By Stephanie Soucheray |
Like many people, Gene Kay has always subscribed to the belief that regular cardiovascular exercise is the magic bullet for optimal heart health. It stresses the heart in a way that makes it stronger — cardiac output increases, as do heart rate and blood pressure. It has been proven in countless studies to lower blood pressure, reduce bad cholesterol, control weight, and lower blood sugar. For most of us, it would seem, there’s no better medicine.
Until recently, Kay was a lifelong athlete. He competed in cross-country ski races for 30 years, completing more than 75 ski marathons as a masters-level athlete. Two years ago, he celebrated his 54th birthday by finishing the 54K American Birkebeiner Classic in Wisconsin, the largest cross-country ski marathon in North America.
“I felt great, finished in the elite class, and was proud of my performance,” says Kay.
A few months later, however, he noticed that he was getting out of breath while sweeping his garage floor, and that his heart was racing when he climbed the stairs in his Plymouth, Minn., home. He could still run eight miles with ease. But at rest, his heart sometimes felt like it was skipping a beat.
“It made no sense,” says Kay. “When I was just sitting around, it seemed like my heart was working really hard.”
Kay, who was used to training eight to 10 hours per week, decided to take a month off. But rest didn’t help, and neither did meditation, yoga, changing his diet, or cutting caffeine. Dealing with stress, watching his nutrition — nothing seemed to have an impact.
So he consulted his doctor, who prescribed cardiac testing, including treadmill stress tests and a cMRI. The results showed Kay had developed a heart arrhythmia, or abnormal heart rhythm, and though it sounds benign, it’s a potentially fatal condition if left untreated. In his case, it was premature ventricular contractions, or PVCs.
PVCs are an electrical misfiring in the heart’s lower chambers (the ventricles) that cause extra, unproductive heartbeats. People usually notice a PVC when they’re resting, and may sense that their heart is skipping a beat, or feel a hollow sensation in their chest.
Kay’s tests showed he was suffering more than 20,000 PVCs daily. These missed beats were causing his heart to race into a state called tachycardia (an irregular or faster-than-normal heartbeat at rest), which can lead to sudden death.
Kay suddenly went from being an elite athlete to an invalid.
Arrhythmias on the Rise
The arrhythmia diagnosis was a shock to Kay — and his disbelief is common among athletes who believe their chosen sports are protecting, not harming, their hearts.
In recent years, several prominent athletes have been sidelined with arrhythmias, including Basque pro cyclist Haimar Zubeldia and Norwegian Olympic cross-country skier Marit Bjørgen, among others. Both National Football League star Reggie White, who died at 43 in 2004, and legendary ultramarathoner Micah True, who died at 58 in 2012, suffered from fatal arrhythmias. Prominent bicycle racer Lennard Zinn — who quit racing in 2013 due to an arrhythmia — says, “Everyone I knew could name six guys with arrhythmias. I started to see it as this defining problem among people like me.”
“Extreme exercise puts the body in an inflammatory state,” explains Mimi Guarneri, MD, an integrative cardiologist in La Jolla, Calif., and author of The Heart Speaks. Yes, endurance exercise can strengthen the heart — but sometimes the stress of training or racing is more than the muscle can repeatedly withstand. “By the time someone crosses the finish line in a marathon or a ski race, their heart is in stress. They almost look septic.”
For some athletes, long bouts of intense endurance exercise repeated over many years can cause their hearts to “misfire.” Over time, the inflammation and disrupted blood flow take a toll and can result in the development of electrical malfunctions and structural changes of the heart.
Endurance-exercise-related arrhythmias are terrifying, yet most people have never heard of them. The condition is a relatively new problem, though growing quickly as more endurance athletes age. Also, it doesn’t have a clear cause — and there are no easy fixes.
To understand what arrhythmias are, it’s important to first understand what they are not. Arrhythmias are not the same as overtraining, which is marked by exhaustion and depression-like symptoms, an increased susceptibility to injury and illness, physical indicators of stress, and, notably, a steady, inexorable decline in performance.
In some people, arrhythmias are the result of a genetic predisposition, but for many athletes who develop them, genetics is not a factor. In these cases, the arrhythmias appear to be caused by extreme endurance exercise, performed at high intensities, over many years. This type of activity can remodel the heart and negatively affect its electrical circuits, resulting in arrhythmias like Kay’s PVCs.
A 2012 review of recent studies, published in the Mayo Clinic Proceedings journal, concluded that “chronic intense and sustained exercise” can induce adaptations in the heart, including increases in right- and left-ventricle volumes and wall thickness, increases in the overall mass of the heart, and enlargement of the left atrium. For example, the review authors note that our hearts’ output can increase from 5 liters of blood per minute at rest to up to 25 liters per minute during intense exercise.
