Masters endurance athletes more at risk of heart arrythmias


Over the last 5-10 years I have become aware of a number of former elite endurance athletes having heart issues. This is counter intuitive given endurance athletes are considered to have strong hearts. However, over the last 10 years research is increasingly showing that the incidence of arrhythmias is higher in athletes, especially in elderly athletes with a lifelong training history in marathons, ultra-marathons, ironman distance triathlons and long distance bicycle races. An arrhythmia is any change from the normal sequence of electrical impulses in the heart. The electrical impulses may happen too fast, too slowly (bradycardia), or erratically so that the heart can’t pump blood effectively.

Bradycardia, defined by a resting heart rate <60 beats min−1, is the most frequent rhythm disturbance in response to endurance training where the resting heart rate can be ~30 beats min−1 and even lower at night. Cyclists Sir Chris Hoy and Tour de France winner Miguel Indurain reportedly had resting heart rates of 30 and 28 beats per minute. Although the bradycardia is usually a harmless adaptation to endurance training, it can become a pathological condition. It was previously thought to affect the electrical activity of the heart that starts in what is called the sinus node (see photo) which is an area of specialized cells in the upper right chamber of the heart that controls the rhythm of your heart.

The most compelling evidence of a link between endurance training and sick sinus syndrome comes from a study of former professional cyclists. Their average heart rate was lower, sick sinus syndrome was more frequent, and pacemaker implantation for bradyarrythmias was more frequent relative to a control group with matched cardiac risk factors. Similarly, a high incidence of pacemaker implantation has been reported in elderly marathon runners.

Historically, this slowing of the heart rate was thought to be the result of a change in the nervous system stimulation of the heart muscle through the sinus node, the pacemaker structure in the heart muscle itself. However, a recent animal study is the first to show that the heart rate adaption to exercise training is not the result of changes in this nervous system control of the heart, and instead is primarily the result of a training-induced remodelling of the sinus node within the heart itself.


Rats were trained for 12 weeks (1 hour per day, 5 days per week) by aerobic interval training (uphill running) alternating between 4 min at 85–90% of the maximum oxygen uptake and 2 min active recovery at 50% of maximum oxygen uptake. Experiments were also carried out in mice that were trained for 4 weeks (1 hour per day, twice a day, 7 days per week) by swimming. Resting heart rates, electrical activity of the heart, as well as actual tissue samples from the sinus node of sedentary and trained animals were analyzed.


The resting heart rate of the trained rats and mice was ~26% and ~20%, respectively, lower than the heart rate of untrained animals. The resting heart rate of exercise-trained human subjects in various studies varies between ~17–26% lower than the heart rate of inactive people, a reduction similar to that observed in the animal models in the present study. This decrease is less than in elite human athletes. However, severe bradycardia or heart rate slowing in human athletes is uncommon. A protein found in the sinus node (the heart’s pacemaker) changed in response to training with a decrease in an important pacemaker protein, known as HCN4, a protein that is responsible for the low heart rate seen in fit animals.

So What?

With lifelong endurance training, research has consistently shown that veteran endurance athletes have a higher incidence of sinus node disease and artificial pacemaker implantation than normal individuals. Historically, we always believed this was due to changes in the nervous system stimulation of the heart. The present study, although done on rats and mice, suggests the slowing of the heart rate may be due to actual remodeling of the sinus node in the heart wall that actually stimulates the heart muscle to beat. The researchers believe that this finding may also help explain syncope (fainting) in the young athlete as well as other heart rhythm disturbances in older athletes including atrial fibrillation, heart block, bundle branch blockand even sudden cardiac death.. They suggest that it is likely that these disturbances may be the consequence of an actual remodeling of other parts of the heart that are responsible for electrical activity in the heart and perhaps in combination with a pre-existing heart condition in the case of sudden cardiac death.

Critically, the researchers suggest endurance exercise is undoubtedly beneficial for the cardiovascular system, but at the same time intense endurance training over many year can have harmful effects, especially in elderly athletes with a lifelong history of training and competing in endurance events like marathons, triathlons and ironman. They conclude that although endurance exercise training can have harmful effects on the heart, it is more than outweighed by the beneficial effects. Importantly, the researchers also know that this animal study’s findings need to be reproduced in humans and that more research is needed before we could draw conclude that too much endurance training is bad for the heart health of veteran athletes who have undertaken years of endurance training.

Source: D’Souza, A. and others (2014). Exercise training reduces resting heart rate via downregulation of the funny channel HCN4. Nature Communications, 5, Article 3775.