes have lower resting heart rates than non-athletes. This has generally been considered a healthy adaptation. Traditionally this was thought be due to increased vagal tone. Several studies have shown that endurance athletes continue to have lower heart rates in the absence of autonomic influence suggesting bradycardia is due to intrinsic changes within the heart. A subset of endurance athletes have very low heart rates with Tour de France cyclists having described heart rates in the 30s. It is unclear whether in these elite athletes with very low heart rates the profound bradycardia is due to autonomic influence or intrinsic changes within the heart. Aim The aim of this study was to determine if extreme bradycardia in athletes is due to excess vagal tone or more profound intrinsic changes within the heart. Methods We recruited three cohorts for this study: non-athlete controls (NA), endurance athletes with a documented resting heart rate >40 (EA) and endurance athletes with a resting heart rate <40 (BA). All participants underwent baseline testing including ECG, echocardiography and VO2 max testing. All participants came back on a second occasion for treatment with dual autonomic blockade (DAB) to determine intrinsic heart rate in the following manner. After resting supine for five minutes resting heart rate was measured. Participants were then administered 0.04mg/kg of intravenous atropine. After five minutes participants were then administered 0.05mg/kg of intravenous metoprolol. This was repeated every five minutes until there was no further drop in heart rate or 0.2mg/kg had been administered. The resting heart rate at this stage was recorded as the intrinsic heart rate. Parasympathetic blockade was confirmed by lack of response to Valsalva manoeuvre and sympathetic blockade was confirmed by lack of response to metoprolol. VO2 max testing was then performed to determine maximum heart rate. Results 9 NA (7 male), 10 EA (8 male) and 5 BA (4 male) participated in this study. The average age was similar in all groups (NA 32.9y, EA 32.4y, BA 31.4y). The average resting heart rate was 71.7 in the NA group, 48.3 in the EA group and 41.6 in the BA group (p<0.05 for comparisons between all three groups). Following dual autonomic blockade resting heart rate was 86.0 in the NA group, 76.9 in the EA group and 64.4 in the BA group (p<0.05 for comparisons between all three groups). Maximum heart rate under DAB was 140.1 in the NA group, 138.0 in the EA group and 140.4 in the BA group. These differences were not significant. Conclusion In athletes with very low heart rates, bradycardia is due to more profound intrinsic changes within the heart. Acknowledgement/Funding NHMRC Project Grant

Last Word on Point:Counterpoint.

to the editor: At scientific or clinical meetings or at other academic institutions when I argue that heart rate variability cannot be used in any simple manner to measure autonomic tone or I speak about our work on the resting bradycardia in athletes, I am faced with the problem of a disbelieving

Does Deep Bradycardia Increase the Risk of Arrhythmias and Syncope in Endurance Athletes?

The aim of this study was to evaluate whether endurance athletes who exhibit deep bradycardia are more prone to arrhythmias and reflex syncope than their non-bradycardic peers. 46 healthy men (ages 19-35) were divided into 3 groups based on whether they were sedentary (SED,<2 h/week) or endurance trained (ET,>6 h/week), and non-bradycardic (NB, resting heart rate (HR)≥60 bpm) or bradycardic (B, resting HR<50 bpm). Resting HR was lower in ETB vs. ETNB and SED (43.8±3.1, 61.3±3.3, 66.1±5.9 bpm, respectively; p<0.001). Thus, 16 SED, 13 ETNB and 17 ETB underwent resting echocardiography, maximal exercise test, tilt test (TT) and 24 h-Holter ECG. Subjects were followed-up during 4.7±1.1 years for training, syncope and cardiac events. Our results showed that incidence of arrhythmias and hypotensive susceptibility did not differ between groups. During follow-up, no episode of syncope or near-syncope was reported. However, cardio-inhibitory syncope occurrence tended to be higher in ETB. Left ventricular end-diastolic diameter index was increased in ETB vs. ETNB and was correlated with resting HR (r=- 0.64; p<0.001). As a result, athletes with deep bradycardia do not present more arrhythmias and more hypotensive susceptibility than their non-bradycardic peers. Cardiac enlargement and autonomic alteration both seem to be involved in an athlete's bradycardia.

Rebuttal from Alicia D'Souza, Sanjay Sharma and Mark R. Boyett

We read with great interest the arguments presented by Coote & White (2015) in favour of the traditional view that exercise training decreases resting heart rate by an increase in the tonic discharge of the vagal nerves. However, we are not persuaded. Coote & White (2015) quote Maciel et al. (1985); however, Maciel et al. (1985) showed that the intrinsic heart rate of trained athletes remains lower after full vagal nerve block. Although Ordway et al. (1982) reported that there was no training-induced bradycardia in six cardiac-denervated dogs, there is evidence to the contrary: Kavanagh et al. (1988) reported that in eight highly compliant cardiac transplant patients (with no evidence of cardiac reinnervation) there was. Coote & White (2015) state that the high frequency (HF) component of heart rate variability (HRV) is a robust surrogate for vagal tone and the increase in the HF component in athletes is evidence of increased vagal tone. However, we have argued that HRV cannot be used in any simple way to measure autonomic nerve activity (Monfredi et al. 2014). Our arguments are based on those of Zaza & Lombardi (2001), who showed that the HF component (like other measures of HRV) is highly sensitive to the heart rate. For example, on training Al-Ani et al. (1996) observed a 12 beats min–1 decrease in the resting heart rate (69 decreased to 57 beats min–1) and a 1.5-fold increase in the HF component, whereas Zaza & Lombardi (2001) calculated that a 10 beats min–1 decrease (70 to 60 beats min–1) will cause a 3-fold increase simply because of the decrease in heart rate alone. Coote & White (2015) mention the sensitivity of the baroreceptor–heart rate reflex; this is a commonly used index of autonomic balance, but this too relies on HRV and is therefore flawed (Zaza & Lombardi (2001). The data from Danson & Paterson (2003) quoted by Coote & White (2015) showing a training-induced upregulation of NOS-1 in intracardiac cholinergic ganglia are fascinating; the data indicate an improvement in vagal neurotransmission but this does not prove it is responsible for the training-induced bradycardia. For example, our own data demonstrate a training-induced reduction in the sinus node of mRNA for the M2 receptor and Kir3.1, Kir3.4, HCN4, Cav1.2 and Cav1.3 channels (responsible for the ACh-sensitive currents IK,ACh, If and ICa,L) (D'Souza et al. 2014); these changes potentially reduce the sensitivity of the sinus node to vagal tone. Overall, given that direct recording of cardiac vagal activity is currently unfeasible, the available evidence tips the balance in favour of electrophysiological remodelling of the sinus node to explain the resting bradycardia in athletes. A challenge for neuroscientists is to measure vagal activity to the sinus node directly and not rely on questionable surrogates.

