Physical exercise is associated with haemodynamic changes and alters the loading conditions of the heart. In dynamic exercise the emphasis is on movement with no or minimal development of force. The main haemodynamic features are increases in heart rate and stroke volume, the two components of cardiac output. Systemic vascular resistance drops but the net result is a slight to moderate rise in blood pressure. The load on the heart is predominantly that of volume. In static exercise force is developed with no or minimal movement. The haemodynamic consequences involve a slight elevation of cardiac output, caused by the increase of heart rate, and a more pronounced rise of blood pressure, resulting in a pressure load on the heart. From a theoretical point of view the haemodynamic alterations and the ventricular loading conditions during exercise could, in the long run, lead to left ventricular hypertrophy (LVH). Volume load would lead to enlargement of the left ventricular internal diameter and a proportional increase of wall thickness; this type of adaptation is termed eccentric LVH. The pressure load would induce thickening of the ventricular wall with unchanged internal dimension, or concentric LVH. It was suggested that these cardiac adaptations serve to normalise wall stress.