Sinus bradycardia is quite common in the athlete’s heart in view of the vagal hypertonia. Its severity could be directly proportional to the degree of training, although there is wide interindividual variability according to the achieved training level due to genetic influences. A slow heartbeat with rates around 40–45 bpm is considered normal in trained athletes, and in highly trained athletes, the heart rate could be as low as 35 bpm in physiological conditions. At rest or during sleep, pauses of up to 3 s can normally occur.

Changes in AV conduction are common in view of the increased parasympathetic and decreased sympathetic tones. First-degree AV block is present in approximately 35% of athletes, and Wenckebach second-degree (Mobitz 1) AV block is encountered in up to 10% of athletes. The above-described changes in AV conduction can often be reduced or eliminated by hyperventilation or physical exercise (an exercise stress test could be helpful to demonstrate this). If symptoms occur (dizziness, presyncope, or syncope), regardless of the existing ECG pattern or evidence of Mobitz 2 second-degree or third-degree AV block, they should be promptly investigated.

Signs of LVH (without other sings of ventricular overload) can be seen in up to 40–60% of the athletes.

The presence of additional minor ECG abnormalities (e.g., left atrial enlargement, left axis deviation, ST-T alterations or pathologic Q waves) can warrant further testing with an echocardiography.

Early repolarization pattern (ERP) is a common ECG variant. It is present in 1–5% of the general population and is very common in young athletes, with a prevalence rate of 25–40% (up to 50–80% in highly trained athletes, mostly in leads V2–V5). The ERP pattern is more frequent among young black adults, especially males. In black athletes, ST-segment elevation associated with T wave inversion in leads V1–V4 could be considered a normal variant. The ERP is characterized by an upward concave elevation ≥0.1 mV (up to 4 mm) of the J point in at least two contiguous leads, often with associated tall T waves. It is manifested by an apparent slowing of the inscription of the waveform at the end of the QRS that merges with the ST segment of the complex (“slurring”) or as an end-QRS notch that occurs on the downslope of an R wave (“notching”). It is due to hypervagotonia and bradycardia and is usually attenuated or vanishes in the presence of tachycardia. Moreover, the J- point/ST-segment elevation often disappears with detraining.

The prevalence of incomplete RBBB (QRS < 120 ms) is approximately 35–50% in athletes, compared to 5–10% in young healthy adults. This pattern is more common in endurance sports, which tend to increase right ventricular mass and volume. A fixed splitting of the second heart sound (S2) in the above situation warrants further echocardiographic evaluation in order to rule out a possible atrial septal defect (ASD) or partial pulmonary anomalous venous return (PPAVR). An ECG pattern with a T wave inversion that extends out to V4 in patients aged >12 years could be explicative of cardiomyopathy as ARVC or HCM. A “nonclassic” morphology of RBBB warrants the use of V1 and V2 leads recorded in the second and third intercostal spaces to rule out a Brugada pattern.

A T wave inversion >1 mm in at least two contiguous leads is not rare: it can be found in approximately 2–3% of a young healthy population. Nevertheless, its presence in leads other than III, aVR, and V1 may reflect an underlying ischemic heart disease, volume or pressure overload (aortic valve disease, systemic hypertension, congenital heart disease), or a cardiomyopathy (especially HCM and ARVC) and thus should prompt further diagnostic evaluation (echocardiography, ECG Holter, or, if necessary, MRI). Inverted T waves in young athletes may represent the first and only sign of an underlying cardiomyopathy, in the absence of any other features and before structural changes in the heart can be detected on echocardiography. There are HCM-related mutations in which the ECG changes precede the echocardiographic phenotype; on the other hand, there are cardiomyopathy and CHD that can be overlooked from a not careful echocardiographic evaluation (i.e., apical cardiomyopathy, ACAOS, or other coronary anomalies).

An ST–segment depression > 0.5 mm in two or more leads is rare and is normally associated with a T wave inversion (overload/strain).

The Q waves are defined pathological if their depth exceeds 25% of the depth of the associated R wave or their duration is >40 ms in two contiguous leads (except D3 and aVR). As a rule, pathological Q waves caused by hypertrophic cardiomyopathy are more than 3 mm deep and/or with a duration of >40 ms.

A right atrial enlargement is defined by a P wave amplitude >2.5 mm in any lead. Even taller T waves can often be seen in young people (up to 15%); they are less frequent after the age of 18–20 years (approximately 1%).