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 20th 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 28th 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 28th 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 28th 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. 


[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 SkiersActa 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.


21 Responses to “The enigma of the runner’s heart”

  1. Ewen Says:

    Canute, I hope your running career isn’t over. I was looking forward to following your progress towards a possible marathon a few years down the track. At least you have the data and can monitor your heart for any changes in future months/years. I hope you fall in that 23% of cases that shows apparent recovery.

    In the study of the cross-country skiers, 12.8% developed AF, but I’m wondering if the stress/duration of a 54k event (and similar events the athletes would have trained for/done) predisposes them to the condition? In other words, is excessively long and hard racing more likely to cause AF than ‘moderate length’ racing?

    • canute1 Says:

      Ewen, Thanks for your comment. You raise the crucial issue of whether or not the risk is only appreciable with extreme training. The sweet spot of minimum risk appears to lie somewhere between vigorous walking (eg 60 blocks per week faster than 3 mph) and training for (and racing) a 54Km ski marathon, but that is a wide range. The other intriguing question is whether it is intensity or volume that does the damage. There is very little evidence addressing this question. My own observations suggest that rhythm is much more stable at high intensity. However that observation does not address the question of whether or not the relevant tissue damage occurs at high intensity or high volume.
      As for my own future, I am afraid I have to be patient, and also shrewd in weighing up evidence.

  2. Henry Szwinto Says:

    Hi Canute,
    When I took up running at the age of 38 (now 52) I started training with a heart rate monitor and during one running time trial where I was aware of irregular heart beats before the start the heart rate went up to 235 so I thought I should get it checked out and eventually we were able to confirm AF. I have been aware of irregular heart rythms since I was a teenager playing hockey and for me it is like an engine missfiring intermittently. I can be perfectly fine for months with nothing more than a few ectopics. If I am stressed (training, work, illness, wife) it can happen almost weekly but usually when I go into AF I stay in it for 24-48 hours.
    There are clearly different forms of AF because you say you were never aware of yours. I immediately feel like my engine is spluttering and if it were in a race my heart rate would jump by about 80 bpm and I my pace would drop by about 30 sec/ml. I have captured scenarios on my garmin and will gladly send you graphs for interest.
    Having been through the mill myself I can offer you the following advice. Don’t try too hard to find a reason. There probably isn’t one. Do avoid stimulants and try to avoid stress but accept that even so you will still get episodes of AF. You will not be able to control it. Instead you need to accept it and live with it. (I can assure you that living with it can be pretty tough. On 2 occassions I have been on the start line of the London Marathon in 2.35 form only to go into AF in the first 400 metres.) There are treatments available including lazer ablation but I personally am not ready for that yet. Drug treatments tend to reduce cardiac output so are pointless if you are a racer but I use them short term as rescue medication. I for one will not give up racing but I do drop out of races if it happens at an inconvienient time. I am surprised you can’t feel the AF but if you could then I would say racing and hard training would not be dangerous as long as you are prepared to drop out. Even still I am defintiely sure that I would rather die in a race than sitting watching the telly.
    One last comment about some of the studies you refer too. There still is the potential for them to be flawed. Sedentary people tend to be type B personalities and rarely look for adreniline rushes and competition. The type A personalities are more likely to be striving for success and be heavy trainers. As AF can be stimulated by adrenaline and cortisol the type A personalities are likely to be more prone. In other words it may not be the heavy training it may just be because we are competitive.
    All the best Henry

  3. canute1 Says:

    Thank you for that very interesting comment. I agree there are many varieties of AF. One of the most important features is whether or not there are any signs of other cardiac abnormality. In the large studies, it is only those with AF together with some other cardiac abnormality who have a poor outcome. In the Stockholm cohort, those with no other abnormality actually has a longer life expectancy than the age-matched general population. Two other indicators of good outcome are an association with premature atrial contractions (which I have) and onset at age before 60 (which was true of you but not me, unfortunately).

