Crazy heart rhythms

There is little doubt that the balance of benefits and risks to the well-being of the heart arising from regular running favours the benefits.  The risk of heart attack following a marathon is small but real, though it is generally accepted that this risk often arises from underlying heart abnormality.  However there is one heart problem that is relatively common and might arise largely from factors related to fitness itself.  That is atrial fibrillation.

Atrial fibrillation is a disturbance of heart rhythm in which the electrical events that initiate contraction do not arise in a regular manner from the sinoatrial node embedded in the muscle of the right atrium of the heart, but instead arises in a chaotic manner from a variety of different sites in the walls of the atria.  Instead of a well organized contraction of the  atria followed by a regular contraction of the ventricles, the walls of the atria contract in a poorly coordinated manner and blood is not transferred to the ventricles in a way that ensures efficient filling of the ventricles before ventricular contraction ejects the blood into the pulmonary artery (that connects the right ventricle to the lungs) and the aorta (that carries blood from the left ventricle to the rest of the body).  Usually a person with atrial fibrillation feels fatigued and may be aware of palpitations – an irregular heart beat.

The evidence for increased risk in endurance athletes

Many studies report that atrial fibrillation is more common in endurance athletes.  In a 5 year follow-up of 146 young elite athletes from a larger sample 1772 elite athletes who had been found to have heart rhythm disturbances, 13 (9%) had atrial fibrillation (Furlanello et al Atrial fibrillation in elite athletes. J Cardiovasc Electrophysiol. 1998;9(8 Suppl):S63-8.)    In 5 of the these 13 young athletes, an underlying heart abnormality was found (most commonly abnormality of the  electrical conduction path from atria to ventricles known as the Wolf-Parkinson-White syndrome, but in 8 athletes, no underlying cause was detectable. 

In a meta-analysis that examined pooled data from 6 previously published studies comparing a total of 655 athletes with 985 age and sex matched non-athletes (with all members of both groups drawn from clinic attenders), there were 147 cases of atrial fibrillation among athletes and 116 among the non-athletes  (Abdulla J, Nielsen JR  Is the risk of atrial fibrillation higher in athletes than in the general population? A systematic review and meta-analysis. Europace. 2009;11(9):1156-9.).  Mean age was 51+/-9 years and 93% were men. The authors concluded that the risk of atrial fibrillation is significantly higher in athletes compared with non- athletes, but that this finding should be confirmed further in large-scale prospective longitudinal studies.

In a prospective longitudinal study, individuals representative of the group of interest  (eg male endurance athletes) are recruited before they are known to have any abnormality and followed over a period of years.  This provides an estimate of the risk that members of that group will develop the problem over the number of years of the follow-up.  Such a prospective longitudinal study, of long distance skiers, has just been published this month  (Grimsmo J, Grundvold I, Maehlum S, Arnesen H. 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 Rehabil. 2010 Feb ;17(1):100-5.)   Grimsmo and colleagues studied cross-country skiers with a long history of training, from three different age groups, identified on the basis of participating in the Birkebeiner ski marathon, an annual 54 Km cross-county race from Rena to Lillehammer, in Norway. 122 individuals entered the study in 1976 and of these 78 were available for the follow-up assessment in 2004-2006.   12.8% of those followed up over the period of 28-30 years had ‘lone’ atrial fibrillation that was not accounted for by any other underlying heart abnormality.  The mean age of onset of the atrial fibrillation was 58 years.  Although atrial fibrillation 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.   There seems little doubt that male endurance athletes have a substantially increased risk of atrial fibrillation.

Is endurance training the cause of the problem?

In the study by Grimsmo and colleagues, the factors that were associated with the development of atrial fibrillation were a long interval between the p wave and the q wave in the electrocardiogram (this indicates a long conduction time between atria and ventricles); a slow heart rate; and a large left atrium.  Slow heart rate and enlarged left atrium are features produced by endurance training. So it is plausible that the endurance training plays a causal role in the problem.   It is well known that both excess parasympathetic activity (which is responsible for low resting heart rate) and excess of sympathetic activity can predispose to atrial fibrillation, with the parasympathetic form more common in individuals without other evidence of heart disease (Coumel P. Autonomic influences in atrial tachyarrhythmias. J Cardiovasc Electrophysiol. 1996;7(10):999-1007.)   While there is a widespread belief that the increased parasympathetic activity associated with endurance training is a good thing, the link to atrial fibrillation should give us pause for thought.

