CHAPTER 42 The Effects of Training on Echocardiographic Measurements
The heart has a unique capacity for adapting to altered loading conditions. In the face of increased physical demands, the heart increases the volume of blood pumped by increasing stroke volume and heart rate. For short-term needs, the heart can cope with the greater volume or pressure loads. However, when the overload is sustained over time, such as during exercise, left ventricular (LV) hypertrophy (i.e., an increase in LV muscle mass) develops. Left ventricular hypertrophy is a physiologic phenomenon described in human and equine athletes as “athlete’s heart.” Pathologic LV hypertrophy can be induced by chronic hypertension and cardiac valvular disease and the ensuing pressure overload. Pathologic LV hypertrophy is distinguished from physiologic cardiac hypertrophy by the lability of the latter, with regression of hypertrophy after overload is removed. The increased LV wall thickness in elite athletes and racehorses regresses after deconditioning, whereas ventricular wall thickness in individuals with pathologic LV hypertrophy does not regress.
Cardiac hypertrophy secondary to exercise was first described in humans and animals more than a century ago. Recently, echocardiographic studies in racehorses revealed that the heart of racehorses undergoes hypertrophy and, together with anecdotal reports of record-breaking racehorses having extraordinarily large hearts at postmortem examination, this information has supported the concept that heart size and athletic performance are related. Information about cardiac size and morphology in a horse would ideally enable breeders, buyers, and trainers to predict and select the most talented horses if the theory of correlation between cardiac size and performance holds in practice. During recent years, echocardiographic studies in both Thoroughbreds and Standardbred trotters have supported the correlation between heart size and racing success, particularly in horses racing over longer distances. Studies in 3-day-event, endurance, and show jumping horses are sparse.
The effect of physical training on the human heart has demonstrated two morphologic forms of myocardial response to training: an endurance-trained heart and a strength-trained heart, each of which will be described briefly.
Athletes in endurance training (e.g., long- or middle-distance running or cycling) experience long periods of relatively low-intensity exercise with prolonged elevations in cardiac output and heart rate and a proportionately smaller increase in blood pressure. These changes increase venous filling pressure (preload) and diastolic loading of the heart. According to the Law of Laplace, these changes result in increased LV internal diameter with a proportionate increase in wall thickness until stress is returned to normal. Therefore, endurance-trained athletes are presumed to have eccentric LV hypertrophy characterized by an unchanged relationship between LV wall thickness and LV internal diameter.
In contrast, athletes involved primarily in strength exercise (e.g., weightlifting or sprinting) have short bursts of high-intensity exercise and small increases in cardiac output but great increases in blood pressure. The high systemic blood pressure increases arterial pressure (afterload) and hence the pressure that must be overcome by the myocardium. These athletes develop predominantly increased LV wall thickness with unchanged LV internal diameter. Thus, strength-trained athletes are presumed to develop concentric LV hypertrophy, characterized by a higher wall thickness to internal LV diameter ratio.
In horses, endurance training is exemplified by long-distance training in trotters, National Hunt Thoroughbreds, and endurance horses, whereas strength training may be comparable to sprinting or interval training. Most forms of exercise and training programs fall somewhere between the two extremes, and most horses are probably trained both by interval training and long-distance training.
Athletic training influences function of the cardiac valves, and the prevalence of leaking cardiac valves (valvular regurgitation) is high in both human and equine athletes. When cardiac valves do not close sufficiently, blood flows backward in the cardiac chambers and is not available to working muscles or other vital organ systems. The grade of valvular regurgitation detected in racehorses is typically classified as small, and there is generally no progression in severity of regurgitation over time. These regurgitations often cannot be detected by auscultation but only by use of color Doppler echocardiography, which is a far more sensitive method. The increased prevalence of valvular regurgitation is seen in both human and equine athletes, and although the exact pathogenesis is unknown, it seems likely that altered loading conditions and morphologic and functional changes concurrent with cardiac hypertrophy are prerequisites for development of regurgitant valves.
Two-dimensional (2-D) and M-mode echocardiography are used for measuring the size of the heart and for quantification of functional measurements. For evaluation of valve function, color Doppler echocardiography is used in combination with 2-D echocardiography. Echocardiographic examination of the equine athlete may have numerous purposes. Estimation of LV size is performed in yearlings at sales to predict future racing performance. For horses in training, the effect of training on cardiac growth and adaptation to training can be examined by consecutive examinations over time. It has also been suggested that estimation of cardiac size in flat-racing Thoroughbreds may be helpful for selection of horses to be moved into National Hunt racing, where large heart size is correlated with racing performance. Finally, use of echocardiography for selection of breeding stock has been suggested, but the heritability of cardiac hypertrophy in horses has not been investigated, to our knowledge.
Echocardiographic measurement of heart size in performance horses necessitates greater standardization and consistency of technique than are required for clinical diagnosis. Because the LV mass is measured from the right side of the thorax, a high-quality ultrasound machine capable of imaging at tissue depths up to 30 cm is needed. Although obtaining a short-axis view of the LV from the left side of the thorax requires less penetration depth, use of this imaging window is not recommended because accurate definition of the border of the LV free wall is made difficult by near-field artifact. Fortunately, small portable digital machines with deep penetration are now commercially available. For detailed descriptions of the physics of echocardiography and recommended techniques, readers are referred to the Suggested Reading.
Echocardiographic examination of horses requires a quiet environment, a competent horse handler, and, ideally, a dark room. Shaving the skin and applying plenty of ultrasound coupling gel improves the quality of the images. Sedation of the horse should be avoided, but if it is not possible to keep the heart rate consistently below 40 to 45 beats/minute, romifidine HCl (0.04 mg/kg, administered intravenously [IV]) can be used and has only a minimal effect on the cardiac variables to be measured. The horse’s body weight must be accurately determined because there is a strong relationship between heart size and body weight. A weight tape can be used if a scale is not available.