Athlete's bradycardia may be a multifactorial mechanism

to the editor: Boyett et al. ([1][1]) provides interesting evidences, arguing that endurance training-induced bradycardia seems mostly related to a remodeling of the sinoatrial node. However, we would like to add four complementary elements to extend this paper. #### About intrinsic heart rate. In

Commentaries on Viewpoint: Is the resting bradycardia in athletes the result of remodeling of the sinoatrial node rather than high vagal tone?

Commentaries on Viewpoint: Is the resting bradycardia in athletes the result of remodeling of the sinoatrial node rather than high vagal tone?

Viewpoint: Is the resting bradycardia in athletes the result of remodeling of the sinoatrial node rather than high vagal tone?

it is well known that athletes have a low resting heart rate, i.e., a resting bradycardia and heart rates below 30 beats/min have been reported ([7][1]). For example, Wikipedia states that the Tour de France cyclist, Miguel Indurain, had a resting heart rate of 28 beats/min when race fit. The

Athlete's bradycardia as an embolising disorder? Symptomatic arrhythmias in patients aged less than 50 years.

One hundred and sixty consecutive patients less than 50 years of age (mean 38 years) referred for long term electrocardiographic recording were evaluated retrospectively. Significant cardiac arrhythmias were detected in 51 of 107 (48%) patients examined because of syncope or dizzy spells or both. Of 39 patients examined for cardiac complaints or presumed complex arrhythmias, 15 (38%) had significant arrhythmias. Of 14 patients examined because of otherwise unexplained strokes, nine had slow sinus rates. Of these, one patient had recently undertaken moderately intensive athletic activity and four had been undertaking vigorous athletic activities for several years. All of the 12 active athletes who were followed up on account of syncope or dizzy spells were free of symptoms after reducing their athletic activities. The cardiac rhythm returned to normal in four out of five who underwent repeat long term electrocardiographic recording. It is suggested that vigorous athletic activity in subjects of 30-50 years of age may transform the adaptative bradycardia of the athlete into a condition similar to the embolising sick sinus syndrome.

Ambulatory electrocardiographic findings in young athletes between 14 and 16 years of age.

Ambulatory electrocardiographic recordings were obtained from 35 male athletes between 14 and 16 years old, and from 35 male non-athlete controls of the same ages, in order to determine the effects of regular physical training on cardiac electrical activity. In the young athletes, the heart rates were significantly (P less than 0.01) lower than in the nonathletes. Sinus intervals over 2.00 s were present in five athletes (14%) and one control (3%). First-degree atrioventricular block was detected in eight athletes (23%) and four controls (11%), and second-degree block was detected in seven athletes (20%) and one control (3%) (P less than 0.05). Ventricular premature beats were present in 60% of athletes and 57% of controls. The bradycardia in athletes did not predispose to ventricular ectopic activity, since heart rates at the times of occurrence of extrasystoles were higher in athletes than in controls. Even after two years of regular physical training there are significant differences in sinus nodal function and atrioventricular conduction as between young athletes and controls.

A more explicit estimate for the “implications of athlete's bradycardia on lifespan”

L. A. Kuehn has estimated the dependence of lifespan on exercise, based upon the hypothesis of a fixed total number of heartbeats, and upon a reduction in resting heart rate (“bradycardia”) due to exercise. He did not, however, assign an explicit dependence of resting heart rate decrease upon duration and intensity of exercise. With introduction of such a dependence, Kuehn's result is made more explicit. The dependence also eliminates results which can be viewed as paradoxical, viz. increased lifespan resulting from finite bradycardia with zero time spent on exercise. The extended theory suggests a lifespan increase for moderate amounts of exercise, and a decrease for very large amounts.

Implications of athlete's bradycardia on lifespan

It has been postulated that there may be a rather fixed number of heartbeats in the lifespans of non-hibernating homeothermic mammals, a concept reminiscent of a “heartbeat bank”. Based on this conjecture, simple equations were derived which predict the possible prolongation of the life of an exercising individual compared to that of a sedentary person. It appears that life could be extended, provided that exercise training results in significant reduction in heart rate (athlete's bradycardia).

Autonomic nervous control of cardiac frequency in the exercise-trained rat.

Autonomic nervous control of cardiac frequency in the exercise-trained rat.