A 24-year-old male rower was referred to the cardiologist office for palpitations. He described palpitations that occurred after exercise and denied any lightheadedness or syncope. Echocardiogram was performed, which showed a dilated left ventricle, dilated left atrium, mild concentric left ventricular hypertrophy, and normal left ventricular function. In endurance athletes, cardiac remodeling may occur; distinguishing exercise-induced cardiac adaptations from pathology is important.
Athletic heart syndrome encompasses a variety of significant physiological and morphological changes that occur in a human heart after repetitive strenuous physical exercise. Physical exercise is dependent on the cardiovascular system’s ability to provide oxygenated blood to the critical organs, removing deoxygenated blood from tissues, as well as the lungs’ ability to clear carbon dioxide (CO2). With exercise a greater proportion of the oxygen (O2) is extracted from the blood.
Cardiopulmonary stress testing can be used to assess the athletic performance of an athlete. Gas exchange during rest and exercise can be analyzed. Myocardial oxygen demand is directly related to exercise intensity. The increasing oxygen demands cause an increase in pulmonary oxygen uptake (VO2). Physiological changes that occur with training include lowered blood pressure and heart rate, enhanced contraction and relaxation of both ventricles, as well as an increase in the VO2 max. VO2 max is widely considered to be the gold standard metric for cardiovascular fitness.
Cardiac output is the product of stroke volume and heart rate and may increase 5- to 6-fold during maximal exercise. Heart rate increase accounts for a majority of the augmentation in cardiac output with exercise and may range from 40 bpm at rest to ≥200 bpm in a young maximally exercising athlete.1 Hemodynamic conditions, specifically changes in cardiac output and peripheral vascular resistance (PVR), vary widely across sporting disciplines.
Structural adaptions of the heart with exercise include increases in heart cavity dimensions, augmentation of cardiac output, and increases in heart muscle mass. Although some overlap exists, exercise activity can be segregated into 2 forms with defining hemodynamic differences.
Isotonic exercise (endurance training) involves sustained elevations in cardiac output with normal or reduced PVR. This hemodynamic effect causes a volume challenge for the heart that affects all 4 chambers. Cardiac adaptations seen with daily sustained exercise include an increase in left ventricular (LV) mass, LV chamber dilation, enhanced LV diastolic function, biatrial enlargement, and right ventricular (RV) dilation with increased systolic and diastolic function. Examples of isotonic sports are long-distance running and swimming.
Isometric exercise (strength training) is characterized by increased PVR and normal or only slightly elevated cardiac output. This increase in PVR causes a pressure load on the ventricle with a transient but potentially marked systolic hypertension and LV afterload. Concentric left ventricular hypertrophy (LVH) and reduction in LV diastolic function occur ...