The Equine Heart - how it works to power a racehorse

By Robert Keck

Exciting new advances in ultrasound image technology have provided a better understanding of both the anatomy and function of the heart at rest and during exercise. In the last 30 years many veterinary clinics and universities with equine departments that study equine physiology are able to study the heart of the equine athlete in their own sports performance laboratories, while exercising on a high-speed treadmill.

Considering that heart rate is one of the most frequently measured physiological variables in exercise tests, Thoroughbred racehorse trainers have largely failed to take advantage of the heart rate monitor as standard equipment. However, heart rate monitors are commonplace in eventing and sport horses. Understanding the heart’s function, and its response and adaptation to training, can provide trainers with a competitive edge.


The heart of a Thoroughbred weighs about 1% of the horse’s bodyweight but can be as high as 1.3-1.4% in elite animals. Therefore an average 1000 pound horse has a heart weighing between 8-10 pounds. The horse has a proportionately larger heart per unit of body mass as compared to other mammals. The horse’s heart rate is 20-30 beats per minute at rest and may have a maximal heart rate of 240 beats per minute during maximal exercise. The fact that the horse is able to increase heart rate by nearly 10 times the resting heart rate is a contributing factor to their athletic superiority.

As in all mammals, the heart consists of four chambers with valves that open and close as the heart muscle relaxes and contracts to insure blood flows in the right direction. The two pumping chambers are the left and right ventricles, and the two receiving chambers are the left and right atria. The left ventricle is larger than the right ventricle.

Specialized cells within the heart conduct electrical activity that coordinates the muscles of the heart to contract in order to optimize blood pumping. Electrical impulses of both the atria and ventricles are isolated by a fibrous ring; preventing them from contracting simultaneously. The only point at which electrical activity can pass between the atria and the ventricles is via the Purkinje fibers found in the wall between the left and right ventricle. When the atria contract, blood is delivered to the larger volume ventricle that lies beneath. The right side of the heart receives unoxygenated blood from the body and pumps it to the lungs to allow the red blood cells to uptake oxygen. Oxygenated blood returns to the left side of the heart, and the left ventricle pumps it out the aorta to the rest of the body.
The cardiac cycle consists of a contraction/ejection phase (systole), and a relaxation/filling phase (diastole). Stroke volume (SV) is the volume of blood pumped in each beat, and is influenced by the muscular contraction of the ventricles, their resistance to flow during systolic ejection, and their ability to fill during the diastolic relaxation. The structural integrity of various anatomic components of the heart such as the valves and septa between the chambers affect heart function.

Stroke volume in a 500 kg Thoroughbred is approximately 1.3 litres and can increase by 20-50% during exercise. Cardiac output (CO) is stroke volume (SV) multiplied by heart rate (HR); therefore CO = SV x HR. At rest the cardiac output is approximately 6.6 (25 litres) gallons per minute and increases to an amazing 79 (300 litres) gallons per minute in elite athletes during exercise.

A horse’s total blood volume is approximately 10 gallons, representing 10% of its body weight. At rest 35% of the horse’s blood volume is red blood cells, however they can amazingly increase their red blood cell count on demand to 65% of their blood volume during a race, with up to 50% of the total red blood cells stored in the spleen. The horse has a proportionally larger spleen per unit of body mass as compared to other mammals. The red blood cells are void of a nucleus and have the large protein haemoglobin that transports oxygen. The horse’s heart is able to handle the increased viscosity of the blood. During exercise blood is diverted away from internal organs such as the intestines and kidney to working muscles used in motion.


The heart is a major determinant in VO2 max, a measure of aerobic capacity. VO2 max is the maximal rate of oxygen consumption that can be consumed by the horse. VO2 max is determined by cardiac output (stroke volume x heart rate), lung capacity, and the ability of muscle cells to extract oxygen from the blood. During exercise the oxygen requirement by muscles can increase to 35 times their resting rate. Sydney University studies have shown that training can increase a Thoroughbred’s VO2 max by 20% or more, with this improvement highly attributable to the heart’s pumping capacity.