It is also possible that the mechanism involves atrial scarring.   In general, training effects arise as a result of transient damage to muscle that leads to compensation – this is well established for skeletal muscle and is likely to occur in heart muscle as well.  If the transient damage results in scars (residual fibrous tissue) then these scars might be expected to interfere with the coordinated conduction of electrical signals through the muscle.

What are the consequences of atrial fibrillation?

In the short term, atrial fibrillation usually results in fatigue and limitation of athletic performance.  The evidence for serious long term adverse effects is less straightforward.   The chaotic contraction of the atria can result in clotting of blood within the atria creating a risk that the clots might break free and be transported via the large arteries and produce blockage in the smaller diameter peripheral arteries.  One possible serious consequence is a stroke due to blockage of arteries in the brain.   In a 9 year follow-up study between 1993 and 2002, of 30 athletes with atrial fibrillation, Hoogsteen and colleagues found that by 2002, 3 (10%) were dead; paroxysmal atrial fibrillation continued in 15 (50%) ; permanent atrial fibrillation emerged in 5 (17%) ; and 7 (23%) of them showed no further atrial fibrillation.   Thus at least in this group of athletes, the outcome was worrying.  However it should be noted that these were not specifically described as cases of ‘lone atrial fibrillation’ and hence in at least some cases it is possible that there were other underlying heart abnormalities.

A personal note

Not only do atrial hypertrophy and over-activity of either the parasympathetic or sympathetic divisions of the autonomic nervous system appear to increase the risk of atrial fibrillation but there is also evidence that inflammation can increase the risk.  In the presence of inflammation, the body produces a protein known as C-reactive protein.   A meta-analysis of the relationship between C-reactive protein and recurrence of atrial fibrillation in patients under medical treatment found evidence suggesting that baseline C-reactive protein levels predict the long-term risk of recurrence of atrial fibrillation (Korantzopoulos P, Kalantzi K, Siogas K, Goudevenos JA Long-term prognostic value of baseline C-reactive protein in predicting recurrence of atrial fibrillation after electrical cardioversion. Pacing Clin Electrophysiol. 2008 ;31(10):1272-6.).

Recently I suffered an episode of inflammatory arthritis and as a precaution I cut back on training.  On 13th February, about two weeks after the worst of the joint pain, I did my regular test of aerobic fitness on the elliptical cross-trainer.  In this test, I record heart rate during 2 minutes on each of a series of steps of increasing power output in the range 30 to 232 watts. In recent months, my heart rate at 232 watts is usually around 146-148 which I regard as just a little above my anaerobic threshold.  I can comfortably maintain a breathing rate of 40 breaths per minute, at this heart rate but if I increase further, then my breathing rate increases rapidly up to around 80 per minute.   On 13th Feb, I noted that my heart rate was typically around 5 beats per minute higher than usual on each of the lower steps and by the final step at 232 watts, it settled at 150 beats per minute.  I did not feel stressed, so I simply assumed that I had lost a little fitness in the preceding three weeks of reduced training. 

I examined the Poincare plot which provides an indication of function of the autonomic nervous system.  The plot for the final 1 minute at power output of 232 watts is shown in figure 1. 

Poincare plot during the final minute at a power output of 232 watts

As I have discussed in previous postings the spread of points across the 45 degree line denotes high frequency heart rate variability and is an index of parasympathetic activity, though there is some controversy about the details of the interpretation of the Poincare plot during upper-aerobic exercise.  The measurement that represents the amount of spread at right angles to the 45 degree line (sd1) is 3.9ms, while the quantity presenting spread along the 45 degree line (sd2) is 3.3 ms.  This is fairly typical of what I usually observe when maintaining a constant power output at the upper end of the aerobic range.  

