Tachycardia in athletes: causes and the link with exercise load and pharmacology

In a trained person the heart at rest usually beats more slowly than in the average individual, so a fast pulse in an athlete is a signal worth decoding. The editorial team examines when tachycardia is a normal response to exertion, and when it hides dehydration, overtraining, stimulants or hormonal drugs, and why individual cases require a cardiac work-up.

What is considered tachycardia and why athletes have a different “norm”

In clinical practice, tachycardia refers to a heart rate above 100 beats per minute at rest. During physical exertion the pulse naturally rises, and this is not a disease but a normal reaction of the autonomic nervous system: the sympathetic nerves and adrenaline speed up the sinus node to supply the muscles with oxygen.

In people who systematically train for endurance, a so-called “athlete’s heart” develops. Stroke volume increases, parasympathetic (vagal) tone strengthens, and the resting pulse often drops to 40–60 beats per minute. International criteria for interpreting an athlete’s ECG regard sinus bradycardia as a training adaptation rather than a pathology.

That is why, for an athlete, even a resting pulse of 85–95 — which is not yet formally tachycardia — may be a deviation from their personal norm. A steady rise in the morning pulse of 7–10 beats above the usual level has long been used by coaches as an early marker of under-recovery, although this indicator is individual and has no rigid threshold.

A distinction is drawn between sinus tachycardia, when the rhythm is set by the normal pacemaker, and tachyarrhythmias — supraventricular, atrial fibrillation, ventricular. The first is mostly a reaction to an external cause, the second is a disturbance of the heart’s electrical system that requires an entirely different approach.

Tachycardia linked to exertion and recovery

The most common cause of a fast pulse in an athlete is obvious: intense work. However, after a workout ends the pulse should fall, and the speed of that decline (heart-rate recovery in the first minute) is considered an indicator of the state of autonomic regulation. Slow recovery that is not explained by heat or fatigue is worth noting.

Dehydration reduces the volume of circulating plasma. To maintain cardiac output with a smaller stroke volume, the heart contracts more frequently. This phenomenon is known as “cardiovascular drift”: during prolonged work in the heat the pulse gradually rises even at an unchanged pace. Loss of electrolytes, especially potassium and magnesium, further increases the excitability of the myocardium.

Overload and insufficient recovery are another common cause. In functional overreaching the resting pulse often rises while heart-rate variability falls. Yet in the late stages of overtraining syndrome the picture can be the opposite, so heart rate alone does not make a diagnosis.

Non-sporting factors should not be forgotten either: fever and infections, anaemia (including the iron-deficiency kind common among female runners), hyperthyroidism, sleep deprivation, anxiety, alcohol the night before. Training during an acute viral infection with fever and tachycardia is something sports cardiologists explicitly advise against because of the risk of myocarditis.

• Physiological causes:exertion, heat, altitude, emotional arousal before the start.
• Recovery states:dehydration, sleep deficit, functional overreaching.
• Medical causes:infections, anaemia, hyperthyroidism, electrolyte disturbances.
• Substances:caffeine, stimulants, beta-agonists, thyroid hormones, anabolic steroids.

Stimulants and “fat burners”

Sports pharmacology is a separate and often underestimated cause of tachycardia. Caffeine, in the doses used to improve performance, moderately raises sympathetic activity. On its own it rarely causes marked tachycardia in healthy people, but in pre-workout formulas it is often combined with other stimulants, and the cumulative effect becomes unpredictable.

Synephrine, yohimbine, ephedrine and similar substances stimulate adrenergic receptors and raise pulse and blood pressure. Ephedrine and a number of other stimulants are on WADA’s Prohibited List for the competition period, and some substances found in supplements (for example, DMAA) have been linked to serious cardiovascular events, which became grounds for regulatory bans.

Clenbuterol is a beta-2 agonist that in many countries is used only in veterinary medicine. In sport it is used illegally for “cutting”, and tachycardia and tremor are its most characteristic side effects. In poisoning cases described in the literature, marked tachycardia, hypokalaemia and myocardial ischaemia were observed. Clenbuterol is banned by WADA at all times.

Thyroid hormones (levothyroxine, liothyronine/T3) are used without medical indication as “fat burners”. An excess of thyroid hormone speeds up the sinus rhythm and increases the risk of atrial fibrillation — a well-known effect of thyrotoxicosis. The editorial team stresses: such drugs should be used only as prescribed by an endocrinologist.

Anabolic steroids, hormones and heart rhythm

Anabolic-androgenic steroids (AAS) rarely cause tachycardia directly, but they change the “soil” on which it arises. The Endocrine Society scientific statement on the consequences of doping describes left ventricular hypertrophy, impaired diastolic function, raised blood pressure and adverse lipid changes in AAS users.

A remodelled myocardium is more prone to arrhythmias. Cases of atrial fibrillation and ventricular arrhythmias in young steroid users have been described, and autopsy series of sudden death among them feature cardiomyopathies. The exact rates are unknown, because most studies are observational and cannot separate the effect of steroids from that of other drugs.

Erythrocytosis, which often accompanies the use of testosterone and its derivatives, increases blood viscosity and the load on the heart. Growth hormone and insulin, which also occur in “stacks”, affect water-salt balance and glucose levels; hypoglycaemia caused by insulin is accompanied by marked tachycardia and sweating and can be fatal.

Beta-2 agonists for the treatment of asthma (salbutamol, formoterol) deserve a separate mention. In therapeutic doses, permitted by WADA with restrictions, they can cause a moderate rise in pulse. Athletes with asthma should discuss their treatment regimen with a doctor rather than adjust it on their own.

True arrhythmias that masquerade as a “fast pulse”

Not every tachycardia is sinus. Paroxysmal supraventricular tachycardia begins and ends abruptly, “like a switch”, often at a rate of 150–250 beats per minute. Its cause is an accessory electrical pathway in the heart (as in Wolff–Parkinson–White syndrome) or features of the atrioventricular node. Such episodes can occur both at rest and during training.

Atrial fibrillation occurs more often in veteran endurance athletes than in their sedentary peers. The mechanisms are linked to enlargement of the atria, fibrosis and high vagal tone. The ESC sports cardiology guidelines treat this phenomenon separately and propose individual decisions about continuing training.

The most dangerous are ventricular tachycardias linked to hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, myocarditis or channelopathies. They underlie most cases of sudden cardiac death in young athletes. Fainting during exertion is a “red flag” that always requires investigation.

The practical conclusion: if a fast pulse appears suddenly, does not match the intensity of the work, and is accompanied by dizziness, chest pain, shortness of breath or fainting, this is not a matter of “tweaking supplements” but a reason for an ECG and a consultation with a cardiologist.

Editorial conclusions

In an athlete a fast pulse at rest is atypical, since training usually lowers heart rate. That is why even a moderate rise above the usual pulse is worth treating as information about recovery, hydration or state of health.

A large share of cases is explained by simple causes: dehydration, heat, sleep deprivation, infection or excessive caffeine. They can be removed by adjusting one’s routine.

At the same time, stimulants, clenbuterol, thyroid hormones and anabolic steroids are able both to speed up the pulse directly and to change the structure of the heart, creating the conditions for dangerous arrhythmias. Sudden attacks of a strong heartbeat and fainting require a cardiac work-up.

We also recommend reading our materials on the prevention and diagnosis of tachycardia, on arrhythmia after caffeine and on the effect of anabolic steroids on the cardiovascular system.

References

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