VO2 max expressed as millilitres of O2 per kilogram of bodyweight per minute (or second). At rest the horse absorbs 3 millilitres of oxygen per kilogram of body weight per minute. Maximal rates of oxygen intake vary within breeds and training state, but fit Thoroughbreds have a VO2 max of 160-170 ml./min./kg and elite horses can achieve 200 ml./min./kg. By comparison elite human athletes have a VO2 max of about half or 85 ml./min./kg. Pronghorn antelopes have a VO2 max of 210-310 ml./min./kg.
VO2 max is a high indicator of athletic potential, and has been found to be highly correlated with race times in Thoroughbred horses. A horse with a higher VO2 max had faster times (Harkening et al, 1993). The ability of the horse’s muscle mass to consume oxygen far exceeds the ability of the heart and lungs to provide oxygenated blood. Therefore cardiac output is a limiting factor in performance. Conditions that improve cardiac output positively impact VO2 max.


The heart has two initial responses to exercise, a rise in blood volume pumped and dilation of the blood vessels. The heart rate increases, and beats stronger. The stroke volume may increase from 20-50% above resting rates. Through training the heart becomes more efficient at delivering oxygenated blood to exercising muscles.

Heart mass has been shown to increase with training. This hypertrophy (enlargement) in the heart comes in two ways, a thickening of the heart walls, and an increase in the size of the chambers, especially the left ventricle. Although the effects of training on the heart are not clearly understood, heart mass has been shown to increase up to 33% in 2-year old horses after only 18 weeks of conventional race training (Young, 1999). The increase in heart size results in increased cardiac output. Stroke volume has been shown to increase by 10% in as little as 10 weeks of training (Thomas et al, 1983).

Although not yet proved, it is likely that in addition to the strengthening, improved filling capacity of the pumping chambers when the heart is relaxed may contribute to the increases shown in stroke volume. Interestingly, maximal heart rate does not increase with training, and resting heart rates (unlike humans) do not decrease with training.

Training can improve VO2 max from 10-20% in the first 6-8 weeks of training, after which further improvement is limited. The relationship between VO2 max and velocity is highly correlated, but the differences found in speed and performance of two Thoroughbreds with equal VO2 max can be explained by differences in biomechanics and economy of locomotion.

Although the heart plays an important role in determining several physiological factors related to performance, it is merely one variable in the whole physiological equation that describes the equine athlete. Not only does the heart change and adapt with the rigors of training, but a myriad number of adaptations take place in the muscle fibers at the cellular level. As a result of training, oxidative enzymes in the muscles increase, along with the size and density ofmitochondria, the powerhouse of the cell. Enhanced oxidative capacity results in increased utilization of fat and less reliance on blood glucose and muscle glycogen, being an advantage at both submaximal and maximal exercise, because fat is a more efficient energy fuel.

An improved network in the number and density of capillaries provides more efficient blood flow and transit time to working muscles, which also become more efficient in buffering lactate in anaerobic exercise. Muscle, bone, tendons and ligaments modify their structure with the stresses of training. Depending on the event, the horse develops “metabolic specificity” and neuromuscular coordination for his chosen discipline.


When evaluating the equine heart, ultrasound has become an extremely valuable non-invasive tool, revolutionizing equine cardiology. The heart’s anatomical structure and physiology can be readily determined as well as measurements in heart size, wall thickness, and identifying defective cardiac valve function. Findings can determine pathology of the heart and the cause of poor performance. The ultrasound examination of the heart (echocardiogram) is now considered an integral part of cardiovascular evaluation of equine athletes.

An ultrasound machine works by emitting a beam of high frequency sound waves (>20,000 Hz) from an ultrasound transducer into the body tissues. In general, the waves can penetrate to a maximum of 15 inches (40 cm) and they interact with various tissue types in different ways. The waves can be scattered, refracted or attenuated. The reflected waves are transmitted back to the ultrasound transducer. This information is interpreted by the ultrasound machine which produces a two-dimensional black and white image called a sonogram.

The frequency of the ultrasound waves emitted by the transducer markedly influences the quality of the image, depending on the depth of the tissues. Higher frequency ultrasound waves have a shorter wavelength and yield better resolution of small structures close to the skin surface. However, more energy is absorbed and scattered with high frequency, therefore high frequency transducers have less penetrating ability. Conversely, a lower frequency transducer will have greater depth of penetration but poor resolution. The transducer selected for echocardiography should be the highest frequency available that will penetrate to the depths needed to image the heart in its entirety. Frequencies generally used for veterinary echocardiography range from 2.25-3.5 Mhz for adult horses.