Last summer, when I developed parasympathetc overactivity as I increased training during recovery from my episode of illness, the spread of points across the line was far greater (up to 12 ms).  The only minor feature of note in figure 1 is that there is one point well away from the cluster above the 45 degree line and a matching aberrant point below the line.  These two points indicate that one beat was initiated about 10 milliseconds earlier than might have been expected and was followed by a corresponding lengthening of the next inter-beat interval before normal sinus rhythm resumed.  This 10 ms advance is a trivial advance of the usual beat rate though it might indicate that a location outside of the sinoatrial node had captured the role of initiating that beat.  However I would regard one slightly early beat among around 150 beats as utterly trivial, and therefore I had no qualms about setting off for an easy 8Km run in the lower aerobic zone.  I maintained an easy pace of around 5:30 minute  per Km, which would normally be associated with a heart rate of around 118 bpm.  Because I did not have any concerns, and I felt quite comfortable running, I did not take much notice of my heart rate as I ran. I was therefore amazed when I examined the beat by beat variation afterwards (figure 2.).

Crazy heart rhythm during an easy lower aerobic run

As expected, my heart rate rose steadily over the first two minutes to about 117 bpm but then within the next 6 minutes there were 7 strikingly premature beasts, typically occurring 150-200 milliseconds early.  If this is not an artifact due to monitor malfunction, it suggests that a rogue site was capturing the role of initiating the beat.  Furthermore during that period the heart rate fluctuated a lot more than usual, though it tended mostly to be in the range 100-120 bpm. However, those fluctuations were nothing compared with what happened after around 9 minutes.  The rhythm went haywire, and did not settle until I got home, at around 45 minutes.  The heart rate then settled rapidly reaching around 75 bpm with only modest (and potentially healthy) amount of beat by beat variability, 4 minutes after I stopped running.  What might this mean?  My first conclusion is that my monitor had malfunctioned.  I still do not have any firm evidence to rule out this possibility.  The other possibility is that I experienced about 30 minutes of atrial fibrillation.  However the amazing thing is that I felt quite comfortable running.  Perhaps the run felt slightly more effortful than usual for a lower aerobic run, but after a few weeks of reduced training, that would not have been surprising.

I have not yet resumed full training but have done a number of 8-10Km lower aerobic runs and about 10 sessions on the elliptical cross trainer, since mid February.  There has been no further sign of this crazy rhythm.  Typically, when running my heart rate has been around 620-650 beats/Km, which indicates scarcely any loss of aerobic fitness since mid January.  My observed heart rate during elliptical sessions has been back to normal, and my resting heart rate is around 46 bpm which I regard as healthy.

So at this stage I plan to build up my training cautiously.  As the unusual rhythm occurred when running at any easy pace, I think that long easy runs during which parasympathetic activity would be expected to be higher, might actually be riskier than shorter faster runs, but nonetheless, I will be very cautious about any sessions that might be stressful.

With regard to the longer term, I will simply have to wait and see.  I still have no clear evidence that it was not simply a malfunction of my monitor, and I would be interested to know if others have observed similar patterns with the Polar RS800CX.  Although I do not entirely trust the monitor, I am nonetheless very glad that I have it, as it gives me confidence that if in fact I am developing atrial fibrillation, I will be able to detect it.  The chance of detecting it during a planned clinical ECG recording would be very low at present.  Whatever the eventual outcome, it has confirmed that running when exhibiting any signs of inflammation is probably not a good idea.  On the other hand, I suspect that my life expectancy will be greater if I remain fit, so I am quite happy to keep on running while I monitor the situation.  As for my plan to run a good marathon in 2012, only time will tell.


37 Responses to “Crazy heart rhythms”

  1. Roger Says:

    Hi Canute

    I have had a polar RS800cx since mid- January and have had about 5 occassions where the HR & R-R data seems strange. It has only happened on weekends and at no point during these ‘episodes’ did I feel anything unusual in fact, I have generally felt good. I could understand if the device gave strange readings at the start before I had started sweating but the graphs show the values all the way through the exercise. I have also never noticed the abnormal readings during the exercise only later looking at the software. The abnormal readings that I received are not as condensed as yours are ie. I have a lower frequency of abnormal readings. In the polar R-R page, it won’t allow me to do an error correction.

    • canute1 Says:

      Roger, thanks for that comment. The fact that you do not feel anything unusual is interesting. Either we both have a symptom-less rhythm disturbance or the RS800CX is unpredictable. The question is still open, but your evidence pushes me slightly in the direction of blaming the RS800CX. It is also interesting that it only happens on weekends. Do you drink coffee before running on weekends but not on weekdays?

  2. Thomas Says:

    Now, that’s an interesting article to me personally, because I can remember 5 episodes of this happening within the last 4 or so years, the last one almost exactly one year ago. The first time it happened it scared the hell out of me, but I have since learnt that I’m not about to drop dead when that happens.

