The enigma of the runner’s heart

The heart of the endurance runner is an enigma.  Typically the ventricles are enlarged and the muscular walls at least moderately thickened.  As discussed in my post of 20^th June 2009, the muscle is well perfused, unlike the situation in ischemic heart disease, in which obstruction of the coronary arteries results in a restricted supply of blood to the hypertrophied heart muscle.   Athletes are less likely to die of heart disease and live longer than sedentary individuals [1, 2].  However, as discussed in my blog on 28th February 2010, disturbances of heart rhythm are common. 

Elderly athletes have a very high rate of peculiarities of heart rhythm  For example, Jensen-Urstad and colleagues [3] recorded the electrocardiogram (ECG) continuously for 48 hours in 11 elderly male athletes with a life-long history of strenuous exercise, and 11 age-matched control men who were either sedentary or had been only moderately physically active.  Disturbances of rhythm were more common in the athletes.   Nine of the 11 athletes compared with 4 of the 11 controls had complex abnormalities of ventricular rhythm. In general abnormalities of ventricular rhythm are worrying because such abnormalites might lead to chaotic ventricular contraction (ventricular fibrillation) which is fatal.  In addition 9 of the 11 athletes compared with 4 of the controls exhibited more than 100 premature atrial contractions per day.   Premature atrial contraction is less worrying, though in some circumstances it can precede atrial fibrillation, which is disruptive and can lead to fatal stroke.  The two athletes without complex ventricular rhythms were among the 9 with more than 100 premature atrial contractions per day, so all 11 athletes exhibited a noteworthy disturbance of rhythm, in contrast to 5 of the 11 controls.  Overall, the study suggests that that life-long strenuous athletic training increases the risk of disturbance of heart rhythm. At least some of these disturbances of rhythm are of a type associated with risk of sudden death.

On the other hand, the increased life expectancy of athletes suggests that the benefits of running compensate for the increased risks.  In a 5 year follow up study  of 122 middle-aged or elderly cross-country skiers by Lie & Erikssen [4], of the 23 who were found to have ECG abnormalities at initial screening, almost all continued regular training but none suffered from heart attacks, though two did develop angina.  Overall, this study suggests that progression to serious heart conditions is rare. 

Who is at greatest risk?

Nonetheless, this leaves the question of whether there might be identifiable factors that create greater risk in some athletes.  It is well recognized that a small number of runners collapse and die during races, especially during long races such as the marathon, but the risk of sudden death is trivial compared with the increased life expectancy.  It is widely believed that most of those who die unexpectedly had previously undetected  rare abnormalities such as congenital hypertrophic cardiomyopathy.  However, the very high prevalence of rhythm disturbances in those who have engaged in long-term strenuous training reported by Jensen-Urstad [3] raises the possibility that risk might build up slowly but inexorably during long-term heavy training, and furthermore that the risk might indeed be a direct consequence of the hypertrophy of cardiac muscle arising from training.

Atrial fibrillation (AF)

While I am aware of little evidence apart from that provided by the study of Jensen-Urstad and colleagues [3] to suggest that heavy training might play a causal role in ventricular rhythm disturbances, the evidence that training might contribute to atrial fibrillation (AF) is much stronger.  I reviewed some of this evidence in my posting on 28^th February 2010.  Perhaps most compelling of all was the evidence from the recently reported study by Grimsmo and colleagues [5] demonstrating that 12.8 % of 122 long distance skiers competing in the annual 54 Km cross-county race from Rena to Lillehammer, in Norway developed ‘lone’ AF  (not accounted for by any underlying heart abnormality) during a follow-up period of 28-30 years.  The mean age of onset of the atrial fibrillation was 58 years.  Although AF is quite common among the elderly, occurring in about 5% of men over the age of 65, 12.8% is a very high rate to find among relatively young middle aged men.

AF has significant consequences.  It limits cardiac output and therefore limits performance; it quite often causes significant disruption of every-day activities; and,  more importantly from the perspective of health and longevity, it increases the risk of stroke.  Clots of blood form in the fibrillating left atrium and if dislodged, are prone to be borne via the aorta and the carotid arteries to the brain where they obstruct smaller blood vessels, resulting in a stroke.   The frequency of this in athletes with AF is unknown, but the one longitudinal study of athletes who continued to exercise after developing AF is salutary. In a 9 year follow-up study of 30 athletes with AF, Hoogsteen and colleagues [6] found that 3 (10%) had died; paroxysmal atrial fibrillation continued in 15 (50%) ; permanent atrial fibrillation emerged in 5 (17%) ; and 7 (23%) of showed no further atrial fibrillation.  Of three deaths during the follow-up, one was a sudden death during a race and is likely to have been due to a heart rhythm disturbance.  The other two were attributed to strokes.  Although Hoogsteen re-assuringly concludes that these deaths were not directly attributable to AF, the outcome is disconcerting.

