Athletic Bradycardia
Endurance athletes often have a resting pulse in the 40s, and a few dip to 30 or below. In a trained person with no symptoms that is a normal effect of training, not a disease. But why athletes' hearts slow is still argued over, and in registry data, men who had raced a 90-km ski marathon needed slightly more pacemakers later in life, most of all those with the most races and fastest times.
A slow pulse with no symptoms needs nothing. A slow pulse with dizziness, fainting, or breathlessness or exhaustion on exertion out of proportion to your fitness needs checking, however much you train.
What it is
Bradycardia means a slow heart rate; sinus bradycardia means the slow rhythm still comes from the sinus node, the heart's own pacemaker. For most people a slow pulse is good news, and endurance athletes routinely sit in the 40s — well below the 60–100 "normal range" printed in textbooks, which describes a population rather than any one person. See Resting heart rate.
Where doctors draw the line
The international consensus criteria for reading athletes' electrocardiograms (ECGs, the standard heart tracing) treat sinus bradycardia above 30 beats per minute in a trained athlete without symptoms as a normal, training-related finding that needs no further tests. At or below 30 beats per minute, or with pauses of 3 seconds or longer between beats, doctors should assess how the heart rate responds to exercise.[1] This is a working definition agreed by experts, not the result of an outcome study.
How common very slow readings are
Uncommon, but not rare. On 24-hour heart monitoring of 465 mostly young elite endurance athletes (median age 23), about 4 in 10 dipped to 40 beats per minute or below at some point, 1 in 50 to 30 or below, and 3% had pauses of 3 seconds or more.[2]
Over five and a half years, slow rates and pauses were not linked to health problems. That reassurance is weakest exactly where it matters most, though: only seven athletes went to 30 or below and twelve had the long pauses, and the cohort was young.
Genes play a part as well as training. Athletes whose genetic profile predicted a lower heart rate were about twice as likely to be bradycardic.
Why athletes' hearts slow is still argued over
The traditional explanation is high vagal tone: a strong calming signal from the vagus nerve, the parasympathetic brake that heart rate variability tries to measure. The competing account, argued in a formal exchange of papers between physiologists, is that endurance training physically remodels the sinus node itself, turning down the ion channel that drives its pacemaker current.[3][4]
The difference matters. If the second account is even partly right, some of an athlete's slow heart rate is a lasting structural change rather than a fully reversible shift in nervous-system tone.
Ski marathons and pacemakers
Registry data are consistent with remodelling, though they cannot tell the two accounts apart. Among about 209,000 Swedish long-distance cross-country skiers compared with over half a million non-skiers, men had about 17% more pacemaker implants and about 19% more diagnoses of a slow heart rhythm.[5]
- More racing, more risk. The highest rates were in men who had finished the most races and posted the fastest times.
- A different reason for the pacemaker. A malfunctioning sinus node (sick sinus syndrome) was a more common reason for the pacemaker in skiers than in non-skiers.
- Women showed no excess.
- No extra deaths. Among skiers, death rates did not differ between those who had a pacemaker and those who did not.
An earlier study of the same 90-km race found that men with five or more finishes were about twice as likely to be admitted to hospital with a slow heart rhythm as men who had finished once.[6]
These are associations in registry data, not proof that the training caused the slow rhythms.
Training or disease: watch the response, not the number
The resting number does not tell a trained heart from a failing pacemaker; the response does. A trained heart speeds up normally when you exert yourself and causes no symptoms. A sinus node that is failing does not keep up, and the giveaways are dizziness, fainting, breathlessness or exhaustion on exertion out of proportion to your fitness. Those symptoms with a slow pulse warrant evaluation regardless of how much you train.
Drugs can also slow the heart. On a beta-blocker or another rate-slowing drug, a low resting rate reflects the dose rather than your training.
What to do
- No symptoms, slow pulse, normal exercise capacity: nothing to do. It is not a number to raise or to chase lower.
- A reading at or below 30, or pauses of 3 seconds or more on a tracing or monitor: the athlete criteria call for a check of how your heart rate responds to exercise.
- Dizziness, fainting, or breathlessness or exhaustion out of proportion to your fitness: get evaluated, whatever your training history.
Further reading
- Drezner JA, et al. International criteria for electrocardiographic interpretation in athletes: consensus statement. Br J Sports Med 2017.[7]
- D'Ambrosio P, et al. Bradycardia in Athletes: Prevalence, Mechanisms, and Risks. Circulation 2026.[8]
- Svedberg N, et al. Long-Term Incidence of Bradycardia and Pacemaker Implantations Among Cross-Country Skiers: A Cohort Study. Circulation 2024.[9]
- Andersen K, et al. Risk of arrhythmias in 52 755 long-distance cross-country skiers: a cohort study. Eur Heart J 2013.[10]
- D'Souza A, Sharma S, Boyett MR. CrossTalk opposing view: bradycardia in the trained athlete is attributable to a downregulation of a pacemaker channel in the sinus node. J Physiol 2015.[11]
- Coote JH, White MJ. CrossTalk proposal: bradycardia in the trained athlete is attributable to high vagal tone. J Physiol 2015.[12]