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I read the article about your heart problems and relating it to cycling, and it can’t be right. The heart is a muscle, so how can it be damaged by working it hard? Exercise doesn’t damage muscles. It makes them stronger.
In the two years since I’ve quit racing after developing a heart arrhythmia, I’ve wondered about that same question. In fact, during the first three months since I ended up in the ER with it, I was in denial about it and was convinced that training hard and racing at my age (then 55) was good for my heart. But after three months of tachycardia becoming not only more frequent but also kicking in at lower and lower levels of riding intensity, I stopped denying there was a link and quit racing cold turkey following a pretty good cyclocross race for me after which my heart shot up to 220bpm many minutes into the warm-down.
The more I learn about it, the more it makes sense that endurance athletes over 50, who are extremely fit, can end up with cardiac electrical issues, even though they have none of the classic risk factors for heart disease, and their circulatory plumbing is clear of plaque. The day after I ended up in the ER, doctors performed an angiogram (a.k.a., “catheterization”) on me in the OR, and my cardiologist declared, after having sent a catheter in to inspect them, that I had arteries as healthy as those of a 14-year-old. Nonetheless, I still had an electrical problem.
First of all, don’t underestimate what the heart is doing inside you constantly; the heart does more physical work than any other muscle over a lifetime. While the heart puts out 1-5 watts of power, and the quadriceps can produce 100 watts, the quad only does that in short bursts, and the heart at a resting output of one watt for 80 years puts out 2.5 gigajoules.* You will never ride enough that your power meter will accumulate a total like that!
Then there is the effect of aging. No matter how healthy and fit others might say that I appear, their comment is predicated on my age, and my 57-year-old skin could never be mistaken for either of my daughters’ 20-something-year-old skin. It simply lacks that kind of flexibility and has little of the smoothness I see in my wedding photos from 32 years ago. It stands to reason that tissues throughout my body have undergone a similar transformation over the decades, including my heart muscle.
If I were to do a fast hike today up and down our local 14er, Long’s Peak, I know that my calves would be killing me the next day and would be even worse two days after. And the soreness would be more intense and slower to heal than it would have been when I was 40 years younger. We know that this soreness is due to micro-tearing of the muscle fibers, and it stands to reason that muscles with reduced elasticity will tear more easily than younger, more elastic ones.
But what about an aging heart? Even when lacking the same flexibility it had in its 20s, the volume of blood pumped by the heart can vary from 1.3 to 8 gallons per minute.** Imagine how much blood eight gallons is; my kitchen faucet will not fill a five-gallon bucket in a minute! And blood is thicker than water. To spit out the same amount of water as a human heart pumps blood in an average lifetime, a kitchen faucet would need to be turned on full for over 45 years!* During that time, the heart will pump nearly 1.5 million barrels of blood — enough to fill 200 train tanker cars.*
If you ask a little 11-ounce muscle that lacks the flexibility it had 30 years prior to push out five or six gallons of blood per minute during 700 hours per year of training (as I did through decades of cross-country ski racing, bike racing, and endurance training), it stands to reason that the same kind of micro-tearing would be occurring in the heart as in calves asked to go hard up and down Long’s Peak. The thing that got me a ride in an ambulance from the ER to the downtown cardiac unit after my first heart incident was an elevated level in my blood of troponin, an enzyme that is released when cardiac muscles die. My theory is that micro-tearing in my heart muscle caused the release of troponin. The ER doctor attending to me was Shannon Sovndal, who was at the time a team doctor for the Garmin-Sharp team. When I poo-pooed his troponin finding as likely just being due to a hard workout, he said that whenever he tested the blood of Garmin-Sharp riders (who were all at least 20 years younger than me) after hard workouts, he didn’t find elevated troponin levels.
Were I to do that fast Long’s Peak hike, I would rest my sore legs afterward, and perhaps the microfractures in the muscle cells would heal and not become chronic. But the heart never stops beating while you’re alive, so is it a surprise that a no-longer-youthful heart would become enlarged and exhibit scarring and stiffening in response to this demand on it? Try squeezing a tennis ball in your fist 160 times a minute, or even just 60 times a minute, and see what your arm muscles feel like.
An enlarged, stiffened heart with patchy scar tissue is said to exhibit “Pheidippides cardiomyopathy” after the runner who expired bringing news of Greek victory over Persia at Marathon. Idiopathic cardiomyopathy was the autopsy result of legendary runner Micah True, and his death was attributed to resultant cardiac dysrhythmia. It is not hard to imagine that scarring in the cardiac muscle will change its electrical conductivity, and the heart depends on the proper delivery of electrical impulses. Electrical currents behave similarly in some ways to water currents, and if the water rises too high in a streambed, it will seek a path of less resistance and cut a new channel. The next high-water incident will not need to be as high for water to rush down the new channel, cutting it yet deeper. I have no idea how the electrical currents in my heart decided to take the particular path they did that cause my arrhythmia, but I understand the statement from my cardiologist that, “every time you go into the arrhythmia, you’re training it to happen more easily the next time.”
The cause of Micah True’s death was not unique, but the follow-up was. Due to his fame and being the subject of a widely-reported search and rescue effort after his disappearance, an autopsy was conducted on him, and the results were made public. In contrast, the dearth of information following the deaths in major local events that occurred in the two weeks following publication of Chris Case’s “Cycling To Extremes” was more typical and contributes to our general lack of understanding about heart problems among masters endurance athletes. We will probably never find out the exact cause of death of the 40-year-old triathlete who died after collapsing during the marathon of the Boulder Ironman or that of the 55-year-old, 19-time competitor in the Leadville Trail 100 mountain bike race whose “heart gave out about 20 miles from the finish.” The media generally doesn’t distinguish between “heart attack” and other causes of heart failure, and the exact cause rarely can be diagnosed on the spot. But I think it is reasonable to guess that a 19-time competitor in an event as grueling as the Leadville 100 might have lacked many of the risk factors for heart attack, and there is ever more research to suspect that electrical issues caused by decades of training may have played a role.
According to Friedrich Nietzsche, “That which does not kill us, makes us stronger.” But the reverse may also be true after a certain age.
* Avraham, Regina. 2000. The Circulatory System. Philadelphia, PA: Chelsea House Publishers.
** The Heart and Circulatory System. 2000. Pleasantville, NY: The Reader’s Digest Association, Inc.
Editor’s note: Lennard Zinn is not a medical professional, and this article should not be construed as medical advice.