    Feelings of fatigue do come with that, but it once happened in a race. I felt it very clearly, and when I looked at my HR chart later that day (I was wearing an HRM at the time) I could clearly see the spike, it was way off the scale. Interestingly enough, even though it happened about 3 miles into a 10 mile race I carried on running and did a pretty good time. The feelings of fatigue are real, but you can push through that.

    3 people of the tested group dying is a bit worrying, alright, but that’s a rather small sample size. It won’t stop me from running.

    • canute1 Says:

      Thomas, with regard to the long term risks arising from AF, the risk of stroke is much higher in those with additional risk factors such as high blood pressure etc, I think that leading a healthy lifestyle is the most important thing you can do to improve the prospects of good health in old age – I think running makes a great contribution to a healthy lifestyle. However I am also aware of the need to minimize the risk that AF will become an enduring problem. I am planning to do a post in the near future on the evidence suggesting that overtraining, inflammation and AF are linked. If that hypothesis is correct, it is over-training rather than running that creates the risk; in fact it might be that running without over-training reduces the risk. However this is all speculation and we each to weigh up the evidence and then make our own choice about running.

  3. John Says:

    Hi Canute

    I don’t have your email address. Please forgive messaging you via your blog.

    I came across your blog while searching for references re HRV and Cardiac Vagal Tone (CVT) having had little satisfaction with HRV as a reliable way (for a relatively non-technical person) to determine objectively how well the heart is coping (and would be capable of coping with more training).

    This is personally important to me, as someone who has had in the past year a successful bone marrow transplant but also a concomitant acute inflammatory demyelinating polyneuropathy (AIDP), which I have subsequently learned does affect the vagal nerve.

    Recently I have seen and had a test, not available at present outside research establishments, from which diagnostic information can be derived directly in the form of the subject’s CVT score.

    See US Patent 6442420B1 and for the information which relates to the test equipment.

    Would you mind if I ask you whether you have come across CVT and would be willing to express a view on it?

    Thank you so much for your blog.


    • canute1 Says:

      John, The term CVT was introduced by the respected autonomic nervous system expert, Stephen Porges from University of Maryland in 1995, to describe the inhibitory control exerted by the vagal output from the nucleus ambiguous (in the brain stem) over the heart rate. Stephen Porges is a highly respected scientist, but there is still debate about details of his hypothesis. When Porges proposed his ideas about CVT fifteen years ago, he intended that it would be assessed though an analysis of the fluctuation in heart rate associated with respiration. He defined a Vagal Tone Index calculated by taking the logarithm of a quantity based on variation of heart rate during respiration. A large amount of variation was assumed to be good.

      The Neuroscope device you refer to is a patented device for measuring CVT via measurement of fluctuations in blood pressure. It performs computations based on these measurements of blood pressure fluctuations to generate a single number that represents CVT. Although the details of the computation are not readily available, I think it is likely that it generates a number that is similar to the output of the traditional method of analyzing heart rate variability proposed by Porges. There is still debate about what conclusions can be drawn about levels of stress or fitness from measurements of heart rate variability. I do not think it is likely that any single number will provide a reliable measurement of stress or fitness under differing circumstances. I personally would prefer to have detailed knowledge of how the numbers were derived. So in conclusion I am a little skeptical, but my skepticism is based on general principles rather than knowledge of this particular device.

      • John Says:

        Thank you very much Canute. I guess that’s the wisest position.

        Your Poincare plots seem, however, to meet an important need – the shape of the plots giving an overall sense of condition?

        You obviously have the skills to obtain this data without resorting to heart monitors. Does this mean there is no heart rate monitor on the market that one could obtain the same or similar data from and be able to produce a Poincare plot from?

        Or is the quest for a more meaningful, accessible-to-anyone-interested bell-weather of heart health fruitless?

  4. Ewen Says:

    Canute, I hope it’s just a problem with the monitor rather than something that might disrupt your plans to run a marathon in 2012.

    With my Polar RS 200 I sometimes get unusually high and/or ‘jammed’ readings mid-way through a run if the chest strap becomes loose (can happen as the elastic slips through the buckle a bit) and/or the batteries in the strap are low on power.