The three main types of ultrasounds available to veterinarians and researchers are the M-Mode, Two-Dimensional (2-D), and Doppler. Although M-Mode yields only a one-dimensional (“ice pick”) view of the cardiac structures, it can yield cleaner images of cardiac borders, allowing the researcher to obtain very accurate measurements of cardiac dimensions and critically evaluate cardiac motion over time. Two-dimensional echocardiography allows a plane of tissue, with depth and width, to be imaged in real time. This makes it easier to appreciate the anatomic relationships between various structures. 2-D echocardiography makes available an infinite number of imaging planes of the heart. Doppler echocardiography records blood flow within the cardiovascular system when blood moving toward or away from the transducer causes a Doppler shift. From this shift, it is possible to calculate the velocity of the moving blood.


An ECG (electrocardiogram) is another tool commonly used in evaluating the heart. It measures the heart’s electrical conductivity can identify a part that is not contracting properly. It is the tool of choice for diagnosing arrhythmias. The ECG provides information to the researcher about the quality and rhythm of the heartbeat. The appearance of the ECG changes dramatically from rest to exercise.

Cardiac contractions are the result of a well-orchestrated electrical phenomenon called depolarization. In the myocardium are specialized fibers that are very conductive and allow rapid transmission of electrical impulses across the muscle, telling them to contract. There is uniformity in the sequence and force of both the filling and ejecting chambers, relying on a single impulse initiated by the sinoatrial (S/A or sinus) node. Another node is the A/V node (atrioventricular node) situated between the two chambers.

The ECG measures electrical activity from the P-Wave, QRS, and T-Wave. The P-Wave represents the electrical impulse measured across the atria, whereas the T-Wave measures the repolarization of the ventricles. The QRS represents the electrical impulse as it travels across the ventricles. Measurements between these impulses include the PR and ST segments and the PR and OT intervals, all of which can reveal abnormal heart function.

Electrodes are placed in strategic positions on the skin surface to pick up the heart’s electrical activity. In clinical practice, 12 leads may be used in a diagnostic ECG, but usually there are three standard leads, I, II and III, placed at different areas around the ribcage and chest. Placement of the electrodes are critical, and can change the size and shape of the ECG.


Vascular diseases in horses, such as atherosclerosis, which contributes to strokes and heart attacks, are rare. Two of the most common heart abnormalities are heart murmurs and arrhythmias. 
A heart murmur is the sound of turbulent blood flow, usually caused by an abrupt increase in flow velocity. This turbulence is caused by increased velocity due to a leak or obstruction in one of the heart valves or because of abnormal communication between different parts of the heart. Heart murmurs, which are fairly common, occur in horses of all ages. They are called “innocent” when they are soft, short and variable without any other cardiac pathology. One study detected cardiac murmurs in 81% of 846 Thoroughbred racehorses (Kriz, Hodgson, and Rose 2000).
Congenital heart defects are abnormalities that are present at birth, the most common being ventricular septal defect (VSD) where a hole is found between the two ventricles.

Oxygen-rich blood from the higher pressure left ventricle passes through to the lower pressure right ventricle and pulmonary artery during ventricular systole. Because some blood bypasses the lungs, it is not fully oxygenated and will have an adverse effect on cardiac function. Depending on the size of the hole, the horse may be fully capable of moderate activities without fatigue or shortness of breath. VSD is usually detected on the right side of the chest over the cranial part of the heart, and can be fully diagnosed with 2-D ultrasound and Doppler echocardiography.

Atrial fibrillation is an electrical disorder of the heart rhythm, also know as an arrhythmia. Associated with diminished performance, the normally regular, organized atrial waves become irregular, disorganized and chaotic, and the atria fail to contract normally, leading to an unpredictable and irregular heartbeat. Accurate diagnosis using an electrocardiogram can determine type and severity, and often an oral or injectable drug such as quinidine can be administered to establish a normal rhythm. An arrhythmia can sometimes be caused by myocarditis, where part of the heart muscle tissue has died due to an infectious disease such as strangles, influenza or an internal abscess. Toxic damage to the heart muscle may occur from a severe deficiency of vitamin E or selenium.

The most commonly recognized acquired structural heart disorders are degenerative valvular deformities. These defects, involving a thickening and deformity of the valve leaflets, cause inefficiency of one or more heart valves, resulting in dilation of the chambers trying to handle the regurgitated blood on either side of the damaged valve. If the leak is severe enough, the pressure in the veins leading to the affected side of the heart increases until fluid accumulation (edema) occurs.


For centuries, owners, breeders and trainers have been captivated by the idea that the horse’s heart may be the proverbial “Holy Grail” to understanding athletic performance, and predicting the future elite racehorse.

