Slow Heart Rate in Athletes (Bradycardia): When It Is Normal and When It Is a Symptom

For years it was assumed that athletic bradycardia results solely from increased vagal tone. That is true only in part. The first mechanism is indeed autonomic: endurance training increases parasympathetic influence and reduces sympathetic influence at rest, which slows the sinus node. The second mechanism is intrinsic. In an experimental study published in Nature Communications, the slowing of heart rate after training persisted even after the autonomic nervous system was blocked and was linked to remodeling of ion channels in the sinus node itself, including reduced expression of the HCN4 channel (a study in mice, so it should not be transferred directly to humans).

The third element is the structure of the heart. Regular endurance exercise increases the volume of the heart chambers and the stroke volume (the amount of blood ejected with one beat). At the same cardiac output, fewer beats per minute are enough. That is why athletic bradycardia usually goes with larger chamber dimensions, a slightly thicker left ventricular wall and high aerobic fitness, not with weakened cardiac function. We write about measuring fitness in the entry on VO2max, and about how to train aerobically in the entry on zone 2 training.

The conclusions of this study are both reassuring and nuanced. First, a very low pulse and short pauses are not rare in this group but affect a considerable part of athletes, and over 5.5 years of follow-up they were not linked to a worse prognosis. Second, genetics also matters: people predisposed to a lower pulse more often have bradycardia, even after accounting for fitness. This means two athletes in similar shape can have different resting heart rates, and that is not automatically better or worse fitness.

Limitations must be remembered, though. The cohort consisted of young, mostly healthy elite athletes, and the follow-up lasted a little over five years. The results do not prove that a pulse of 38/min is safe in every recreational athlete, nor do they describe long-term consequences in old age. We return to this question in the next section.

This study broadens the picture: a slow pulse in athletes is generally benign, but in men with the greatest long-term endurance training load, symptomatic sinus node dysfunction requiring a pacemaker is observed slightly more often. The scale is moderate (a rise in risk of less than one fifth), and overall mortality in the athlete group was much lower than in the comparison group, which agrees with the many data on the benefits of regular activity. The authors interpret the results as suggesting that training-related bradycardia carries a higher risk of pacemaker implantation without a detrimental effect on the risk of death.

One thing follows for practice: there is no reason to give up training out of worry about a pacemaker, but it is worth paying attention to symptoms. If a long-time athlete develops new dizziness, a feeling of faintness, reduced exercise tolerance or fatigue out of proportion to training, that is a reason for cardiac assessment, not for explaining it away as 'athlete's heart'. As with resting heart rate in general, context and symptoms weigh more than the number itself.

Features suggesting physiological adaptation are: no symptoms, good exercise tolerance and high fitness, a normal rise in heart rate during exertion (the heart speeds up in proportion to the load), a pulse that rises after a few squats or a short walk, a history of years of endurance training, no family history of sudden death or heart disease, and an ECG consistent with criteria for athletes. In many people the resting pulse gradually rises after a break from training, which is an additional argument for its link to training; this test is sometimes used diagnostically, but the decision to use it is best left to the cardiologist.

Worrying features are: fainting or near-fainting (especially during exertion or without a clear reason), dizziness, new breathlessness, chest pain, palpitations, marked fatigue, a fall in fitness, a pulse below 40 in an untrained person, failure of the heart to speed up with exercise (chronotropic incompetence) and prolonged pauses. Conduction disturbances on the ECG matter too. First-degree atrioventricular block and second-degree block of the Mobitz I (Wenckebach) type occur in athletes and can be benign if not accompanied by symptoms. Mobitz II second-degree block and third-degree (complete) block, however, are not regarded as sports adaptation and require urgent investigation.

Not every bradycardia in a person who trains results from training. Common secondary causes include: hypothyroidism (we write about the thyroid in the entry on TSH and thyroid hormones), drugs (beta-blockers, some antiarrhythmics, verapamil, diltiazem, digoxin, clonidine, and also some psychiatric drugs and eye drops), electrolyte disturbances (especially too high potassium), undernutrition and energy deficiency in athletes (RED-S), anorexia nervosa, hypothermia, raised intracranial pressure, and sleep disorders such as sleep apnea, in which slowing of the nighttime pulse can be marked.

Add to this diseases of the heart's own conduction system: sinus node disease, atrioventricular block and, in younger people, congenital and hereditary conduction disorders. Less often a slow pulse is one manifestation of cardiomyopathy or myocarditis. So in an athlete with symptoms, an unusual ECG or a family history, it is worth doing a fuller cardiac assessment instead of assuming it is surely training.

A separate matter is the difference between the pulse at rest and the pulse on the watch. Optical sensors can be less accurate at very low values, and algorithms smooth over transient pauses. A watch may thus suggest a 'pulse of 33' that an ECG will not confirm, or miss short pauses. Treat the reading from a device as a prompt to talk to a doctor, not a diagnosis. We also write about the accuracy of watch measurements in the article on resting heart rate.

The basis is a resting ECG, which lets you assess rhythm, rate, intervals and conduction disturbances, and which in athletes should be interpreted by criteria for people who train, not by standard population norms. We describe it in the entry on the resting ECG. If symptoms occur in episodes, the key test is Holter ECG (24–48 hours or longer), which records the minimum pulse, pauses and blocks, exactly what may be invisible in a short examination. You will find information on the Holter in the entry on Holter ECG and ambulatory blood pressure monitoring.

An exercise test (described in the entry on the exercise ECG) shows whether the heart speeds up appropriately during exertion and whether conduction disturbances disappear at a higher heart rate (typical of vagal changes). Echocardiography assesses the structure and function of the heart, which helps distinguish an athlete's heart from cardiomyopathy; we describe the topic in the entry on echocardiography. Blood tests usually include TSH, blood count, electrolytes (including potassium and magnesium) and, as indicated, markers of cardiac injury. The indications for individual tests are set by a doctor, ideally a cardiologist or sports medicine physician.

It is also worth remembering sports screening. In competitive athletes, screening tests including the ECG are sometimes used before the season; the scope and frequency depend on the country, discipline and age. For an amateur athlete a reasonable approach is a resting ECG once, at the start of regular intensive training or after age 35, and thereafter if symptoms appear.

The second trap is attributing everything to the athlete's heart. A person who trains, whose heart slows markedly more than usual, who starts to feel dizzy or faints, should be examined and not reassured with the phrase 'that is normal in athletes'. What is normal in one healthy trained person may be a symptom of disease in another.

For most people who train, a slow resting pulse is good news: a sign that the heart works economically. The best safeguard, though, is not the number but attention to symptoms and periodic cardiac assessment, especially after age 35, with a family history or when the character of training changes. If your watch shows very low values, write them down, get an ECG and discuss the result with a doctor who knows the criteria for interpretation in athletes, instead of trusting only the device or only the belief that 'athletes just have that'.