Service de Physiologie et d’Explorations Fonctionnelles, CHU de Strasbourg, Strasbourg, FRANCE
Address for correspondence: Stéphane Doutreleau, M.D., Ph.D., Service de Physiologie et d’Explorations Fonctionnelles, CHU de Strasbourg—NHC, 1 place de l’hôpital, 67091 Strasbourg Cedex, France; E-mail: firstname.lastname@example.org.
Submitted for publication April 2012.
Accepted for publication September 2012.
ABSTRACT: Training induces volume- and time-dependent morphological and functional changes in the heart. Heart rhythm disorders, such as atrial arrhythmia (including atrial fibrillation and atrial flutter), are a well-established consequence of such long-term endurance practice. Although resting bradycardia and first-degree atrioventricular persist in veteran athletes, a higher conduction system impairment has never been reported neither at rest nor during exercise. We report here two cases of Type II second-degree atrioventricular block occurring during exercise in middle-age well-trained athletes. Because animal and human studies suggest that a progressive myocardial fibrosis could explain such phenomenon, long-term training could also have consequences on the conduction pathways.
Chronic exercise leads to cardiovascular remodeling in well-trained endurance athletes and is often associated with abnormal ECG findings at rest (6). The more frequent particularities, such as first-degree or Mobitz 1 atrioventricular (AV) blocks, disappear with an acute bout of exercise, thus confirming a training-induced effect. However, AV block induced by exercise is uncommon in athletes and is not part of the cardiac changes commonly called “athlete’s heart.” Thus, it requires a careful, complete diagnostic evaluation. We report here two cases of exercise-induced second-degree AV block during training in two 56-yr-old well-trained male triathletes. They were informed that their cases would be submitted for publication, and they gave their written consent.
The characteristics of the two athletes are summarized in Table 1. Both were competitive triathletes, regularly training for at least 30 yr.
The first man reported, for approximately 1 yr, a chest discomfort concomitant with a decrease in heart rate when running, which was reportedly “divided by two,” as observed on his heart rate monitor. The physical examination, resting ECG (Fig. 1A), and echocardiogram (Table 1) were in the normal range. During incremental maximal exercise testing, a symptomatic intermittent change to a 2:1 Type II second-degree AV block was observed at a heart rate of 130 bpm, which spontaneously regressed during the recovery period (Fig. 2A). Coronarography and cardiovascular magnetic resonance imaging (MRI) were normal. Lyme serology and western blot were positive for Borrelia burgdorferi. A treatment with ceftriaxone for 4 wk and doxycycline for 2 wk was started without beneficial effect. No electrophysiological assessment was performed.
In this second case, the athlete reported an exercise-induced sensation of having his “legs cut off” 3 months after the beginning of the new training season. The physical examination and the echocardiogram (Table 1) were in the normal range. The ECG at rest showed a complete right bundle branch block (Fig. 1B). During the bicycle incremental maximal exercise testing, an acute change to a 2:1 Type II second-degree AV block was observed at a heart rate of 126 bpm (Fig. 2B). Coronarography, cardiovascular MRI, and Lyme serology were normal. The electrophysiological assessment revealed AV block within the bundle of His induced by atrial pacing (prolonged HV interval = 95 ms; HR = 120 bpm).
In both cases, a 6-month detraining period (i.e., light exercising) did not lead to any improvement, and training could not be continued. Therefore, the patients accepted the implantation of a dual chamber pacemaker (Accent®, St. Jude Medical, St. Paul, MN). Both started sports practice again without any symptom and with the initial performance level. To avoid acute drop in exercise heart rate, the maximal heart rate was programmed at 170 bpm and a specific algorithm was used to enable physiological AV conduction during exercise (called Ventricular Intrinsic Preference, VIP®, St. Jude Medical). All the parameters were controlled with an incremental exercise testing.
