“Skiing causes an enlargement of the heart, and this enlarged heart can perform more work than the normal heart,” wrote a Dr. Henschen. “There is therefore, a physiologic enlargement of the heart, due to athletic activity.’’
Today, skiers are still being used to investigate how endurance training can change the heart. A recent study by Swedish researchers found that elite nordic skiers frequently developed heart arrhythmias. While most people assume that endurance training has only positive effects on cardiovascular health, a growing body of work suggests that a lifetime of exercise can contribute to cardiac abnormalities.
“Basically, this study shows, that even though physical activity is generally healthy, athletes committed to endurance sports at elite level have higher risk of suffering from a heart rhythm disorder,” said lead researcher Kasper Andersen of Upsala University. “There seems to be a relation with the duration of the sport commitment and at which level the athletes competed.”
The study surveyed skiers who completed Sweden’s Vasaloppet, one of the longest and most popular races in the world. In all, over 47,000 skiers who competed between 1989 and 1998 were included, and those who had competed seven or more of the races had a 29 percent higher frequency of heart arrhythmias.
But Dr. Andresen said that the increase in arrthymias did not lead to an increase in fatalities. So what does this mean for athletes?
The Anatomy of Arrhythmia
Several kinds of irregular heartbeats are included in the loose grouping of arrhythmia. A heart can beat too quickly or too slowly, it can beat too early, or it can simply beat erratically. There are different specific causes of arrhythmia, but all of them are at the most basic level problems with either the structure of the heart or the electrical impulses which cause the heart muscle to contract.
For those who don’t remember high school biology, here’s a basic refresher on the heart. In humans, the heart has four chambers and two different pumping circuits, a low-pressure one to the lungs and a higher-pressure one to the body. Low-oxygen blood returning from the body is pumped through veins into the right atrium, into the right ventricle, and then to the lungs, where it picks up oxygen. The refreshed blood is then sent into left atrium, the left ventricle, and back into the body through the arteries.
All of this movement is caused by powerful muscle contractions, which must be perfectly timed in the different parts of the heart. The atria contract at the same time, about a tenth of a second before the ventricles, and this pattern explains the characteristic “bump-bump” heard through a stethoscope.
The electrical signals which cause the muscle contractions come from pacemaker cells, which are located in the right atrium. The electrical stimuli can pass directly from cell to cell in the heart, meaning that all of the muscles can contract in unison. Once the muscles in the atria contract, the signal passes through a node which controls the pause before the ventricles contract.
How can this process go wrong? Sometimes, instead of producing one strong electrical pulse, the heart produces many weak ones, leading to a fibrillation or a flutter. Other times, the structure of the heart itself may change, for example due to coronary heart disease or vascular disease. Another possible cause is that the electrical circuits may have changed or grown; sometimes additional cells outside the ventricles produce electrical impulses.
In the Swedish study, the most common arrhythmias found in skiers were the erratic and usual heartbeat in the right atria, called atrial fibrillation, and the slow heartbeat, called bradycardia.
What’s So Bad About Bradycardia?
Bradycardia is defined as a hearbeat under 60 beats per minute, which doesn’t actually get at the underlying causes of the syndrome. For endurance athletes, definitions such as these aren’t particularly useful because having a heart rate under 60 beats per minute is not unusual.
“What’s too slow for you may depend on your age and physical condition,” the American Heart Association writes on its website. “Physically active adults often have a resting heart rate slower than 60 BPM but it doesn’t cause problems.”
Bradycardia is one symptom of the condition known as “athlete’s heart”, in which the resting pulse slows, the left ventricle enlarges, and the heart walls become thicker. These changes are due to regular aerobic exercise; the large muscles in the body require more oxygen to contract and as a result more blood must be pumped in each beat of the heart.