    • canute1 Says:

      Ewen, Yes, I hope that poor contact between belt and skin might be the answer, but it does not quite fit the picture. However, I will continue to collect evidence.

  5. Rick Says:
    Hi Canute I have had Tachycardia for over 20 years +, I had hospital tests on a tread mill and i was told my type of tachycardia was not dangerours but i could have an operation to cure it.
    First you must check your pulse with your fingers if this happens again, you would feel your heart beating very fast and palpitations from your throat.
    But I have heard of a lot of runners with HRM’s getting erratic signals when the battery starts to run low so check this first. so don’t worry, but if in doubt see your doctor straight away.

    • canute1 Says:

      Rick, thanks for that comment. As you imply the first thing to exclude is either flat battery or poor electrical contact. It does not appear to be a battery problem , but it is less easy to exclude poor electrical contact.
      I would be interested to know if your rapid heart beat was regular, which would most likely to due to a paroxysmal supraventricular tachyardia (pSVT), or irregular in which case it is likely to be atrial fibrillation (AF). pSVT can arise from various different causes but is often relatively benign. I would expect the risk of blood clots (and hence risk of stroke) to be far less with pSVT than AF. You are right that it is important to get the problem checked out by a doctor. For me, the good news is the problem appears to a very rare occurrence , but because of this it is less easy to make a clear diagnosis. I am still hoping to convince myself that the problem is with the monitor rather than my heart.

  6. Rick Says:
    Canute paroxysmal supraventricular tachyardia is the condition i have.
    I no long use a pulse monitor but when I did I use to see my pulse suddenly shoot up to 180-200 bmp and it would stay high for 5 – 20 mins unless i stopped my exercise. I did not really get any bad side efforts from the condition.

  7. canute1 Says:

    Rick, A number of very succesful athletes have suffered pSVT, so you are in good company.
    As the Merck article reports, SVT can often be stopped by increasing vagal (parasympathetic) input.

    In the case of atrial fibrillation, it appears that vagal input can slow the atrial sinus to a point where rogue sites can take over the role of initiating the beat. But in other circumstances, too much adrenaline brings on AF. I think that in athletes the risk of AF comes mainly from too much vagal input.

  8. canute1 Says:

    I produce Poincare plots using Microsoft excel because it allows me to adjust the scale on the axis to fit the illustrations I post. However, Polar Protrainer software will produce Poincare plots for any selected time period of a beat by beat HR record (a so-called R-R record – it records each R-R interval; the interval between successive R peaks in the QRS complex of the ECG trace.) The essential requirement is the beat by beat record of heart rate. I collect this data using the Polar RS800cx., but there are other monitors that will produce R-R records. Once you have the R-R record transferred from the monitor to the computer, it is merely a matter of selecting the time period of interest and selecting ‘scattergram’ from the view menu in Polar Protrainer.

    Before I had Protrainer, I used some software that I had written myself to extract the R-R intervals and to produce the plots. There are other good freely downloadable software packages that will analyse HR data.

    However, producing the plot is relatively straightforward. The potentially more tricky part is interpreting it. For resting data, the spread of point across the 45 degree line is a fairly good indication of parasympathetic input to the heart. For data acquired while exercising, interpretation is more complex. First, it is necessary to maintain a steady work rate and steady mean heart rate for a long enough period – a least one minute preferably a few minutes. But even at a steady work rate, the interpretation in terms of parasympathetic and sympathetic input to the heart is a more ambiguous than at rest – so unless you have good access to the scientific literature on the topic, it is probably best to focus on resting data.

    However even for resting data , the question of what measurement best indicates stress level is not completely straightforward because stress can be manifest in different ways. It is a little too simplistic to merely to conclude that high parasympathetic output and low sympathetic output together indicate freedom from stress – though this is a fairly good assumption under many circumstances.

    Unfortunately much of the accessible material presented on websites tends to be an over-simplification. Even scientific papers on the topic of autonomic nervous system and stress reflect opinions regarding interpretation of data, as much as fact, and the only way to get a balanced view is to read a range of scientific papers. Unfortunately much of the material written for non-scientists tends to promote an over-simplistic view. One should be especially cautious with material written by someone selling a product.

