The relationship between the volume of aerobic exercise and health benefits has been described alternatively as curvilinear or U shaped with the current consensus favoring the former .
The curvilinear relationship between aerobic exercise volume and cardiovascular and all cause mortality is firmly founded in multiple large epidemiologic studies. The suggestion that the curve turns upward at some range of exercise volume and becomes U shaped has not been actually demonstrated in large epidemiologic studies. and is conjectural.
.A reported increase in atrial fibrillation, foci of myocardial fibrosis and increased coronary artery calcification may provide mechanisms for this proposed ascending portion of the proposed U shaped curve which is the graphic representation of the "Extreme exercise hypothesis".
Is it possible or likely that there may be other deleterious effects of too much of a good thing in regard to aerobic exercise.?Sinus node disease and cardiac conduction defects might also represent long term deleterious effects of long time aerobic exercise.I say "might" because there is suggestive but not conclusive data to that effect.
My personal experience ( 35 years of marathon running and development of a left bundle branch block (LBBB) and an exercise induced,high grade second degree AV block requiring a pacemaker) and personal knowledge of two other long time, local runners also needing a pacemaker) peaked my interest.
But so much for numerator based reasoning what is the evidence for long time aerobic exercise contributing to the development of clinically relevant bradycardia induced by sinus node disease and/or A-V blocks. Case series and some epidemiologic studies provide some insight.
Andersen et al (1) published a widely quoted cohort study of 52.755 cross country skiers who participated in the Vasaloppet,a 90 kilometer cross country ski race,said to be the oldest and largest cross country event in the world.
Outcomes of interest were hospitalizations for atrial fibrillation (AF) or bradyarrhythmias( BA) as documented in Swedish national registries. When comparison were made between those who skied the race more times ( five or more) with those who skied only once there was a statistically significant increase in the hazard ratios for both AF and BA.For AF the HR was 1.29 (1.04 -1.61,for BA the HR was 2.10 (1.28-3.47).
A similar trend for AF and BA was noted when the faster skiers were compared with slower skiers but failed to reach statistical significance.
The bradyarrhythmias were mainly second degree heart blocks but the hospital codes did not distinguish between type 1 and 2 which is an important distinction as type1 (Wenckeback) is recognized in endurance athletes and is not usually considered an indication for pace maker implantation.
This was very coarse grain study and such important data such as history of elevated blood pressure,diabetes,obesity,alcohol abuse,habitual level of exercise, etc were not available ..
Baldesberger at al (2) studied 62 former professional cyclists who had long since retired from competition . and compared them to 62 age matched golfers for controls. Two had pacemakers.None had bundle branch blocks or second degree AV blocks while six were said to have sinus node disease based on heart rates less than 40 per minute. A question that the authors wanted to answer was -does the slow heart rate , first degree heart block and type 1 second degree block said to be common in competitive racers persist in later years after their period of heavy training has ended. Their persistence would suggest that vagal tone which is usually the proposed mechanism for those cardiac finding is not correct and that electrical remodeling of the SA node and AV node might be responsible. Though a small study these data suggesting increased risk of sinus node disease seem to be the best evidence so far since a comparison was made with age matched controls
The remaining data are simply case reports.
Dr R Northcote (3) published a study of the bradycardias seen in 20 long time, older endurance athletes in Scotland.Nine of the twenty had heart rates less than 35,six had a prolonged P-R interval and four had Mobitz type 2 heart block which disappeared with exercise..One of the 20 had a pacemaker implanted. A follow-up publication in 1999 (4) indicated that 2 more of the original group has been implanted with a pacemaker.
Doutreleau et al (3) published a report of 2 active endurance athletes with type 2 second degree heart block that occurred during exercise. The authors claimed erroneously that their publication was the first to report a high degree AV block either at rest or with exercise, somehow having missed Northcote 's2 reports. Exercise induced heart block is uncommon.
The athlete's bradycardia has traditionally been attributed to high vagal tone but an alternative proposed mechanism is electrical remodeling, specifically downregulation of the so called funny channel AKA HCN4. In older endurance athletes "fibrosis" of the SA noted is often proposed as the culprit but remodeling is an alternative explanation. The sparse data so far available suggest that SA node disease may be more common in endurance athletes while there is less compelling data implicating AV blocks.
In a comprehensive review of the "extreme exercise hypothesis" by Eijsvogels in 2018 (6) there is no discussion of the issue of bradyarrhythmias but perhaps clinically significant BA should at least be considered candidates for still another consequence of too much of a good thing.
In 1964 writing in the same journal Dr. Lev and Dr. Lenegre separately described age related fibrosis of the conduction system as a cause of heart block in the elderly. In 1999 ,JJ Schott (7) identified two families with progressive cardiac conduction defects related to a mutation in the gene encoding for the sodium channel SCN5A.
How could one know given for example an older endurance athlete with a heart block if Lev/Lenegre disease were responsible or if the block was somehow induced by excessive aerobic activity?
1) Andersen K et al Risk of arrhythmias in 52,755 long-distance cross-country skiers: a cohort study.Eur Heart J. 2013 3624 31, Dec 34 (47)
2)Baldesberger,S et al Sinus node disease and arrhythmias in the long term follow-up of former professional cyclists.Euro Heart Journal 2008, 29, 71-78
3)Northcote, R et al Electrocardiographic findings in male veteran endurance athletes. British Heart J. 1989,61,155-160
4)Hood,A and Northcote, R of Cardiac assessment of veteran endurance athletes, a 12 year follow up study. British J Sports Med. 1999, 33, 239-243
5)D'Souza, A,Cross talk opposing view: Bradycardia in the trained athlete is attributable to a downregulation of a pacemaker channel in the sinus node. J Physiol 2015 Apr 15 593 (pt 8)1749-1741
(6) Eijsvogels T. et al The "extreme exercise hypothesis":Recent findings and cardiovascular health implications Current Threat Options Cardio Med (2018)20:84
(7) Schott, JJ et al Cardiac conduction defects associated with mutations in SCN5A .Nature Genetics 23:20-21 1999
Addendum : 12/12/20 In the original posting the section of Lev/Lenegre and SCN5A was inadvertently omitted,
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