The large hearts found in elite human athletes are well-documented. In the 1920’s the “Flying Finn” Paavo Nurmi, who won 12 Olympic medals in track including 9 Golds and set world records from 1500 meters to 20 kilometers, had a heart three times larger than normal (Costill). At postmortem, the legendary 7-time Boston Marathon winner Clarence De Mar was shown to have an enlarged heart and massive coronary arteries (Costill).

In 1989, it was believed that Secretariat, American Triple Crown winner of 1973, had a heart weighing over 10 kg (22 lbs.), and may have had a VO2 max of 240 ml./kg./min. Autopsies showed that the great Australian racehorse Phar Lap had a heart weighing 6.4 kg. (14.1 lbs), 20% larger than normal, and Key to the Mint, American champion 3-year old of 1972 and excellent broodmare sire, had a heart weighing 7.2 kg (15.8 lbs). Secretariat’s rival and runner-up Sham had one of the heaviest hearts recorded, weighing in at 18 lbs. (8.2 kg).

Some of the first studies that scientifically attempted to correlate heart size with race performance were conducted in the 1950’s and early 60’s. The Heart Score concept was first discovered and developed by Dr. James D. Steel, a professor of veterinary medicine at the University of Sydney in Australia in 1953. Using ECG (electrocardiography) to studying herbivores, he began studying the occurrence of heart disease in racehorses. His examinations led him to the development of the “Heart Score” which was his term to describe the correlation between the QRS (intraventricular conduction time) complexes and the performances of several elite versus average racehorses at the time. He believed that the higher heart score number based on the QRS duration using the standard bipolar leads must be correlated with the larger heart size and weight found in superior racehorses.

Steel developed a ranking system that placed male horses with a heart score of 120 or more (116 or more for fillies and mares) in the large heart category, between 103-120 in the medium to normal category, and 103 or less in the small heart category. His conclusion was based on the assumption that the QRS represents the time required for the electric wave to spread and depolarize the ventricular mass. He believed that the QRS interval corresponds to the beginning and end of ventricular depolarization. As the ventricular muscle mass increases, a longer time will be necessary for the ventricular depolarization to take place. Therefore, he believed the higher the heart score the larger the heart mass (and size) Unfortunately, Steel was wrong!

Steel’s conclusions seemed logical at a time when equine cardiology was in its infancy. But in the horse (and hoofed mammals) the depolarization process differs from that of small animals because of the very widespread distribution of the Purkinje network. These fibers extend throughout the myocardium and ventricular depolarization takes place from multiple sites. The electromotive forces therefore tend to cancel each other out; consequently, no wavefronts are formed, and the overall effect of the ventricular depolarization on the ECG is minimal. (Celia 1999) 
Today, we know that ECGs provide little or no information about the relative or absolute sizes of the ventricles. An ECG cannot measure heart size and cannot be used to correlate its size and / or mass. In several studies, heart score showed a relationship neither with body weight nor with ventricular mass, as determined by echocardiograph. Heart score did not correlate with heart size and cannot be regarded as an index for predicting potential performance (Lightowler et al 2004). Although a study using Danish Standardbreds showed a correlation between heart score and Timeform ratings, using these scores to determine heart size has largely been disproved.


Current research in the field of equine exercise physiology continues to investigate the heart and cardiac output. The size of the heart is a key determinant of maximal stroke volume, cardiac output and therefore aerobic capacity, and several new studies have proved this relationship.

A recent breakthrough study demonstrated a significant linear relationship between British Horseracing Board Official rating or Timeform rating and heart size measured by echocardiography in 200 horses engaged in National Hunt racing (over jumps)  (Young and Wood, 2001). It is the first study that positively correlates heart size to performance.

Additionally, a significant strong relationship has been found between left ventricular mass (and other measurements of cardiac size) and VO2 max in Thoroughbred racehorses exercising on a high-speed treadmill. (Young et al 2002).

Interestingly, no such relationships have been reliably been found when horses employed in flat racing were examined, suggesting that, as might be expected, VO2 max and heart size are more important predictors of performance for equine athletes running longer distances.
It must be emphasized that these research studies were conducted on older racehorses that were already racing and training, very different from an untrained yearling.


Understanding the equine heart and its role in equine physiology will remain of great interest to breeders, owners and trainers. Future use of heart rate monitors and heart evaluations using ultrasound technology to identify heart pathology and abnormality will undoubtedly contribute to future breakthroughs in training and racing. The equine heart still remains just one variable in the elusive equation that makes for a great racehorse.