    I would not claim to be a reliable unbiased source of information, but I do try to weigh up as much evidence as I can before I write my blog posts. I will do another post not too far in the future reporting my views about assessment of stress and over-training

  9. Paul Says:

    Canute, another interesting post. I am not particularly well-informed about such medical things but it would seem more than coincidence that two of the best triathletes Australia has ever produced – Greg Welch and Emma Carney, both multiple world champions – would suffer from a ventricular tachycardia. I suspect that in years to come we will understand this relationship (causal link?) a little better. Paul

  10. canute1 Says:

    Paul, thanks for your comment. The occurrence of ventricular tachycardia in two of the all-time greats of triathlon is worrying. Unlike supraventricular tachycardia, which is often benign, VT is potentially a very serious problem. It tends to be arise from local damage to heart muscle such as might exist following a nonfatal heart attack. I do not know of any direct evidence that extreme athletic training can cause local damage that is severe enough to produce VT. However, the evidence that the benefits of training arise from compensation for minor damage to muscle raises the possibility that extreme training might produce damage that is severe enough to lead to VT.

    Overall evidence indicates that running increases life expectancy, so I am quite happy to continue running – but the frequent instances of tachycardias, both supraventricular and ventricular in elite athletes does raise some concern about extreme training. I think the possible link to inflammation is also an important issue to consider. This is both good and bad news – good news insofar as if the risks are only appreciable at times when there is inflammation we can minimize the risk by avoiding hard training when suffering an inflammatory disorder – but it is bad news if it makes us into hypochondriacs trying to decide whether or not it is safe to do a hard training session. For the moment, I think the evidence is far too slender to justify changes in training unless there is clear-cut evidence of either tachycardia or very irregular pulse –in such circumstances, it is important to get an expert evaluation.

    • Paul Says:

      I agree with your summation. My own (very non scientific) guess is that the extreme training/racing performed by some endurance athletes may expose an existing underlying weakness or predisposition to such a condition. For most of the rest of us, the exercise we do is just plain good for us!

  11. John Says:


    Two steps forwards one step back. After your last comment I though “ha, I just have to use the Polar software to produce a scattergram from a resting pulse session”. Unfortunately my S610 doesn’t seem to record R-R data, at least not at the level of discrimination required.

    So I went back to the Suunto (recording at 2 s intervals) – Suunto have confirmed their software does not produce scattergrams.

    I succeeded in exporting the data from a session and I’m looking at a column of IBI data in Excel. But I realised plot had a Y axis not just an X. Your Y axis seems to be IBI+1???

    I’m a mathematical numty but I don’t understand how plotting the same value against itself plus one is going to show anything other than a mathematical shift of the data?

    Have I missed something? Can you clarify?

    • John Says:

      Sorry – I think I am being unduly thick. I see that a Poincare is self-referential, using the previous measurement and the current measurement respectively to give the Y and X values?

  12. canute1 Says:

    The main point of the Poincare plot is it shows the relationship between the duration of one inter-beat interval and the next inter-beat interval. A moderate change in inter-beat interval from one beat to the next demonstrates a healthy amount of parasympathetic influence. However very large changes from beat to beat might indicate the capture of the pace-maker role by a rogue site (outside the sinoatrial node) and this might be unhealthy. So the Poincare plot is illuminating but needs to be interpreted taking account of a variety of factors.

    I think that inspection of the Poincare plot is more informative than calculating a single measurement of Heart Rate Variability such as the RMSSD (root mean square of successive differences) because it allows one to see whether or not large variability is due to many moderately large differences between successive beats (probably healthy) or a smaller number of very large differences (maybe unhealthy).

    • John Says:

      Thank you Canute, I think my limited grey cells can grasp that.

      Assuming there were equal numbers of “high/low” and “low/high” instances in the data that would – I’m surmising – mean that a plot which had something of the appearance of butterfly wings either side of the 45 degree line (pointing up and to the right, as one looks at the plot) indicates some possible problem?

      It may interest you to know that the Neuroscope can produce data (using challenge tests such as deep breathing or the Valsalver manoeuvre) that allows one to distinguish between damage to the vagal nerve that has affected the parasympathetic response and damage that has not. I’m not selling it, just interested, as it’s given me a lot of comfort!

      I re-did the Polar OwnIndex score, by way of saturating the search field and discovered that my previous score of 48 (prior to the transplant) had dropped to 44. However, I am 51, so neither is that bad, for what the score is worth.

