2.2.16 The pathophysiology of reduced exercise tolerance
2.2.16 The pathophysiology of reduced exercise tolerance

In horses, the most significant consideration in heart disease is the effect on exercise tolerance. Unless there is a sudden change in cardiac output, or decompensation of an equilibrium, exercise intolerance is usually the primary presenting sign in horses with heart disease. In addition, once exercise capacity is reduced, long-term changes occur which further reduce the athletic performance of the animal.

Exercise intolerance results from a reduction in the cardiac reserve which is present in normal animals to allow them to cope with increased demand. The reduction in reserve is largely a result of homeostatic mechanisms which mainblood pressure in the face of cardiac disease. The very nature of these compensatory homeostatic mechanisms results in vital organs being saved from reduced perfusion at the expense of less essential organs such as skeletal muscle which are relatively underperfused. There may be a reduced preload reserve because the venous tone is increased. This means that there is less scope for increasing cardiac output via the Frank-Starling mechanism and that exercise capacity will be limited. Animals with LV volume overload may develop abnorhigh pulmonary artery pressure during exercise, which may reduce the efficiency of gaseous exchange and even cause exercise-induced pulmonary haemorrhage. Alternatively, if cardiac output falls, gaseous exchange cannot take place efficiently, resulting in high blood carbon dioxide levels and low arterial oxygen. In addition to cardiac changes, there are changes in the systemic circulation in animals with significant heart disease. The blood supply to skeletal muscle is reduced at rest and the arterioles may be stiff, preventing the usual increase in blood supply to exercising muscle. In the long-term, the capillary supply to skeletal muscle becomes less extensive. These mechanisms result in decreased muscle efficiency.