Type II second-degree AV block when exercising has been rarely reported in the literature in patients and, a fortiori, in athletes. Only one AV block case has been reported in an asymptomatic 19-yr-old soccer player during a cycle ergometer test (7). However, the AV block was complete and training could not be considered as the cause for this young athlete. We report here two cases of patients with nonischemic, second-degree AV block occurring during exercise. Although the origin of AV block was possibly different in each of these two cases, long-term endurance sports practice could explain the clinical presentation in these two middle-age athletes.
An increase in exercise heart rate requires both an increase in sinus rate and a concomitant shortening of the AV nodal and bundle of His refractory period, resulting in a 1:1 ventricular response (1). Except for the sinus node, the conducting system is not under vagal influence, and the exercise-induced shortening of the refractory period depends only on sympathomimetic stimulation (1,9). The vagolytic effect of exercise usually abolishes nodal block and normalizes resting first- and second-degree AV (Mobitz 1) block. Conversely, exercise may aggravate or precipitate Type II second-degree AV block by increasing the sinus rate without concomitant shortening of the refractory period of the relevant AV conducting tissue.
In the first case presented here, exercise-induced second-degree AV block was possibly due to Lyme carditis, the most common tick-borne disease in Europe. Cardiac complications are rare, but when present, the most frequent conduction disturbance is fluctuating resting AV blocks of different degrees (11). In the present case, IgM plasma levels were in the normal range, indicating that the disease was probably in its late stage and could explain the lack of beneficial effect from the medications. An exercise-induced AV block has never been reported in this context. According to electrophysiological assessment published in the literature (16), different localizations of conduction pathways have been described; therefore, exercise could potentially precipitate or aggravate the conduction abnormalities (see the mechanisms mentioned).
In the second case, none of the well-known causes of exercise-induced AV block, such as Lyme carditis, heart disease, or medication use, could be identified (10). This phenomenon is rare and usually secondary to an exercise-induced myocardial ischemia in the right coronary territory (5). We cannot exclude the possibility that an exercise-induced coronary spasm occurred during exercise in these two cases. However, no sign of ischemia was detected on the ECG before the block (ruling out myocardial ischemia), and such conduction disturbances have never been reported during coronary spasm.
Chronic and high-intensity endurance training may have an effect on both the structural and functional adaptation of the heart (14) and long-term sports practice is an independent risk factor for atrial fibrillation and atrial flutter (4,13). The effect on conduction pathways has been described in young athletes, with a longer resting refractory period for AV node conduction in response to an increased parasympathetic activity and/or a decrease in sympathetic tone and intrinsic adaptation at rest (15,18). Animal and human studies suggest a possible progressive myocardial fibrosis predominant in both the left and right atria and in the right ventricle (3,10,12). Because conduction pathways are predominantly localized in the right cavities and because myocardial fibrosis is mainly identified in the interventricular septum (10), long-term training might have an effect on the conduction system. The mechanisms responsible for such an evolution are not clear. The literature (10) suggests that it could result from a combination between acute exercise, biochemical changes (i.e., serum cardiac troponin increase after a long exercise) due to right myocardial injury, or a chronic myocardial remodeling with cardiac fibrosis. In these two cases, a right ventricular biopsy could have been of interest to demonstrate a patchy right myocardial fibrosis. Although sampling of endomyocardial biopsy is relatively safe, we chose not to do it because no late gadolinium enhancement was found in these two patients. This approach could be discussed because the voxel resolution for the late gadolinium enhancement in cardiovascular MRI is approximately 1.8 × 1.2 × 6 mm (17). Moreover, a normal cardiac imaging cannot exclude small regions of focal fibrosis or light diffuse interstitial fibrosis.
Some studies revealed a persistent sinus bradycardia in elderly male athletes. The implantation of a permanent pacemaker has been reported in four veteran athletes (8): three were former marathon runners (two pacemakers were implanted for asymptomatic complete resting AV block, and one was implanted for a 15-s asystole). The fourth was a former boxer admitted for loss of consciousness secondary to a 30-s asystole. A larger recent case report series compared former professional cyclists to age-matched controls (mean age, 66 yr) (2). The results of this study showed that although the incidence of sinus node disease and atrial arrhythmia at rest was higher in the group of athletes, there was no significant difference in terms of PR interval or in the occurrence of AV block.
