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More on abnormal heart rates in cross country skiers

Tue, Mar  2, 2010 - By Peter Vackx

I am a cardiac electrophysiologist from the U of Toronto. I am writing because I am a former competitive soccer player dealing with, and having experienced, exactly what Ken Dawson is going through. My condition has become quite advanced and I have recently altered the focus of my research on understanding precisely what was described in the article by Ken, Abnormal heart rates in cross country skiers.

The "racing" heart can be caused by many factors such as: 1) congenital conditions (without apparent structural disease), 2) genetic mutations of some key known (and unknown) genes involved in electrical control of the heart, 3) molecular/functional/structural changes in the heart (that are not usually characterized as abnormal) and others.

The most prevalent condition, particularly in trained aerobic athletes such as soccer players, basketball players and especially X-country skiers, rowers and speed skaters, is without question atrial fibrillation (AF). In fact, the increased incidence of this condition in athletes like Ken is expected; you will no doubt have a low heart rate (HR) and a slightly or significantly (physiologically) enlarged heart (called an athlete's heart).

Both these conditions (i.e. slowed HRs and enlarged hearts) are predisposing factors for AF. Since you are getting this condition at a young age, it is possible the condition will advance and you be a member of the "aging athlete group" who are very often suffer from AF.

Based on my experience, when I first started to get AF, the most common occurrences of AF were either at night (often right after a large meal) or just before an event (i.e. during your warmup). Both are distressing and relatively benign.  The problem is that the condition often progresses to a chronic condition which can be deadly as a result of vulnerability to stroke.

It is my opinion that you should be skeptical and weary of the current treatment strategies, especially when the condition begins to take its chronic form. The treatment approach is designed essentially to prevent stroke and not to correct the AF. For active individuals this essentially means a major life-style change. I found the approach to be unacceptable for myself. I now use a system of self monitoring (for extra beats) combined with an appropriate dosing of an old antiarrhythmic drug called flecainide.

This old drug was recently shown to have an action on the myocytes of the heart (atrium) that is (I believe) critical for the initiation of bouts of AF (and therefore a very powerful agent to prevent AF). The drug can have side-effects but these are likely to occur primarily in people with structural heart disease (i.e. signs of advanced heart disease or heart failure).

There is an article (very readable) that nicely summarizes AF in the aging athlete:

Endurance sport practice as a risk factor for atrial fibrillation and atrial flutter."
Mont L, Elosua R, Brugada J. Europace. 2009 Jan;11(1):11-7. Epub 2008 Nov 6.

I believe the ideas in the paper by Mont are not widely accepted but I think this article summarizes the condition extremely well.

I would also be happy to answer any questions related to this fascinating phenomenon.

Peter Backx, U of Toronto