While the authors reiterated that cardiovascular exercise is good for heart health in modest amounts, years of extreme cardio can result in “repetitive injury,” which can take the form of an arrhythmia.
Strong evidence that long-term endurance training can cause arrhythmias was published in the European Heart Journal in 2013. The study followed 919 participants in the Swedish Vasaloppet race (a 90K cross-country ski race) who were first diagnosed with arrhythmias at a mean age of 56.8. Skiers who’d completed the race five or more times were twice as likely to develop bradyarrhythmias (an abnormally slow heartbeat) than those who had completed only one. The study concluded, “Among male participants … a faster finishing time and a high number of completed races were associated with higher risk of arrhythmia.”
In other words, the more experience, the more training, and the better the athletes, the more likely they were to develop an arrhythmia.
The most common arrhythmia documented in the Vasaloppet study was atrial fibrillation (AF or AFib), often the first heart problem athletes encounter. AFib occurs when the heart’s upper chambers beat too quickly and are out of sync with the lower chambers; this can result in shortness of breath, palpitations, or fatigue. In a 2011 review article published in Cardiovascular Medicine, the authors concluded that long-term endurance training produces left-atrial structural changes, which can cause AFib in athletes of all ages.
According to some studies, continual, prolonged strenuous exercise (more than two-and-a-half hours at an intense effort) produces chronic inflammation that can change the heart, promoting cardiac fibrosis (hardening or scarring of the heart), stiff arteries, and calcification. These changes can lead to Phidippides cardiomyopathy, named after the ancient Greek who ran 175 miles and then died. This condition is defined by an enlarged heart dotted with patches of fibrosis. The patches can cause ventricular tachyarrhythmias (which is the lower chambers of the heart beating too quickly) in the athlete, which can lead to sudden death in rare cases.
The European Heart Journal published a study in 2008 that compared 108 male marathoners who were over age 50 and had completed five or more marathons with control groups representative of the general public. The study found that the marathoners had stiffer arteries and more coronary artery calcification than the controls.
In a paper presented at the 2010 American College of Cardiology annual meeting, cardiologists found that 25 men who had run the Twin Cities Marathon for 25 consecutive years had a higher calcified-plaque volume than nonathletic peers. These calcium deposits and plaque can narrow the aortic valve, which can lead to heart disease.
In Search of Answers
So at what point does the scale tip and beneficial exercise become hazardous? It’s a question that is being researched and debated in the medical community.
Paul Thompson, MD, chief of cardiology at Hartford Hospital in Connecticut and for years a dedicated marathon runner, takes a pro-exercise stance. In a review of studies concerning the cardiac effects of chronic endurance exercise that was published in Physiological Reviews in 2015, he and his fellow authors issued a reassuring note: “The best evidence remains that physical activity and exercise training benefit the population.” Or, as the review concludes, the problem for most people “is too little and not too much exercise.”
Some experts, however, believe the solution is more complex and needs to take more into consideration, including cumulative workouts over the years, family history, nutrition, and inflammation.
The answer lies in a gray area, says John Mandrola, MD, a cardiac electrophysiologist at Baptist Health Louisville in Kentucky and an avid masters bicycle road and cyclocross racer.
“The dose of exercise that causes damage is unknown, as is an individual’s susceptibility to varying training loads. We don’t know the ideal exercise regimen, or if there is one. I know what is too little exercise; I know what is too much; but there’s a large space in between,” he explains. “Just like everything else in life, even exercise has an upper limit.”
What that threshold might be still needs more study, experts agree.
Age itself may seem to be a predisposing factor. After all, Kay was 54 when he developed an abnormal number of PVCs, and the mean diagnosis age of the Vasaloppet study was 56.8.
The many studies on the subject, however, have not found a “magic cutoff” — an age when athletes become more susceptible to developing arrhythmias, says Lawrence Creswell, MD, a cardiac surgeon at the University of Mississippi who authors the popular . Arrhythmias can develop at any age.
Numerous experts attribute the recent spike in athletes with arrhythmias to the fact that many masters athletes are baby boomers who first began jogging in the 1970s and incorporated endurance events into their lifestyles. “More and more people are getting older and getting into endurance training,” Guarneri explains. “More people are running marathons. More people live a sedentary life, which they compensate for with extreme exercise.”
And it’s a trend with legs: The number of marathon finishers increased 140 percent from 1990 to 2013, according to Running USA. Unfortunately, the scientific research hasn’t caught up to racing demographics.