In conclusion, Type II exercise-induced, paroxysmal AV block has been rarely reported in athletes in the literature. In such cases, a complete cardiac evaluation is required. Long-term endurance training might play a role in this clinical presentation. Numerous electrophysiological studies should be performed in these patients. Finally, long-term follow-up of former endurance athletes is necessary.
The authors declare that no funding has been received for this work and no professional relationships or manufacturers will benefit from the results of this report.
Results of the present study do not constitute endorsement of the American College of Sports Medicine.
1. Bakst A, Goldberg B, Schamroth L. Significance of exercise-induced second degree atrioventricular block. Br Heart J
. 1975; 37 (9): 984–6.
2. Baldesberger S, Bauersfeld U, Candinas R, et al.. Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists. Eur Heart J
. 2008; 29 (1): 71–8.
3. Benito B, Gay-Jordi G, Serrano-Mollar A, et al.. Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training. Circulation
. 2011; 123 (1): 13–22.
4. Claessen G, Colyn E, La Gerche A, et al.. Long-term endurance sport is a risk factor for development of lone atrial flutter. Heart
. 2011; 97 (11): 918–22.
5. Coplan NL, Morales MC, Romanello P, et al.. Exercise-related atrioventricular block. Influence of myocardial ischemia. Chest
. 1991; 100 (6): 1728–30.
6. Corrado D, Pelliccia A, Heidbuchel H, et al.. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J
. 2010; 31 (2): 243–59.
7. Crisafulli A, Melis F, Lai AC, et al.. Haemodynamics during a complete exercise induced atrioventricular block. Br J Sports Med
. 2002; 36 (1): 69–70.
8. Hood S, Northcote RJ. Cardiac assessment of veteran endurance athletes: a 12 year follow up study. Br J Sports Med
. 1999; 33 (4): 239–43.
9. Kapa S, Venkatachalam KL, Asirvatham SJ. The autonomic nervous system in cardiac electrophysiology: an elegant interaction and emerging concepts. Cardiol Rev
. 2010; 18 (6): 275–84.
10. La Gerche A, Burns AT, Mooney DJ, et al.. Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes. Eur Heart J
. 2012; 33 (8): 998–1006.
11. Lelovas P, Dontas I, Bassiakou E, et al.. Cardiac implications of Lyme disease, diagnosis and therapeutic approach. Int J Cardiol
. 2008; 129 (1): 15–21.
12. Lindsay MM, Dunn FG. Biochemical evidence of myocardial fibrosis in veteran endurance athletes. Br J Sports Med
. 2007; 41 (7): 447–52.
13. Mont L, Elosua R, Brugada J. Endurance sport practice as a risk factor for atrial fibrillation and atrial flutter. Europace
. 2009; 11 (1): 11–7.
14. Prior DL, La Gerche A. The athlete’s heart. Heart
. 2012; 98 (12): 947–55.
15. Stein B, Eschenhagen T, Rudiger J, et al.. Increased expression of constitutive nitric oxide synthase III, but not inducible nitric oxide synthase II, in human heart failure. J Am Coll Cardiol
. 1998; 32 (5): 1179–86.
16. van der Linde MR, Crijns HJ, de Koning J, et al.. Range of atrioventricular conduction disturbances in Lyme borreliosis: a report of four cases and review of other published reports. Br Heart J
. 1990; 63 (3): 162–8.
17. Vohringer M, Mahrholdt H, Yilmaz A, et al.. Significance of late gadolinium enhancement in cardiovascular magnetic resonance imaging (CMR). Herz
. 2007; 32 (2): 129–37.
18. Zeppilli P, Fenici R, Sassara M, et al.. Wenckebach second-degree A-V block in top-ranking athletes: an old problem revisited. Am Heart J
. 1980; 100 (3): 281–94.