Don't miss a moment from Paris-Roubaix and Unbound Gravel, to the Giro d’Italia, Tour de France, Vuelta a España, and everything in between when you join Outside+.
Have a question for Lennard? Please email him at email@example.com to be included in Technical FAQ.
You mentioned that problems related to ventricular contraction are more dangerous from a cycling perspective. I was recently diagnosed with PVCs and put on metoprolol, a blood pressure medicine, to “calm” my heart. Are you saying it is dangerous for me to ride hard?
No, I’m not saying that. Though indeed they do appear in the ventricles, PVCs (Premature Ventricular Complexes) are far different from ventricular tachycardia and ventricular fibrillation, which are what I was referring to when I discussed ventricular arrhythmias; the latter are conditions that can cause death. By contrast, PVCs, while they do send a lot less blood to the body than a normal heartbeat would, do not happen continuously. They are “premature” in the sense that the heart contracts before the ventricles have had time to fill completely with blood. This could be life-threatening, I suppose, if they happened on every beat, or perhaps even on every other beat, but they do not. The most I have ever heard of is a PVC every fourth beat on average. A high percentage of people experience PVCs occasionally. For you to be on medication for them, I assume yours occur more than occasionally.
In Chapter 4 of The Haywire Heart, I go into the details of how the electrical signals that produce PVCs (as well as PACs, Premature Atrial Complexes) arise. PVCs can be caused by healthy cardiac pacemaker cells but are more often created by clusters of cells that have somehow gained “enhanced automaticity” and are behaving like pacemaker cells. In the heart of a highly-trained athlete, the stimulation from the sino-atrial (SA) node can be so infrequent (at rest) that pacemaker cells or rogue cells behaving as pacemaker cells occasionally fire on their own. PVCs can happen so frequently in some elite masters athletes (on the order of 25,000 PVCs per day) that blood flow is significantly reduced and treatment, or at least a great reduction in athletic workload, is mandated.
If your PVCs occur during exercise, rather than at rest, then I don’t get the point of riding hard anyway with that condition. I realize that may come as anathema to you and certainly would have to me before I developed a cardiac arrhythmia myself. Now, it is clear as day to me that, if my heart is not going to beat in sinus rhythm when I am exercising, I will not ask it to. Why would I? What’s the point of trying to compare my ride to a PR or to somebody else or to prove something, when my ride will be slow because my heart will not be circulating as much blood as it could without arrhythmia? For me, it comes as a pretty clear message to find a different type or intensity of exercise that won’t put my heart into arrhythmia.
Whether your PVCs pose any danger to you is an individual thing and not something I would have any way of knowing. That would be a subject for discussion with your cardiologist.
With great interest, I read your tech column response in regards to Štybar’s afib and ablation. I’m 65 now and still not the same aerobic animal I was prior to a botched ablation in 2014. I developed pericarditis from damage done in an ablation that persisted for months. Almost two years after the ablation, I had a near-fatal pulmonary embolism. I’m lucky to be here.
The point being, with regards to Štybar wanting to go back to racing so quickly after an ablation — I hope someone gets to him and can convince him to chill. As you are well aware, any procedure involving your heart and general anesthesia is no joke.
So, I am mainly curious about your opinion as to why long-time endurance athletes are way more prone to developing cardiac arrhythmias and, most importantly, why some get “lucky” and have atrial fibrillation vs. some that develop the WAY more serious Vtach [ventricular fibrillation]. I would love to hear your theory on the causation of PVCs and arrhythmias.
I bought your book back in 2017 and still refer people to it that are unfortunate enough to go down the road you and I have. My own personal theory is having a resting pulse in the 30s or 40s for a long period of time changes the micro distances in the electrical conduction pathways forever, and arrhythmias can develop.
Can you steer me somewhere to find references regards how some develop AFib while others sadly have Vtach? Another guess on my part-those athletes with higher max heart rates are more likely to have Vtach? Thanks for all you do and offer to all of us old athletes!