    I am inclined to speculate that all three of these indicators of good outcome (lack of other abnormality, association with PACs, and young age at onset) might be typical of athletes who develop AF. This leads to the optimistic speculation that AF in athletes may be associated with relatively good outcome – despite the worrying findings of the small study by Hoogsteen.

    I also agree that it is possible that the observed high prevalence of AF in athletes is not necessarily due directly to training – personality and other lifestyle factors might also contribute.
    In light of all the uncertainties, I think that each individual has to make their own decision over whether they continue running. The safest plan is probably to continue with only moderate intensity exercise, but if you really enjoy racing, and take the attitude that you are happy to tolerate the uncertain risks associated with racing, this seems quite reasonable to me. It is no more irrational that engaging in mountaineering; a sport which can make life much richer, but also entails risk.
    My current decision is to continue with moderate intensity exercise for the time being, but I will review this decision from time to time as more evidence becomes available.

    I would be very interested to see any garmin recordings you have. Please contact me via email at

    Note added March 2012: my email address is now

  4. Barbara Says:

    Keep me updated, please

  5. mark Says:

    55… diagnosed with afib at 52. I’ve been a life long runner with a clear heart and continue to log about thirty miles a week, plus biking and moderate weights.
    I take aspirin and 25mg of toprol… Aware of the stroke issues and lead a very normal life…. I’m lucky in that I never feel my afib, which I’m in 7/24.
    As mentioned above there are many forms of afib… and leaning to managing it is crucial… good luck to all.

    • canute1 Says:

      Mark, Thanks for your comment.

      There was an encouraging study of the outcome of lone AF (i.e. AF absence of other heart disease) over a thirty year period carried out by Jahangir and colleagues (Circulation 2007;115:3050-3056). They compared outcome in 76 patients with lone AF, with that in age and sex matched individuals from the general population, They found a 68% survival after 30 years in the AF group compared with 57% survival in the matched subjects in the general population. Risk for stroke or transient ischemic attack (TIA) was similar to the expected population risk during the initial 25 years of follow-up (12% of AF cases suffered stoke or TIA, compared with 11% from the matched general population at 25 years), but the risk increased more in the AF cases after 25 years, so it may be that the risk of stroke assocated with lone AF starts to become appreciable only when other problems related to aging emerge. By 30 years, 5 of the 76 AF cases had suffered stoke and 12 had suffered TIA. However, among ther 17 who suffered stroke or TIA over the 30 year period, the cerebrovascular event was attributable to embolism (the expected mechanism by which AF causes stroke or TIA) in only 4 cases, and to probable embolism in the presence of atherosclerotic disease in a further 3 cases. All who suffered a stroke or TIA had an additional risk factor such as high blood pressure, diabetes or heart failure. Since risk of diabetes, and of high blood pressure is reduced in athletes compared with the general population, these data suggest that in athletes, the risk of either death, stroke or TIA due to AF is likely to be small.

      However as you imply, is is important to be well informed about the many issues that might affect oucome and to devise a sensible strategy based on consultation with an expert.