      Subsequent to getting confirmation from the Neuroscope that my parasympathetic response appears to be within normal healthy range, I have been doing a longer cycle rides – nothing like pro level of course, and concentrating on deep breathing to “wake up” the response as much as possible. I’ve found very little difficulty in coping with 2 hour continuous rides including moderate climbs.

      That said, as I wrote this, I realised I could try a Poincare plot from today’s ride. Have to say the results leave me unsure! A 10 minute selection of IBI data, during which I did a steady 90 metre climb, bpm was “steady” between 120 and 140, produces what looks to me like a pretty strange plot. Can I share it?

      • canute1 Says:


        Several factors cause departure from a symmetrical ellipsoidal distribution of points in the Poincare plot.

        For a fit person at rest, the decreases in heart rate (driven by parasympathetic fluctuations) tend to be more abrupt than the increases in heart rate. Therefore the Poincare plot (of inter-beat intervals -IBI) tend to be asymmetrical with a large number of points displaced a relativley large distance above the 45 degree line, representing moderately large increases in IBI, while the majority of displacements below the 45 degree line (shortening of IBI) tend to smaller.

        If there are slow changes in HR that produce a substantial spread along the 45 degree line, the Poincare plot looks like a comet tail because the HRV tends to be less in a period when mean HR is higher (ie the head of the comet points towards the bottom left corner of the plot.

        So both a comet shape and an asymmetry that produce great displacements above the 45 degree line are normal features. I am not sure if this answers you question about the butterfly shape.

        Thanks for the information about the neuroscope challenge procedures. I agree that various challenge procedures can be used to help distinguish ‘healthy’ from ‘unhealthy’ parasympathetic activity

        I am happy to look at any of your Poincare plots, though cannot offer to provide a clinical diagnosis. If you want to, you can send them as attachments to

  13. John Bedson Says:

    I’m sorry to give you the bad news, but to me that trace shows atrial fibrillation. Your running days are probably over. The trace also shows some premature atrial contractions (above the line) and premature ventricle contractions (below the line). You need to see an electrophysiologist immediately. See: to see similar traces and to understand what you are looking at. Email me if you need more deatils or help.

    • canute1 Says:

      Thank you. I agree that the HR trace shown in my posting is strongly suggestive of atrial fibrillation, and furthermore shows evidence of premature beats preceding the onset of AF. A 12 lead ECG performed in the clinic revealed no abnormality apart from the anticipated hypertrophy, which is a common consequence of athletic training.

      However on careful observation of the HR recordings performed using my Polar RS800cx when running I have obtained evidence that overt AF only occurs on days when I take salbutamol for asthma, so perhaps I can minimize the risk of overt AF by stopping use of salbutamol. I am a little more concerned about the frequency of premature beats and have arranged to have a 24 hour Holter monitor recording which I hope will clarify the seriousness of this problem.

  14. John Bedson Says:

    An ECG will not show the presence of AF unless you happen to go into an AF attack during the 30 seconds of the EGC, which is unlikely. Similarly a 24 holter will only catch AF if it comes that day. However it will show any ectopic beats that day.

    Each time you get an AF episode (and you ARE getting them) the atria is “stunned” for a few days afterwards and is not beating correctly. You are at risk of thrombotic embolism in that time and would be wise to take daily aspirin to give limited protection. You should NOT be exercising while the atria are stunned, you should be resting.

    Moreover the atria will “remodel” itself even during a short episode. That means that the “wiring” or more correctly the “substrate” of your atria will be more open to the next attack. It can take up to a month for this remodelling to fully reverse. If you keep getting attacks the remodelling will accelerate and you will be on a dangerous path.

    You need to get clear of attacks for several weeks. But I regret to say that now that AF has reared its ugly head you will most likely see it reoccur for the rest of your life. Yes it is probably the salbutamol causing these attacks, but when you cut that out it will progress to something else. AF moves from one cause to the next. It is a pig of an illness. I’ve had it for eight years. In the early stages you will be optimistic and keep thinking that the latest “cure” has fixed the problem. But like an enemy that never gives up it will keep coming back to bite you from another direction.

    • canute1 Says:

      Thanks. I agree that neither a brief ECG in the clinic nor a 24 hour Holter recording will diagnose AF if there is no episode during the acquisition period. However as you point out the 24 hour Holter should give me an indication of the frequency of premature beats. Do you consider that frequency of atrial premature beats is a useful indicator of severity of risk of AF?

