Exercise-induced cardiac remodeling : a potential cause of pathological changes in the equine heart?

Abstract: Cardiac remodeling is a response to exercise that has been reported in a number of different species. Intensified training will lead to an increasing demand on the cardiovascular capacity, because of the requirements of enhanced oxygen delivery, metabolism and thermoregulation. An increased cardiac output is therefore needed, but it will only be able to change through an increased stroke volume as the maximal heart rate stays the same. An increased heart size is therefore the only way the animal can improve its cardiac capacity. Cardiac murmurs and valvular regurgitations may develop along with the enlargement of the heart. Whether these changes are physiological or pathological has been discussed. This study aims to investigate how the equine heart responds to exercise, if cardiac remodeling can induce pathological changes in the heart and if upper airway obstructions can contribute to these pathological alterations. An increased heart size can be seen after periods of intense exercise. This is caused by hypertrophy of the cardiomyocytes and, perhaps also, the formation of new cardiomyocytes from progenitor cells. The hypertrophy may lead to secondary pathological changes in terms of valvular regurgitations and arrhythmias. It seems like most valvular regurgitations occur due to leaking valves as the hypertrophy progresses. Arrhythmias can develop due to regurgitations and hypertrophy that effects areas important to the conducting system. Most arrhythmias, however, seem to be induced by imbalances in the autonomic nervous system, and may also occur as a result of exercise-induced changes in the heart through increased sensitivity to cholinergic stimulation. The most common cardiac causes of exercise intolerance in the horses seems to be mitral regurgitations and atrial fibrillation. Hypoxia associated with airway obstructions is a contributing factor to the cardiac remodeling as it causes a more excessive hypertrophy and potentially induces arrhythmias due to disturbances in the potassium homeostasis.