My tachygrams

On 28^th February, I had posted a heart rate record made in R-R mode (that is, a record that gives the beat by beat variation in heart rate) during one of my easy-paced runs that showed wild beat to beat fluctuations that looked like AF – though I had been entirely unaware of any symptoms during the run.   The definitive diagnosis of AF depends on a demonstration of absence of the P waves that reflect the orderly conduction of an electrical impulse from the sino-atrial node where it is generated, through the walls of the atria to the atrio-ventricular node, from which point it spreads through the  ventricles producing the powerful ventricular contraction that ejects blood into the arteries. The record of R-R intervals (the tachygram) is based on detection of the sharp R wave associated with ventricular contraction, but contains no information about the P wave.  Therefore, my wild tachygram is not absolute proof of AF, though the comments which John Bedson recently posted on my post of 28^th February maintain that the evidence of AF is unequivocal and  further, he suggests that my running career is over.

John has extensive experience of AF and I respect his opinion.  However this leaves me in a quandary.  I had of course been to see a doctor after I had discovered the crazy heart rhythm, and have had some investigations.  So far the only feature the investigations have revealed is ventricular enlargement, but this is an expected consequence of my history of extensive running and other heavy exercise in young adult life, and my more modest but fairly regular running in recent years.  As far as my official medical record goes, no significant abnormality has yet been identified.

Nonetheless, I have scrutinized the tachygrams recorded in the majority of my training sessions over the past 8 months, and at this stage have concluded that the picture is one that warrants some caution.  I have had the wildly fluctuating rhythm on four occasions, lasting from a few minutes to half an hour, though never accompanied by any conscious awareness of symptoms.  On three of these occasions I had inhaled salbutamol before the run to relieve wheeziness due to asthma.  Since I have only used the salbutamol inhaler on 8 occasions over the eight month period, the data indicate that I have had the wild rhythm on 37% percent of the occasions when I have used salbutamol, and much fewer than 1% of occasions when I have not used salbutamol.  So a link between the wild rhythm and salbutamol is unlikely to be a chance occurrence.  Salbutamol relaxes the smooth muscle in the bronchi thereby relieving the wheeze of asthma, but can activate the adrenaline receptors in heart muscle, so it seems quite likely that salbutamol has caused accelerated and perhaps chaotic heart beat.   I have now abandoned use of salbutamol and have no intention of ever using it again, except in an emergency. At present after a run, my peak airways flow is around 200-250 liters per minute whereas it is in the range 500-600 litres per minute after use of salbutamol.  I will have to find some other way of dealing with the asthma that does not involve adrenaline-like medication. 

My future

Is my running career over, as John Bedson suggests? In general rhythm disturbances get worse as one gets older, and it is likely that my crazy heart rhythms will get worse, though it is noteworthy that in the 30 cases of AF followed by Hoogsteen [6], apparent recovery occurred in 23% while  17% progressed to persistent AF, and 50% continued to have episodes of AF.  

The ultimate decision might be forced upon me by the outcome of further cardiac investigations but if a reasonably thorough series of investigations reveals no significant abnormality, I will have to make a decision based on a careful appraisal of the evidence.  The full picture must take account of  both the risk and benefits.  While the study by Grimsmo provides compelling evidence that heavy endurance training can cause AF, the overall picture is more complex.

Beneficial effects of exercise

A study by Mozzafarian and colleagues [7] reveals that light to moderate exercise actually reduces the risk of AF.   Within a sample of over 5 thousand elderly individuals, those who exercised with moderate intensity had a 39 percent reduction in liklihood of suffering AF in comparison with sedentary individuals (that is, a relative risk of suffering AF of 61%). Even those reported to exercise at high intensity had a modest reduction compared to sedentary individuals, having a relative risk of 71%.  High intensity was not defined precisely but almost certainly was less intense than the exercise taken by the skiers studied by Grimsmo [5].  Although Mozzafarian and colleagues did not define high intensity clearly, they did provide an estimate of the reduction in risk produced by fairly vigorous walking.  Those in the highest quartile (i.e. the top 25% of the sample) for distance and pace of walking had only half the risk of developing AF compared with the lowest quartile.  Those who walked 60 or more blocks per week had a risk that was 56% of the risk among those who walked 4 or less blocks per week.  Similarly, those who walked at greater than 3 miles per hour had a risk that was only 59% the risk of those who walked more slowly than 2 miles per hour.  Thus, at least up to the upper end of the scale of recreational walking, the risk of AF decreases steadily with increasing volume and intensity of exercise.

It is also necessary to consider the other benefits of exercise.  There is good evidence that quite vigorous exercise increases life expectancy [1]; reduces risk of cancer [8]; lowers blood pressure and lowers risk of ischemic heart disease [2]; and there is rapidly accumulating evidence that it is associated with improved memory and other aspects of brain function [10].  Furthermore the overall evaluation of risks and benefits should take account of the fact that I simply enjoy running in the woods and meadows

These considerations lead me to conclude that if I do have AF, complete cessation of running would probably decrease my overall quality of life and longevity.  However, the challenge is to decide what is the optimum amount and type of exercise.

