My wife, who, bless her, seems to care about my long-term health, sent me some articles this morning about athletes and atrial fibrillation. Now, most of us know that runners and other endurance athletes are at higher risk as they get older for developing atrial fibrillation (rapid heart rate triggered within the upper chamber of the heart receiving blood from the lungs), but these articles go a bit deeper into both why this might happen, and what to do about it. I was intrigued to read them after I saw this introduction:
“The endurance athlete is special. These are not the people who run a marathon; they are the types who ride their bike to the marathon, run the 26.2 miles, then ride home.
The normal exerciser sweats, breathes hard, and occasionally pushes his heart rate close to maximum. The competitive chronic endurance athlete pushes well past that threshold on a regular basis—for years and decades. Going over the limit—in dose and intensity—is what defines these individuals.
Endurance athletes endure fluid shifts, changes in pH and electrolytes, and fluctuations in blood pressure. Their atria are exposed to chronic volume and pressure overload. Athletes live in a disordered autonomic milieu—spikes of sympathetic outflow interrupt a persistently high parasympathetic tone. The athletic heart is exposed to extreme tachycardia and long periods of profound bradycardia.
And it is not only the physical effects. Endurance athletes who compete may also develop mental and emotional stressors. Although the incidence is not known, some athletes use substances to enhance performance or promote rest—many of which are arrhythmogenic. In addition, those who exercise as a vocation rather than a hobby may endure self-esteem issues, which have been correlated [3] with greater inflammatory responses to stress.”
I shuddered with a recognition – every sentence in that applies to me, except for the one about PEDs. So I read on. (I’ll provide the link to the article, but, caution, it is written mostly in medical/cardiologese. Even as an MD, I can can understand the words used, but it’s a bit more difficult than deciphering James Joyce or Thomas Pynchon. EG, this sentence: “Vagal stimulation further shortens AP duration, then sympathetic stimulation enhances Ca-current, which has a net depolarizing effect and can lead to rapid repetitive firing.”) Article (you’ll need a Medscape account to read, I think.)
Anyway, this gist of it seems to be a theory that some of us have the advantage of conduction pathways near the top of our heart, where the veins from the lungs are bringing blood back, which work a bit differently, along with some structural differences in the atrium itself, which help reduce the risk that all that chaos during intense and/or prolonged exercise described above will trigger a bout of arrhythmia in our heart. Others who don’t have these variations might develop AF. The older you are, the longer you’ve put yourself through the ringer, and the faster you are, the more likely you will experience AF.
So what to do if you develop AF with no discernible cause other than you are a “competitive chronic endurance athlete [who] pushes well past that threshold on a regular basis—for years and decades.”? Apparently, you have three choices: medication, which would significantly inhibit the quality of your training, surgery, which, in addition to its inherent risks, fails 15-35% of the time, or simply stop being a competitive endurance athlete, as defined above.
The good news is, AF is not really life threatening. But it’s still worth being aware of the symptoms: Heart palpitations (feeling that your heart is racing or fluttering) • Awareness that the heart is beating • Chest pain, pressure, or discomfort • Abdominal pain • Shortness of breath • Lightheadedness • Fatigue or lack of energy • Exercise intolerance