  6. Ronald Friedman Says:

    I’m 67, have been running 22 years. I was never a fast runner, yet nevertheless raced consistently, averaging 12-15 races per year. This past year I decided to train intensively, and lose weight. I’m 5’10”, and dropped from 184 to 164 lbs. Ran 39 races this year ranging from one half marathon through multiple 10K, 5 mile, 4 mile and 5K races. Trained very hard for months. Hill repeats, speed work, etc. Broke all my PRs between May and September and in mid-September developed paroxysmal afib. Very depressing; went through a right atrial ablation with no change in afib. Have has since mid-September about 15 – 20 episodes lasting from two hours to 36 hours each. I am working with two very respected electrophysiologists, but for now – we’re keeping the afib in abeyance with Toprol XL, 50 mg. once a day. My already-low resting hr of 57 is now about 47, and when I run I feel as though I’ve gained back the 20 pounds I lost. My 5K race times went from 27 minutes to 33 minutes, and the last 5K two weeks ago triggered, 2 hours later, that 36 hour afib episode. So where does that leave me? For now, I can run albeit slowly. I find the first 10 minutes are difficult; then if I run for a total of 30 minutes the remaining 20 minutes are easier. I won’t race for now. We’ll see how I do on the Toprol XL after another month. May then try Propafenone, which is much less of a beta blocker and may allow faster running while still controlling afib. I’ll also consider the left side ablation, even though it does carry some risk. BUT here’s the key question. Why should I consider continuing to race? Might I be doing more damage if in fact the Propafenone and/or the left side ablation allow me to race? Should I just be happy I could break my PRs, run 39 races this year, and switch to a regimen of moderate running, and perhaps biking/swimming and/or walking, all with moderation? I’ll have to give up the love of the competition and the successes….. but doesn’t that make sense in terms of my overall health and longevity? I’m new at this; doing lots of research and I much appreciate finding this article and the posts/comments. I welcome commiseration and advice!

    • canute1 Says:

      Your experience has been terribly frustrating. It seems unfair that an activity which should have been a source of satisfaction, good health and happiness, has left you feeling puzzled and perhaps less healthy – though with regard to overall health, the issue is not clear. On the whole runners live longer than non-athletes, and there is very little evidence that even those who athletes who suffer AF have an adverse long term outcome.

      With regard to what you should do in the future, I do not think there is any clear guidance. In light of the fairly strong evidence that a large amount of endurance training and/or racing is associated with increased risk of AF, the safest option is probably to engage in regular moderate exercise. However, the available long term evidence, mainly from studies of cross-country skiers, is that some individuals who continue to train and race, suffer a deterioration of AF, while in others the AF resolves. I think each individual needs to weigh up the options taking account of the available evidence, and how much racing matters to them.

      It seems to me that the fact the 36 hour episode of AF came on several hours after the race in Sept suggests that the trigger might be a combination of metabolic changes in the body that affect the function of the autonomic nervous system for a period of hours or days after exercise. It is fairly well established that following events such as a marathon, many athletes exhibit a shift towards excessive parasympathetic activity and also show evidence suggesting transient trauma to heart muscle. It is plausible that these changes, perhaps exacerbated by changes in the concentration of electrolytes (sodium, potassium, calcium) in the blood, might destabilize heart rhythm. This does suggest that if only we understood clearly the way in which these various factors might interact to destabilise heart rhythm, we might be able to develop strategies to prevent the onset of AF. I consider that a heart rate monitor that records R-R intervals can assist in identifying the circumstances that increase the frequency of abnormal rhythms, though the interpretation of R-R records can be tricky.

      In my own case, it is not clear that I have ever had AF. The medical investigations have not revealed any abnormality. My own observations of my heart rate, using a monitor with capacity to record the R-R intervals, is that I do experience occasional spikes which are likely to be due to premature atrial contractions – though occasion premature atrial contractions are not abnormal for a person in their late 60’s. I noted on one occasion when I became quite dehydrated after getting off-route on a long run in arid terrain on a very hot day, the monitor revealed more frequent sharp spikes in the R-R trace – indicating either less good contact between belt and skin, or premature atrial contractions. Since that occasion I have been more careful to ensure adequate hydration and have had less frequent sharp spikes in the R-R record. In my own circumstances, I think that the balance of evidence indicates that continued training and racing is likely to be beneficial for my long term health. Nonetheless, I believe it is worthwhile to continue to perform R-R recording to monitor the occurrence of spikes, even though the ambiguity of interpreting the spikes means that the HRM cannot provide definitive evidence.