With regard to type of exercise, it is interesting to note that all instances of crazy rhythm have occurred when I was running in the low aerobic zone. It has never appeared during tempo runs, long interval sessions (1000m or 2000m repeats) or HIIT sessions.  On one occasion it had developed during a low aerobic run and disappeared when I increased HR into the mid-aerobic zone, as I climbed a steep hill.  On another occasion it occured as my heart rate decreased while jogging duirng the ‘cool down’ after a run.  It has never occurred during sessions of elliptical cross training, even though I generally push my cardiovascular system harder on the elliptical than when running.  Nonetheless, the study by Jensen-Urstad [3] suggests that the risk is associated with intensity, and the study by Mazzafarian [7] shows that the risk of AF is lowest for those who exercise at moderate intensity, so at least for the time being I will avoid high intensity sessions. 

The bliss of ignorance

I would never have known about the possibility of AF if I had not performed R-R recordings.  In light of the frequency of heart rhythm disturbances in elderly athletes reported by Jensen-Urstad [3], I wonder whether indeed a high proportion of elderly runners might actually have similar evidence of crazy rhythms but continue to run in blissful ignorance.  However I do not regard ignorance as blissful.  I would rather know as many facts as there are to know.  I am greatly reassured that whatever decisions I make regarding type and amount of running in the future, I can use my heart rate monitor to keep a close eye on whether or not my problems are deteriorating. This gives me the confidence to experiment cautiously. 

One crucial issue is whether there are any practical markers of deterioration that will provide advance warning of AF.   Examination of the tachygrams on those occasions when I have developed the crazy rhythm, reveals clear evidence of premature atrial contractions (PACs) – sharp spikes in which the rate of a singe beat is more than 30% higher than the surrounding beats, before the onset of the crazy rhythm.  As shown by Jensen-Urstad [3], PACs are common in elderly people and especially common in runners.  In most instances they are no related to AF.  Furthermore, as far as I can see I have a lower frequency of PACs than the elderly runner studied by Jensen-Urstad.   However in my case, there appears to be a clear relationship between PACs and the crazy rhythm and therefore, at least for the time being, I will regard frequency of PACs as a guide to either deterioration or improvement.  

An additional reason for regular monitoring it the possibility of seeking active treatment.  Medication can be effective in some cases, though several experts advocate a relatively minor surgical procedure in which a burst of radio frequency energy is employed the ablate the tissue that appears to be source of the chaotic rhythms, usually near the point where the pulmonary vein enters the left atrium.   However there is a small but appreciable mortality associated with this procedure, and despite the optimism of those who advocate the procedure, long term outcome remains uncertain.   A recent review carried out under the Health Technology Assessment programme [11] advised caution regarding this procedure.

As for my future racing career, I will simply have to see what story the tachygrams tell me.  For the near future, I am making no plans to race nor setting high performance goals for the next few months. 

References

[1] Paffenberger Jr RS, Hyde RT, Wing AL, et al. (1986) Physical activity, all-cause mortality, and longevity of college alumni. N Engl J Med.  314:605–14.

[2]  Berlin JA, Colditz GA. (1990) A meta-analysis of physical activity in the prevention of coronary heart disease. Am J Epidemiol. 132:612–28.

[3] K Jensen-Urstad, F Bouvier, B Saltin,M Jensen-Urstad (1998) High prevalence of arrhythmias in elderly male athletes with a lifelong history of regular strenuous exercise Heart 1998;79:161–164

[4] Lie H & Erikssen (198 ) Five-year Follow-up of ECG Aberrations, Latent Coronary Heart Disease and Cardiopulmonary Fitness in Various Age Groups of Norwegian Cross-country Skiers.  Acta Medica Scandinavica 216 (4),  377 – 383

[5] Grimsmo J, Grundvold I, Maehlum S, Arnesen H, (2010) High prevalence of atrial fibrillation in long-term endurance cross-country skiers: echocardiographic findings and possible predictors–a 28-30 years follow-up study. Eur J Cardiovasc Prev Rehahil. 17(1): 100-105

[6] Hoogsteen J, Schep GGG, VanHemel NM, Van Der Wall EE (2004) Paroxysmal atrial fibrillation in male endurance athletes: a 9 year follow-up.  Europace 6(3): 222-8

[7] Mozaffarian D, Furberg CD, Psaty BM & Siscovick D. (2008)  Physical Activity and Incidence of Atrial Fibrillation in Older Adults: The Cardiovascular Health Study. Circulation. 118;800-807.

[8] Jones et al (2010) Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer J Appl Physiol 108:343-348

[9] Smith, JP,  Blumenthal JA, Hoffman BM, Cooper H, Strauman TA, Welsh-Bohmer K, Browndyke JN, Sherwood A. (2010)  Aerobic exercise and neurocognitive performance: a meta-analytic review of randomized controlled trials.  Psychosomatic Medicine. 72(3):239-52.

[10] Rodgers M, McKenna C, Palmer S, Chambers D, Van Hout S, Golder S, Pepper C, Todd D, Woolacott N. (2008) Curative catheter ablation in atrial fibrillation and typical atrial flutter: systematic review and economic evaluation  Health technology assessment (Winchester, England), 12(34):iii-iv, xi-xiii, 1-198.