as a competitive badge of honor, proof that they are really fit. Unfortunately,
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, 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,
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, or SAN,
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, is a small group of cells in the right atrium of the heart. It sets the pace ?for heart contraction,
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, 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,
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, 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,
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,” 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,
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, 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,
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, one of four known “funny channels.” Discovered by coauthor and cardiac electrophysiologist

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