Secondary to long-term exercise, cardiac adaptations occur. These are mostly physiological adaptations and are considered benign. However, in some cases the adaptation may have negative consequences, or may not only be benign. The normal physiological cardiac adaptation to long-term exercise is termed “athletes heart”, and includes both structural, electrical (autonomic) and functional adaptation. It is considered typical for a competitive athlete in endurance sports, to have sinus bardycardia, sinus arrythmia, AV-block I (or even AV-block II, Type 1), early repolarisation changes as well as QRS-signs of left ventricular hypertrophy (LVH) on standard 12-lead ECG. The structural adaptations, as readily shown by echocardiography, includes larger cardiac dimensions (walls and cavities). The level of adaptation will depend on the age, gender, ethnicity and body size of the athlete, as well as on the type of sport, duration of the sporting career and on external factors such as doping and drugs. Importantly, the adaptation of the athletes heart is associated with improved systolic and/or diastolic function, and is thus considered to be “good”. However, it has been suggested, by Heidbuchel and others, that the adaptation to long-term intensive endurance activity, in some cases may have a negative effect on the right ventricle (RV). Indeed, the RV is submitted to a disproportionate hemodynamic load, compared to the LV, during intense activity. This may lead to transient exercise-induced RV dysfunction and to chronic RV remodelling. Remodelling includes fibrosis and could in turn, lead to increased risk of ventricular arrhythmias. Importantly, a standard resting-echocardiography, focusing on the LV, will miss these changes. The RV function is most important, and may possibly be best evaluated during exercise, by either cardiac MRI and/or echocardiography. Furthermore, physiological adaptation to exercise may be dangerous, when it is added to an existing underlying disease. For example, in patients with hypertrophic cardiomyopathy (HCM) the degree of hypertrophy is a prognostic marker, and is associated with increased risk of malignant arrhythmias and sudden cardiac death (SCD). We know, that medications (beta-blockade) may reduce the level of hypertrophy in HCM, showing that it is possible to influence. Conversely, although the majority of hypertrophy in HCM, is genetically determined, it may be aggravated by the adaptation secondary to sporting activity. When the diagnosis of HCM is made, sporting eligibility is restricted, to reduce the risk of SCD. Another example, is aortic insufficiency (AI), where sporting eligibility applies for all sports, in athletes with mild-moderate AI’s with normal LV size and function and without arrhythmias. However, bradykardia in “athletes heart” may result in increased regurgitation by lengthening the diastolic duration, as may cardiac dilatation secondary to exercise. Finally, physiological adaptation to exercise is associated with an increased risk of atrial fibrillation (AF). An overweight, physically inactive patient with hypertension do have a high risk of accompanying AF, much more so than a lean, regularly active individual. However, long-lasting endurance activity, is associated with an increased risk of AF, and at a younger age, than non-athletes. This is attributed to the increase in atrial dimensions as well as the autonomic changes associated with athletes heart. Many athletes with AF, have a low cardiovascular risk profile, but anticoagulation should be considered when necessary, to reduce the risk of cardiovascular complications, such as stroke.