      • Ronald Friedman Says:

        You have been incredibly helpful. First, I’ll learn about R-R. What sort of monitor do I need to determine R-R? I’ll do research on this in the next day; have been busy at work since I received your reply. But yes, it is so frustrating. Your advice is what I do plan to do, going forward. There is no clear path. The good news is that I don’t need to, nor could even likely, break my PRs from this summer. Broadening my exercise routine, incorporating biking, walking, and moderate, non-racing running, is just a mind shift I’ll have to work on. As is oft-said, running/racing is as much or more mental as physical; now, shifting gears is the mental/psychological challenge. And it just, I guess, mirrors life’s other challenges in that regard.



    • mark Says:

      Ronald… welcome to the club 😉
      I’m 56, I’ve been a life long runner and I’m in Afib 7/24, have been for about 7 years.
      I too was on toporol and hated the “heavy legs” that came with it… as I ran with a heart monitor and kept a log, I realized that 50mg. daily didn’t change a thing vs. no drug. I got off the drug two years ago and feel a lot better… I take nothing for rate control, and aspirin and fish oil for “thinning” and I’m happy with my choices…
      My doc’s want me to get on a blood thinner (NFW)… and my heart’s ability to pump is in the mid to high range with zero plaque…
      I would check to make sure your heart is pumping correctly… doubt if you have a plaque problem but check it and consider dropping your dose to 25mg.
      Wear a monitor keep a log and your body will tell you !
      Best of luck.


      • Ronald Friedman Says:

        Hi, Mark,
        Your email just now made my day. I’ve been pretty down after such a good year. One does everything by the book, as it were, and then – this. I had an angiogram three years ago in connection with another issue that turned out not to be heart-related. My doctor said my heart had nothing in it but blood and muscle. No plaque. Recent carotoid sonograms show no plaque at all. My big fear is – am I hurting myself when pushing and when in afib? How about the stroke issue? Do you feel the afib? I can feel it, and it of course is scary. But this is all new to me. Have you considered or have had ablations?



      • Mark Says:

        No ablation for me… I feel fine, no symptoms even while running. I don’t want a doc messing that up. My only concern is stroke. I’m less at risk due to the constant afib and frankly the aspirin vs warafin cohorts are statistically similar…. Aspirin is not a panacea and you still need to watch for bleeding. I’d try the polar monitor and them log your results and how you feel on various dosage…. If you are already on a blood thinner you can’t go cold turkey. Lastly Dr Natalie has the biggest following for ablations…. The stats overall however are not encouraging Happy Holidays and fun runs… Mark

        Sent from my iPhone

    • canute1 Says:

      If you do decide to get a monitor that records R-R intervals, there are two models to consider: Polar RS800cx and Suunto t6. I have the polar RS800cx. I have been a little frustrated by some minor aspects of the engineering (eg poorly designed attachment of watch to wrist strap) but it appears to record high quality R-R data provided there is good contact between the chest belt and the skin. As far as I gather, Suunto t6 records similarly high quality data, but I have no personal experience with it.

      The cost is non-trivial, but now, after more than two years experience with the RS800cx, I consider it has been of great benefit. It has given me much greater confidence that I can identify circumstances that increase the frequency of premature atrial contractions (PACs). As described above, it allowed me to confirm the danger of dehydration. On the other hand, it has demonstrated that for me that high intensity training and hard racing produce only a trivial increases in the frequency of PACs,. Furthermore, there is no sign of deterioration after prolonged periods of heavy training. So I feel optimistic about the future, but also confident that if there were to be a marked deterioration, there is a good chance that I would identify the deterioration at an early stage.

  7. Is prolonged vigorous training bad for your health? « Canute’s Efficient Running Site Says:

    […] is strong evidence that prolonged endurance training increases the risk of atrial fibrillation (as reviewed in my post in June 2010 and several subsequent posts).  In those posts I also reviewed the evidence for increase in other […]

  8. mike Says:

    I have been involved in all sorts of sports and running etc for decades I am now 59. Three years ago I started developing PACs within a year that was turning into afib and every two or three months a trip to the ER for conversion Now the good news all that exercise made me a great candidate for ablation. I now 18 months ( post surgery) free of symptoms except for a few (think 6-12 PACs) when I am recovering from aerobic work outs So just keep running but talk to a good cardiologist when you are worried about symptoms

    • canute1 Says:

      Thanks for your comment. I am pleased to hear of the good outcome of your ablation.