  15. John Bedson Says:

    The holter monitor will be a waste of time and money. Ectopic beat prove nothing; lots of people have them and they do not get AF. Your doctors don’t know how to interpret the polar data which clearly shows (assuming that you have a structurally sound heart) that you have adrenergically mediated atrial fibrillation. You are not vagal; you are adrenergic. Sympathetic tone is shortening your atrial refractory period (the time that the atria cannot carry the beat signal) and allowing ectopic (beats not from the sinus node) to take over the pacemaking.

    You could try cutting down on salt and increasing magnesium and potassium intake. Make sure you are well hydrated especially when running.

    You might need beta blockers. If you need anti arrhythmic medication it should be either propafenone or sotalol.

    This is a good forum to ask questions about your condition:

  16. John Bedson Says:

    The test that you need next is an echocardiogram. That will show if your heart is sound, which it probably is. If the echocardiogram is good then you will know that you have paroxysmal, lone, adrenergic, atrial fibrillation. Knowing what you have is a good start to trying to fix it. But the adrenergic can become permanent so don’t think that this is a benign illness. It is not.

    • canute1 Says:

      Thanks for your comments. I agree with you that some doctors are skeptical about Polar data. My own first reaction when I saw the wild fluctuations in the HR record was to assume it was noise of the recording system. (I am a doctor but not a cardiologiost). The reason I posted the data was to elicit comments, and your comments provide much food for thought.
      However I had not phrased my question about the value of investigating the ectopics with a Holter recording clearly enough. In Courmel’s original papers in which he made the distinction between on adrenergic and vagal AF (for example, his article in European Heart Journal 1994), he stated that the adrenergic form is likely to be associated with an intrinsic problem in the atrial muscle. It seems to me that the first thing in investigating AF is to look carefully for evidence of intrinsic cardiac abnormality. In my question to you about the value of the Holter I had meant, what use is an investigation of ectopics in trying to identify possible abnormalities that might underlie AF. In particular, are there features such as an increase in the PR interval in the beats preceding an atrial ectopic; if so this might be a clue to the initaition of AF. Furthermore in view of the fact that the Polar data only provides indirect evidence of ventricular ectopics, I would be interested to know if I am generating an appreciable number of VE’s and if so, are there any identifiable precursers of VEs
      However I note that you recommend that an echocardiogram as the most important investigation. I assume that will provide a good measure of the coordination of the pumping action of the heart. Circumstantial evidence indicates that my heart is a fairly efficient pump (at least provided the beat in initiated properly) but I acknowledge I should not take this for granted and that an echo is probably a good idea.

  17. John Bedson Says:

    I’ll continue this discussion with you by email.

  18. Laurent Says:


    my name Laurent. Please excuse my poor english (I am French)…
    I bought a polar RS800CX few weeks ago. It seemed to work pretty well until I asked my wife to try it the last 2 weeks. It turned out she showed a very similar heart beat curve to Fig2. At the end of her 2 runs, the chart becomes hectic. I can send you the charts by email if you want. I asked her to go and see a cardiologist because I doubt It is just an artifact (Never happens to me, and happened to her the 2 times she used the Polar, with a very consistant pattern of abnormalities onset…).
    Before we see the doctor, I would appreciate to have your opinion and more information abour your medical condition. Have you seen an electrophysiologist yet?
    Thanks in advance for your advices


  19. canute1 Says:

    Laurent, the medical investigations I have had so far have not demonstrated any definite heart abnormality. I am still waiting for a three week continuous ECG recording.

    It is clear that the R-R traces produced by a Polar heart rate monitor do not provide reliable evidence regarding abnormal heart rhythm. Artifacts are common. These can arise from either a malfunction of the computer or due to poor electrode contact. Therefore, if your wife is getting abnormal R-R traces, the first thing is to check the quality of the electrode contact carefully. It may be best to use warm water to moisten the electrodes.

    I would be happy to offer my opinion on the traces if you send them to me at However, my opinion is not a specialist medical opinion. If your wife continues to obtain abnormal R-R records after checking the electrodes, it would be best if she consults a cardiologist or electrophysiologist.

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  24. jhon Says:

    Nice post. Very important topic. I read full article. I think Ectopic beat prove nothing; lots of people have them and they do not get AF

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