Dr. Paul Thompson of the Hartford Hospital noted in a 2002 paper that bradycardia has been shown to occur in a staggering 91% of endurance athletes. But athlete’s heart isn’t known to have any dangerous side effects, and once athletes stop training, their heart eventually returns to normal. So if bradycardia is simply caused by physiological adaptation to exercise, it probably isn’t a problem.
Another potential cause of bradycardia is what is called atrioventricular block, when the electrical signal from the atria are not fully transmitted to the ventricles. First-degree block is when the electrical impulses are simply transmitted more slowly to the ventricles, causing a delay in the pumping action. In second-degree block, not all of the signals actually reach the ventricles, and in third-degree block, none of the electrical impulses reach the ventricles.
A widely cited 1982 study by Finnish researchers using elite skiers and runners as test subjects found that endurance athletes were more than twice as likely to show first-degree heart block and more than four times as likely to show second-degree heart block compared to the controls. In some cases, the atrioventricular block lasted more than an hour, but the symptoms always disappeared as the heart rate increased during exercise.
The Finnish team did not find believe that these cases of atrioventricular block were particularly dangerous, but they did note that in a small number of cases second-degree heart block can develop into full-blown heart block, which is fatal.
All in all, a review paper in the New England Journal of Medicine noted that athletes shouldn’t be alarmed by bardycardia or first-degree heart block.
“Trained athletes are particularly prone to bradycardia, with heart rates below 40 beats per minute common at rest,” wrote Dr. Michael Mangrum and Dr. John DiMarco. “In one series, sinus pauses lasting between two and three seconds were found in 37 percent of athletes during sleep.”
However, there are some more sinister causes of bradycardia, such as heart disease, low thyroid levels, or electrolyte imbalances. In terms of effects, the danger of the condition is that the body does not receive enough oxygen because blood is moving so slowly and getting refreshed at a lower rate. If a skier has a low resting heart rate and experiences fainting, dizziness, chest pain, low blood pressure, shortness of breath, confusion or trouble focusing, then bradycardia could be the underlying cause and ought to be examined more closely.
All Aflutter About Atrial Fibrillation
The Swedish study isn’t the first to allege that atrial fibrillation (AF) is more common among endurance athletes. A 1997 paper by Finnish researchers showed that elite orienteers were more than five times more likely than the sedentary population to experience AF.
Interestingly, study after study has shown that male athletes are more inclined towards AF than women. AF also frequently appears for the first time in resting situations rather than during exercise.
Unlike bradycardia, the prevalence of AF isn’t simply an issue of definition. There’s no way around the fact that the syndrome is caused by abnormalities in electrical signaling, which is never a positive development. While not always life-threatening, AF can lead to palpitations, chest pain, fainting, stroke, and congestive heart failure.
Most AF cases in athletes are what is called lone atrial fibrillation, which means that there are no accompanying heart defects. While AF is often caused by heart attacks, abnormal heart valves, congenital heart defects, or sleep apnea, in lone AF no other disease is present. Lone AF is caused by electrical disorders rather than structural ones, and it’s rare to have serious complications from lone AF.
Researchers aren’t sure exactly why athletes have a higher prevalence of AF, but inflammation caused by training might be one cause. Inflammation leads an increase in the production of C-reactive protein (CRP), which is positively associated with AF, although why is unclear. Scientists have also hypothesized that the enlargement of the heart chambers might have some effect on electrical signaling.
New Zealand rower Nicola Coles woke up from a nap several weeks before the Beijing Olympics with AF, which persisted for more than 24 hours. After going to the hospital, doctors found that the only way to return her heartbeat to normal was cardioversion, a procedure using electricity and drugs to convert the heart rate.
Coles didn’t experience AF again and went on to place fifth in the women’s pair. But as her case shows, even without complications, AF is uncomfortable and requires treatment if it doesn’t disappear on its own.
“Although having a benign course, regular follow-up of patients with lone AF is warranted,” a group of Dutch researchers led by Dr. Bas Schoonderwoerd wrote in a 2008 paper. “In time, risk factors such as hypertension, heart failure, diabetes, and peripheral vascular disease may develop, changing prognosis.”