I can answer the first half of your first question, namely, “Why us long-term endurance athletes are way more prone to developing cardiac arrhythmias?” The second part about why some are less lucky with their arrhythmia type than others I can’t answer because nobody knows why some athletes get AF and some get VT.
As for the causation of PVCs and arrhythmias, that is a much more involved answer than I could give in this column. As I mentioned in my prior answer to Mark, I go into detail in the book about what brings on the electrical impulses that cause PVCs. The book also addresses causes of arrhythmias in general.
I can say briefly that sustaining an atrial arrhythmia requires an abnormal “substrate,” which is a cardiologist’s word for the atrial muscle. As Dr. John Mandrola writes in The Haywire Heart, “Typical conditions that cause an abnormal atrial substrate are inflammation, stretch, atria enlargement and scarring.” Making the assumption that you are talking about arrhythmias in highly-trained cyclists, you might be interested in studies Mandrola discusses in our book of rats and mice that were put on 6- to 16-week exercise regimens. Regarding the results of one of those studies, he writes, “Compared to a group of sedentary mice, the trained group had lower heart rates, enlarged atria and ventricles, and atrial fibrosis (scarring). The trained mice in this study also had enhanced vulnerability to AF [atrial fibrillation].” That right there is a description of the abnormal atrial substrate he mentioned as being required to sustain an arrhythmia; it confirmed the findings in other studies of exercised mice and rats. It also lined up with some studies of human masters endurance athletes described in the book.
I just read your response to the question about Štybar’s arrhythmia. I discovered I had an exercised induce arrhythmia about 15 years ago, when I was mountain bike racing. I had a Polar heart rate monitor, and the graphs of my heart rate during a race showed that it would occasionally spike to around 220 bpm. When I started going downhill, or reduced efforts, it would come back to normal. I continued racing into my 40s with no real issues other than mild nervousness about it. Then it started happening in spin classes, and at much lower efforts than before. I had stress tests on the treadmill, but for about four tries it didn’t trigger the event. Finally, a cardiologist friend of mine put me on a bike and bingo! – there it was. I have the atrial version (a four-letter acronym I can never remember), and I was told it was controllable and non-life-threatening.
Since then, I have been on a low-dose beta-blocker, which keeps my heart rate from spiking. I have not had an incident since while on the bike. We did discuss ablation, but as my cardiologist said, “Why would I recommend something that has a 0.1 percent chance of killing you when there is a solution that you are happy with that has zero risk”. Fair. I am not a professional athlete and am not going to be getting Strava KOMs anytime soon – except maybe for downhill segments. But since my max HR is now only about 155 (at age 60) I am also aware that my maximum sustainable power output is going to be diminished.
Finally, I had an incidence of AFib on Labour Day two years ago. They had to do cardioversion to get me back in rhythm, but there have been no long-term effects. Again, there was discussion of ablation, but the doctor basically said that if the beta-blockers are doing their work, why mess with it.
All this to say that people are frightened at the very mention of an arrhythmia. Absolutely, everyone should get it checked out, but it is neither a death sentence nor a guarantee of a life of inactivity. “Touch wood,” mine has just made a chunky slow guy a bit slower…
Thanks for this perspective. It is indeed not a death sentence nor a guarantee of a life of inactivity. Since my diagnosis of arrhythmia (and failure of two ablation attempts to fix it), my life has completely changed, and, while the changes initially did not come easily, it’s not a bad thing. I don’t race (bikes or cross-country skis) anymore, and I now could care less when somebody passes me on a bike or on skis. I ride an e-bike to still be able to do fun mountain rides and not be confined to short, slow rides within a short radius of my house. Skate skiing I now only do on flat terrain, and when track skiing on hilly terrain at altitude, I now only do the classic technique (kick and glide). Mostly, for 5-6 months of the year, I backcountry ski with people my own age, which is plodding up mountains with skins on our skis and then powder-skiing back down. I am 62 and do things like tending my koi pond and gardening that were inconceivable before I developed arrhythmia at age 55. I love my life and do not feel I’m missing anything by no longer racing other people or feeling the burn of hard workouts.
