slow heartbeat in athletes is not so funny
Changes in the ‘funny channel’ of heart’s pacemaker may be behind sinus bradycardia
by Bethany Brookshire
May 21, 2014
“Yeah, I brought my heart rate down from 80 to 45 beats per minute resting….” The boasting drawl came from behind me as I waited in the starting corral of the Rock and Roll Marathon in Raleigh, N.C. It may seem like an odd comment to those not in endurance sports, but for distance runners, cyclists, swimmers and triathletes, a sluggish resting heart rate can be a matter of pride.
No one knew exactly what causes athletes to have this slow heartbeat, a condition called sinus bradycardia. Now, a study by cardiac physiologist Alicia D’Souza and colleagues from the University of Manchester in England finds the answer in certain “funny channels” in the sinoatrial node, the pacemaker for the heart. The slower heart rate isn’t as funny — it has fewer funny channels to transmit current that controls the activity of the heart cells. The results suggest a mechanism for sinus bradycardia in athletes, and also might help scientists understand why athletes can have heart problems later in life.
The study started close to home. “I had a Ph.D. student, Will Morris,” says Mark Boyett, a cardiac physiologist and lead author of the study. “He’s a cardiologist and he’s also a very keen cyclist. He was telling me that his heart rate when he is race-fit is 42 beats per minute!” A normal heart beats at around 70 beats per minute at rest. A professional athlete in top condition will cut that number in half.
Many amateur athletes wear their reduced heart rates as a competitive badge of honor, proof that they are really fit. Unfortunately, sinus bradycardia is not always an effect worth boasting about. Lifelong athletes with low heart rates need pacemakers later in life much more often than the general population. D’Souza and Boyett became interested in how sinus bradycardia occurs.
The sinoatrial node, or SAN, is a small group of cells in the right atrium of the heart. It sets the pace for heart contraction, spreading electrical signals through the rest of the muscle. The SAN is controlled both from electrical channels within the node and by the vagus nerve, which relays signals from the brain. When D’Souza and Boyett started to examine sinus bradycardia in athletes, most scientists assumed that it was causes by changes in the signals coming from the vagus nerve.
But it wasn’t quite so simple. “We looked into it but it was a case of the emperor’s new clothes. We found no evidence that the vagus nerve was causing sinus bradycardia,” Boyett says. So the researchers set up an experiment. They took mice and rats and made athletes out of them, training the rats to run long distance for 12 weeks and the mice to become swimmers for four weeks. The fit rodents all displayed sinus bradycardia, with much slower heart rates compared with their couch-potato counterparts.
The authors focused on the ion channels that control electrical current in the sinoatrial node. They noticed decreases in a particular ion channel called HCN4, one of four known “funny channels.” Discovered by coauthor and cardiac electrophysiologist Dario DiFrancesco at the University of Milan in Italy, funny channels are key pacemakers that help to determine heart rate. “It is now widely accepted that the HCN4 channel is a marker of pacemaker tissue and controls pacemaking and cardiac rate in a variety of conditions,” DiFrancesco explains. “Whenever changes of cardiac rate are involved, it is natural to think that HCN4 channels may be involved.”
The results, published May 13 in Nature Communications, show that endurance training remodels the heart and reduces resting heart rate by altering the number of funny channels. In the rodents, these changes reversed when the animals were allowed to fall off the exercise wagon.
The findings suggest that “the sinus node has an intrinsic ability to react against the chronically increased heart rate” associated with endurance training, says cardiac physiologist Elizabetta Cerbai of the University of Florence, Italy. The study, she says, has uncovered one of the ways in which the changeable heart can modify itself. Cerbai also notes that long-term sinus node sickness is not limited to athletes. The mechanisms uncovered in this study could also benefit the studies of other heart problems such as heart failure.
Matteo Mangoni, a molecular physiologist at the University of Montpellier in France, found the study to be innovative, and is curious to see what would happen with even longer training regimens. While the rodents did undergo some impressive endurance training, it couldn’t equal the years and years of training that most endurance athletes put in. “It will be important to understand if this same mechanism that appears to be operant in moderately trained mice is also responsible for severe bradycardia and atrial rhythm disease sometimes observed in endurance sportsmen,” he says.
D’Souza agrees that their next step is to look at sinus bradycardia after longer training and in older animals. “It’s speculation at this point,” she explains. “Our data is in response to very short-term training, so we have to be cautious in interpreting our results.”
Boyett points out that the bradycardia was reversible in their young, fit animals, as it is in young athletes when they take time off from training. “But in older athletes it may not be reversible.” So for now, he says, the main message is “everything in moderation.”