A separate trio of Dutch scientists followed a cohort of endurance athletes for ten years, and in a 2004 paper noted that AF developed in to permanent, chronic AF in fifteen percent of the study subjects.
Athletes should also be concerned about AF because it means that the heart is not pumping blood efficiently. Instead of producing one big electrical signal, the pacemaker cells in the atria beat chaotically, producing a group of weaker electrical signals. As a result, the atria pumps quickly; however, not all of these signals reach the ventricles, so they pump more slowly. The end result is that pumping is not as powerful.
So What’s the Big Deal?
“The absolute incidence of death during or within one hour of sports participation among U.S. high school and college athletes is one death per year for every 133,000 men and 769,000 women,” Dr. Thompson wrote in his 2002 paper. “These numbers overestimate the incidence of cardiac events, because of the 136 deaths, only 100 were caused by cardiac disease.”
An individual skier who shows signs of bradycardia or atrial defibrillation has only a miniscule chance of dropping dead on the trails; if their heart is otherwise healthy, the arrhythmias found by the Swedish researchers aren’t necessarily dangerous.
The more important finding of their study on the Vasaloppet skiers, however, was that as skiers trained and raced more and more, they because more likely to develop arrhythmias.
This concept is supported by previous research showing that there is some threshold of lifetime training volume above which arrhythmias become markedly more common. As athletes move into middle age and keep training, they are more likely to experience AF, and as they continue to age, they show more risk factors for serious complications – although even these complications are not as prevalent or as dangerous as some of the other heart problems which are common in the rest of the population.
In short, the more a skier trains, the more the heart restructures itself to deal with the stress of exercise – for better or for worse.
“The veteran athlete may not be as healthy as believed with many established areas lacking conclusive evidence to support the benefits of a lifelong career in high intensive endurance exercise,” a team of international researchers noted in a paper just last year.
While it’s not a reason to stop training, skiers should be cautious about heart health. It’s often difficult to tell whether abnormalities are due to athlete’s heart or an underlying condition, but if a skier is blacking out on the trails or experiences heart palpitations, they need to head to the doctor’s office.
Hoogsteen J, Schep G, van Hemel NM, van der Wall EE. Paroxysmal atrial fibrillation in male endurance athletes: a 9 year follow up. Europace 2004;6(3):222-228.
Karjalainen J, Kujala UM, Kaprio J, Sarna S, Viitasalo M. Lone atrial fibrillation in vigorously exercising middle-aged men: a case-control study. British Medical Journal 1998;316:1784.
Mangrum JM, DiMarco JP. The Evaluation and Management of bradycardia. New England Journal of Medicine 200;342(10)703-709.
Partarrieu J. “Link Between Elite Cross-Country Skiing And Increased Risk Of Subsequent Arrhythmias“. Medical News Today, August 31, 2011. Web. 10 Sep, 2011.
Schoonderwoerd BA, Smit MD, Pen L, Van Gelder IC. New risk factors for atrial fibrillation: causes of ‘not-so-lone atrial fibrillation.’ Europace 2008:10(6):668-673.
Swanson DR. Atrial fibrillation in athletes: implicit literature-based connections suggest that overtraining and subsequent inflammation may be a contributory mechanism. Medical hypotheses 2006:66(6)1085-1092.
Thompson P. Exercise and the Heart: The Good, the Bad, and the Ugly. Dialogues in Cardiovascular Medicine 2002;7:143-162.
Viitasalo MT, Kala R, Eisalo A. Ambulatory electrocardiographic recording in endurance athletes. British Heart Journal 1982;47:213-220.
Wilson M, O’Hanlon R, Basavarajaiah S, George K, Green D, Ainslie P, Sharma S, Prasad S, Murrell C, Thijssen D, Nevill A, Whyte G. Cardiovascular function and the veteran athlete. European Journal of Applied Physiology 2010;3:459-478.