As an interventional cardiologist (not an electrophysiologist), I do appreciate your quality explanation in this article. I would only like to offer two suggestions:
– catheter placement in the “groin” is perhaps more eloquent than the “crotch”
– for several years now we have been using suture closure (as well as other) techniques to lower the risk of bleeding, avoid prolonged manual pressure, and minimize bed rest/allow for early ambulation. I routinely do 14 Fr venous procedures (most ablation catheters are much smaller) and allow patients to sit up to 45 degrees immediately and ambulate in 2 hours.
I was diagnosed with Afib in the summer of 2019 after having multiple episodes of tachycardia following bike races (I am 55 and was racing W50+). I was also having ~6000 PACs a day and occasional episodes of SVT — supraventricular tachycardia, literally meaning racing heart rate in the chambers above the ventricles, namely, the atria — which had begun during my first pregnancy 25 years earlier. The arrhythmias were becoming frequent and severe enough to keep me from racing bikes, so my cardiologist proposed ablating both the SVT and the Afib. I had the ablation procedure in the fall of 2019 and intended to return to racing bikes the following year.
At the time of the ablation, I had not understood that ablating for Afib is different than ablating for other types of arrhythmias; as I’m sure you know, instead of isolating a specific conductive path, the Afib ablation involves burning around the entire circumference of a pulmonary vein. This can affect the vagal inputs to the heart, as seems to have happened in my case. My resting heart rate immediately went from 60 to about 95 (1.5 years later it has settled at 84 bpm) and my HRV [heart rate variability, which is the variation in the beat-to-beat interval; more is preferable. Research suggests that people with higher HRV at rest tend to give more appropriate emotional responses than people with low HRV at rest] completely tanked. It now averages around 11 (RMSSD) [root mean square successive difference: a time-domain measure of heart period variability] according to Whoop. Because my vagal tone [continuous baseline parasympathetic action provided by the vagus nerve] was trashed by the ablation, my ability to recover from efforts is significantly reduced; once my heart rate goes up, it doesn’t want to come back down. As a result of these changes, I no longer race or even ride hard. I believe the reduction in vagal tone has also had a significant effect on my mental health; since my parasympathetic system is degraded, I am operating in more of a “fight-or-flight” regime all the time.
I was surprised to read in online journal articles that an increased HR and decreased HRV following Afib ablation are correlated with a reduced likelihood of Afib recurrence—and thus from an electrophysiologist’s perspective, these changes are good. From my perspective, however, they are a disaster. I may not have Afib anymore, but my quality of life has been significantly impaired, and I worry about the long-term health implications of having such a low vagal tone and poor HRV.
I have not found a single paper that discusses or even acknowledges this tradeoff. I asked my electrophysiologist (whom I like and trust) whether there was anything I could do to help recover my vagal tone (like using an external vagus nerve stimulator) and he seemed entirely unfamiliar with this issue.
Have you heard of this problem with Afib ablations before? Do you have any resources that discuss the health implications of poor post-ablation vagal tone, or possible treatment options?
Yes, I have heard of this from others after AF ablations. I know of no treatment options, which does not mean that none exist. If anybody writes in with suggestions, I will pass them on to you. Best wishes with this.
Lennard Zinn, our longtime technical writer, joined VeloNews in 1987. He is also a custom frame builder (www.zinncycles.com) and purveyor of non-custom huge bikes (bikeclydesdale.com), a former U.S. national team rider, co-author of “The Haywire Heart,” and author of many bicycle books including “Zinn and the Art of Road Bike Maintenance,” “DVD, as well as “Zinn and the Art of Triathlon Bikes” and “Zinn’s Cycling Primer: Maintenance Tips and Skill Building for Cyclists.” He holds a bachelor’s in physics from Colorado College.
Follow @lennardzinn on Twitter.