I've been putting off writing this post for some time for several reasons. One, the subject matter is complex and usually requires a knowledge of both physiology and medicine. The other problem is that I don't know if I could do the subject "justice" in a single post. However, after some additional thought, I decided to go ahead since an education about cardiac arrhythmia and single lead ECG interpretation could potentially help prevent some life changing events. In conjunction with this post, please read these as well:
So here goes:
The problem:(Taken from this review)
- Even though there are innumerable health benefits from long standing endurance exercise there are also some consequences.
- The one we will address in this post centers around the risk of atrial fibrillation.
What is the magnitude of the problem?
Here is a good review of the etiology, risk factors and theory:
In this review several studies are discussed that describe why this may occur:
One of the first studies on AF in athletes was conducted by
Karjalainen et al., who reported a prevalence of AF of 5.3% in vet-
eran orienteers (aged 47 ± 7 years). Grimsmo et al. reported a
higher prevalence of AF (12.8%) in older (59–88 years) cross-country
skiers. By contrast, Pelliccia et al. reported a very low prevalence
of paroxysmal AF of 0.3% in young elite endurance athletes (mean age
24 ± 6 years). Thus, the diagnostic efforts for identifying SEE-
associated AF should mostly focus on middle-aged long-term endur-
ance male athletes (~45–65 years). This target group comprises
middle-aged men who have been engaged in regular structured SEE
training for years (such as veteran marathon runners who still have
some performance expectations in Masters categories), and especially
those with previous experience at the ‘elite’or competitive level. At a
younger age, the prevalence of AF is usually very low and beyond the
age of 65 AF is likely to be caused, at least partially, by age-related struc-
tural heart disease independent from SEE itself.
In a recent review, Carpenter et al. highlighted that ‘vagal AF’
remains an under-recognized entity, with no universal definition,
etiology, or diagnostic criteria. The observation of atrioventricu-
lar block, asystolic periods, sinus bradycardia and an increase in
heart rate variability (HRV) have been used as criteria to define
vagal AF. Vagal stimuli such as eating, sleeping, relaxation
following stress or exercise and alcohol consumption have been im-
plicated. Carpenter and colleagues underlined that vagal-driven AF
might actually explain many cases of paroxysmal AF among endur-
What exactly is atrial fibrillation? To answer that we need to first consider the normal electrical flow through the heart leading to orderly contraction of all chambers.
The sino-atrial node (pacemaker area) usually controls impulse initiation in the atria (small chamber on top of the heart).
The atria contracts first, filling the main chamber (ventricle), which in turn contracts due to the impulses traveling through the atrioventricular node (then His bundle, right and left bundles as above), pumping out a bolus of blood to the systemic circulation (from left ventricle) or to the lungs (from right ventricle). If the atrial cells (or nearby cells) become inappropriately excitable and initiate contractile activity chaotically, that is atrial fibrillation. Since the activity is without any coordination, no real pumping action occurs and the atria simply quiver. If an isolated (non ventricular) area creates a single abnormal impulse, an "atrial premature contraction" APC occurs. If this arises in the ventricle, a ventricular premature contraction VPC is the result.
Why is atrial fibrillation (AF) dangerous? By itself, AF can lead to very rapid ventricular rates with heart rates quite high, enough to cause a heart attack in a vulnerable individual with coronary occlusion. The AV node may not transmit each atrial impulse, so various degrees of block may occur. In addition, the ventricular bundles may have varying degrees of "refractory times" - periods immediately after an impulse where they can't be excited again until they recover. This could lead to the atrial impulse being conducted in an aberrent fashion, with abnormal looking electrical activity seen on ECG.
Back to AF.
What's the other danger of AF? The other consequence may be even worse - the occurrence of stroke. Why - AF leads to stasis of blood in the atria (since there is no real organized contraction) and the chance of a blood clot forming is high. If the AF spontaneously corrects and goes back to "sinus rhythm", organized contractile function returns and the clot may be pushed out of the heart to the systemic circulation including the brain. When the clot lodges in a cerebral vessel, blockade of blood flow will cause a stroke with potential permanent damage to that area.
So to summarize:
- AF is dangerous and can lead to stroke.
- It is not uncommon in athletes who have done long standing endurance exercise for many years - just the kind of training that seems so desirable.
- It is associated with higher vagal activity including higher HRV. This seems almost paradoxical since higher resting HRV is usually felt to be a sign of better cardiac health and fitness. While this may be so, one needs to be alert to the fact that AF is an associated finding.
- It may be associated with some fibrosis and also structural change in chamber dynamics.
This diagram (taken from here) illustrates the U shaped risk of AF with increasing endurance exercise:
What can we do about reducing the risk of AF (besides cutting back on exercise)?
As noted above, certain life style changes such as caffeine and alcohol reduction may help, although I'm unaware of any prospective studies examining this. I don't think reducing training volume will go over big with most readers....
What else can we do - Observation of early warning signs of AF.
What are the early risk factors we can see?
Although these studies were not done in athletes, it seems sensible to presume that excessive atrial premature activity would also be a risk factor in athletic AF.
How do we pick up this activity with a chest belt monitor (Polar H10)?
It's actually not difficult. It can be done in a number of ways, but the best is by using Fatmaxxer to record the RR data. Other ways include looking for excess artifacts in Kubios/Runalyze etc, then going to the trouble of getting a Holter monitor (24 hr recording) through your physician. If you have Kubios premium and a Movesense ECG, you have a perfect arrhythmia detection combo. Coaches and researchers may want to consider that investment.
Fatmaxxer will record a 10 sec strip of good quality ECG data (sample rate 130 Hz) from your Polar H10. Please see this for details. It will not record "normal" RR intervals which greatly simplifies the process. We will need to differentiate noise from atrial or ventricular activity which is as follows.
What does a normal strip look like?
- Regular, narrow complexes, separated by the same spacing. Although there is heart rate variability in here, it's too small to see visually.
The electrical baseline is jumping and that is producing distortions - they are not of any concern.
How about multiple atrial premature complexes?
- I circled the normal ones in green, the early, premature beats in red. They are all narrow and the QRS is identical looking. There is a reset of the SA node by the APC (non compensatory pause) noted in orange since the gap is > 2x the RR distance:
Ventricular beats are going to be wider, not have a P wave and have a "compensatory" pause:
And here is a classic VPC captured by Fatmaxxer during one of my sessions:
- The wide complex is circled in red, the lack of a P wave is circled in orange and the larger than normal T wave is circled in green.
How many are too many?
That's a tough one to answer. Sometimes it's obvious. Here is a section from one of the participants from out Frontiers DFA a1 validation study (whose data was excluded):
I circled the normal in black, APCs in red - they run in a paired pattern - normal, then two abnormal then repeat. It almost resembles AF, but there are P waves visible:
- I circled the P waves and the arrow shows where the P is "hidden" under the T wave.
- This would be something to take seriously and investigate.
I would recommend some of the recommendations in the above studies - high order ectopy (doublets, triplets) and high frequency APCs (>30 per hour).
- Atrial fib is common in endurance athletes. The high risk candidate is middle age with a history of many years of endurance training (sound familiar).
- Additional risk factors include frequent APCs, either at rest and/or during exercise. High resting HRV and high vagal tone also may be involved.
- A fib can lead to stroke which can be irreversible.
- With simple consumer HRM equipment and free software, one can identify APCs, their frequency and consult a specialist before a problem develops.