      Subsequent to writing this post I had a fairly comprehensive cardiac examination which revealed no abnormality apart from signs of large ventricles, consistent with athletic training. I have continued to record my heart rate using the Polar RS800CX and have been pleased to demonstrate beyond reasonable doubt that at least some of the dramatic abnormalities I had observed previously were artefacts. For example, running in a rain sodden vest almost always produces many dramatic spikes. Nonetheless I believe that some of the spikes I observe in the R-R record are genuine PACs. I think that the frequency of PACs I observe at present is consistent with my age. However I think it is worthwhile to continue to record the R-R traces, in order to detect any tendency for increasing frequency of PACs.

  9. mike Says:

    I would also add the statistics on treating Afib with ablation are extremely good well over a 90% success rate ( if you include those Pts that require a touch up or second procedure). The recovery time is about a week or less. On the other had no medication has really proven effective, blood thinners will thin your blood but they do nothing for the Afib. A number of other factors however do contribute to Afib; Coffee, smoking, sugar, alcohol, dehydration, electrolyte imbalance, and anxiety are all common triggers. That being said all surgeons are not equal. Dr. Athill in San Diego did mine he has a long record of research in the field. I would highly recommend him. Unless you are in San Diego and can use him. Id ask other experts who they really would trust. That being said often insurance companies will want you to take warfarin forever rather than have a costly surgery. I had to take meds that have proven ineffective (fecainade) for a year before they would do the surgery.

    If you want to go the organic route I did have some success with Taurine and Arginne. In Japan they have used these substances for ages. In America a fellow named George Eby is the big advocate for these and you should read his articles I however only had limited success with this approach, but about the worst side effect is a little Diarrhea so its not a big risk. I hope this helps someone out there it took a couple years of my life to solve.

    • canute1 Says:

      Yes, from the accounts of individuals I know who have had ablation, the rate of good outcomes from ablation appears to have increased in recent years. Nonetheless, it is a technically demanding procedure and I think it is likely that outcome depends strongly on the expertise of the surgeon.
      I think the point you make about the many factors that increase the risk of AF (or PACs) is very important. I think it is sensible for an elderly runner to identify any circumstances that produce an increase in rate of PACs, as it is plausible that taking steps to minimize PACs will reduce the risk of onset of AF. I have observed that PACs appear more common when I get dehydrated, so I am now very careful to avoid serious dehydration.

  10. Jack R. Says:

    You mention that the premature beats in a PAC are at least 30% greater than surrounding beats. I have read your blog, and I have used a Polar H7 to record RR intervals during exercise, and at high heart rates (90% MHR) I’ve seen runs of what look like PACs, (same short first beat and then a long beat, just as you show in your blog,) but the first beat is NOT more than 30% faster than surrounding beats. At most it’s no more than 15% faster, and most in the run of PACs are no more than 11% greater than surrounding heart beats. Are these PAC’s?

    • canute1 Says:


      You raise a good point. I sometimes experience the same phenomenon at high HR. It indicates that a muscle cell in the atrium has fired and triggered contraction a little earlier than expected. This might either be a cell in the sinoatrial (SA) node or outside the SA node. Granted that there is likely to be high level stimulation by adrenaline at high HR promoting rapid firing of the SA node, I would not regard slightly early firing of a cell in the SA node as a pathological event. Alternatively, it might indicate that a cell outside the SA node has fired. Since normal contraction is initiated by the SA node, I suppose this should be regarded as possibly pathological. However, granted that a high level of adrenaline is likely to promote firing of all cardiac muscle cells, I would not regard it as evidence that there is a seriously pathological ‘rogue cell’ prone to fire with little provocation.

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