Age is a consideration only in that an older adult may have spent more years training hard than a younger person. It’s the cumulative effect of chronic inflammation on the heart — chronic exercise stress piled on top of chronic life stress — that makes the real impact, Guarneri says. That is what can change the structure and functioning of someone’s heart.
Taking It to Heart
Skier Gene Kay was past the point of prevention when he was diagnosed, so he began working with his doctors. Treatment for PVCs can include anti-arrhythmic drugs, including beta-blockers and calcium channel blockers, both of which come with side effects and other risks. Both classes of drugs work to reduce your heart rate and cardiac output, so you have to be carefully monitored when you begin taking them.
Kay’s doctors decided he was a good candidate for cardiac ablation, a procedure that destroys the area of the heart causing the electrical misfirings. Kay’s procedure lasted 14 hours: He described it as a game of “pin the tail on the donkey” between the cardiologist and the electrical pulses in different parts of his heart.
One week after the ablation, Kay was back at the cardiologist’s office. “They had me on a treadmill and took my heart rate up to 180. I felt good.” Still, his doctors gave him conflicting advice about how and when he should return to his training.
“One cardiologist told me to resume all activities. Another told me to be active but give up racing,” says Kay. He took the latter advice.
Doctors aren’t quick to advise younger athletes to give up their chosen sports. Mandrola, for one, says he would caution against a competitive, endurance-heavy lifestyle only if someone had a family history of heart disease or a history of smoking. Avoiding excess is one important precaution (for more preventive measures, see “5 Things You Can Do to Prevent Arrhythmias,” below), but in many cases, this advice falls on deaf ears.
“Very few athletes in their 30s and 40s would change their mind [about endurance exercise] because of some nebulous future risk,” says Mandrola, alluding to the need for more research. “It’s way too much fun.”
Heart arrhythmias in endurance athletes is a growing problem, but because it’s not yet widely recognized, cardiologists and other healthcare professionals don’t yet have a can’t-fail formula to prevent avid exercisers from developing the condition. Still, they agree there are some steps you can take to reduce your risk:
Lennard Zinn is well known to most cyclists. A former member of the U.S. national cycling team, owner of custom bike-frame builder Zinn Cycles in Boulder, Colo., author of the celebratedbooks, and a writer for VeloNews, Zinn has been a 40-year presence in the endurance-sport world.But in 2013, when he was 55, Zinn became a cautionary tale among his peers when he wrote about his struggles with PVCs, tachycardias, and cardiac ablations in a series of groundbreaking VeloNews articles. It was one of the first comprehensive reports on arrhythmias in endurance athletes.Zinn experienced PVCs at rest beginning in his 40s, but he continued to exercise and race while wearing a heart-rate monitor. “I wasn’t bothered by the sensation of the PVC,” Zinn says. But a PVC during a training race against himself up Boulder’s Flagstaff Mountain forced Zinn to stop in his tracks.“My heart skipped, and my heart monitor read 155. I looked at it again and it was 218, then 220 as I was halfway up the steepest pitch,” says Zinn. “I thought, ‘I should stop. This is not a good idea.’”Zinn called his primary-care physician, who recommended he go straight to the ER. There, a team of cardiologists began testing.Like many athletes, Zinn denied that anything serious could be wrong with his heart: He had clear arteries, a slow resting-heart rate, and low blood pressure.He decided to keep exercising while doctors ran him through weeks of testing. He wore an EKG monitor, but his incidents of tachycardia increased in frequency, and his doctors diagnosed him with multifocal atrial tachycardia.Because his resting heart rate and blood pressure were already so low, most anti-arrhythmic drugs weren’t an option; they would have produced serious side effects.Eventually, Zinn was recommended for cardiac ablation. But his doctors weren’t able to find any of the electrical hot spots causing the tachycardias in his heart.“The surgeons blasted me with adrenaline to try to get the arrhythmia going, but they couldn’t,” he notes.Within months, Zinn decided to quit racing for fear it would lead to more arrhythmias, or worse, a stroke.Like many athletes, he had a hard time adapting to his new normal. But the more he talked about his condition, the more he heard stories about other athletes his age facing the same problems.After consulting with doctors, Zinn felt his best chance at healing his heart would be to give up his competitive cycling career.“At first, it was certainly hard,” says Zinn. “But now, I’m a better husband and father. I can enjoy a vacation without thinking about needing three hours of the day to exercise.”
Listen in ascopy chief Steve Waryan, a longtime endurance athlete, shares the story of his arrhythmia and recovery with senior fitness editor Maggie Fazeli Fard.