I have had the pleasure of working with many veterinary undergraduates in the last 40 years. One of my responsibilities has been to help students learn how to examine the cardiovascular system of the horse and cow and appropriately interpret their findings. My perspectives on the cardiovascular system are drawn from that experience, from my clinical work and research, and from an ever-growing fascination with how beautifully orchestrated the cardiovascular response to exercise really is. What follows is an attempt to overview heart rate and rhythm in the horse at rest and exercise.

Physical Examination - The ‘Unstable’ Heart

When you first start examining patients as a veterinary undergraduate, you are very keen to (gently) poke and prod every animal you come across, and you are an absolute sponge for new information. Realising you are able to interrogate cardiovascular function by palpating the peripheral pulse is very empowering! And once you find a pulse on a healthy cow, you simply hang on and count, and the pulse waves come to you in a more or less steady stream, 60-80 times a minute. You can confidently anticipate when the next one is going to arrive.

Then you examine a horse, a horse, perhaps, in its late teens - quiet, cooperative, neutral about seeing you and not in the least concerned (she has seen it all before - she’s been dealing with veterinary students for 12 years). You palpate the pulse and suddenly all of your confidence disappears. One minute you have the artery, the next you don’t, one minute the pulse wave is very strong, and then it disappears - and you’re sure you didn’t move your fingers. The book says the rate should be 28-40, but in this horse, well, sometimes it’s 40 and sometimes it’s 12! So you decide to listen to the heart with your brand-new stethoscope - and that doesn’t help one bit! It was much easier to feel the pulse on the three-year-old standing next door - this old mare must surely be ill?

Generations of veterinary students have gone through this. Supposedly healthy horses whose hearts do not beat regularly, horses whose hearts take frequent breaks, who beat much more slowly, and sometimes much more rapidly, than they are supposed to, huge, fit, healthy animals whose pulses are so soft and slow that your cow-trained fingers just can’t register life. Horses sometimes devoid of clear evidence of cardiac activity will suddenly respond to a passing paper bag blowing in the wind with a pounding response that is palpable from several inches away without even touching the animal. And your mother said it was going to be easy!

This is your introduction to equine cardiology - all over the map! Equine cardiology is different. The horse has a huge range of normal resting heart rates, all the way from 16 BPM in a mature fit event horse at rest up to 40 in a resting horse that is nonetheless meeting you for the first time. Seemingly a paradox, the lower the heart rate the more likely you are to encounter rhythm variation. And even at rest, the rate can suddenly flip to over 150 because the horse became aware of something that you had not even noticed. And at exercise, the rate can be 240 or higher in a racehorse approaching the finish line.

The horse also has a huge range of different rhythms, and in a healthy horse none of them are really regular. As we are discovering, regularity is not necessarily the norm at exercise, either! And on top of the lack of rhythm, we sit on the top of horses, which makes us justifiably nervous when things seem not to be quite as we expected. Horses’ hearts also produce a wide range of sounds, most of which are also normal, but which are all the same, very disconcerting. Today, however, we are not interested in sounds so much as rate and rhythm.

Homoeostasis & Simple Diffusion

The best approach to understanding what’s actually going on might be to start with a brief discussion of basic cardiovascular form and function. Some of this will be very basic for some of you, a useful reminder for others, and perhaps for the occasional person among you, news. Regardless, the discussion will bring us all to the same level of understanding, and will frame the rest of the talk.

All living creatures are composed of cells, the smallest functional unit of all free-living lifeforms. Each cell has a cell membrane that forms a complete package separating what’s inside the cell from what’s outside, and defining the limits of the unit. Some lifeforms, such as bacteria for example, and some inhabitants of pond water, consist of only one cell. These single-celled organisms contain within their cell membrane everything they need to survive and reproduce. They gather nutrients from the environment by simple diffusion, and sometimes also by engulfing them. They are unable to exert major changes in their environment, are only able to live in environments that suit their immediate needs, are completely dependent on the environment immediately outside the cell membrane for life support, and depend on outside agencies to move around.

Multicellular organisms, on the other hand, can exert much greater control over their environment. They can take advantage of a broad range of habitats, and have much greater mobility. A horse is an example of a multicellular organism. It is still composed of cells, and just like the single celled organism each cell is still completely dependent on the environment immediately surrounding it for life support, but now the cells number in the trillions, and instead of each cell trying to do everything, they are each quite highly specialised, so they have to depend on each other.

A consequence of complex structure and the specialisation of cells is that while each cell continues to use simple diffusion (among other mechanisms) to get what it needs from the surrounding fluid, that fluid becomes rapidly depleted of what the cell needs, and at the same time, rapidly overburdened by by-products the cell is trying to eliminate.

The more intensely the cell is working (think of a muscle cell in a galloping horse, for example), the more acute the problem. The only option is to have a circulation system. Such a system brings things the cell needs (for example, oxygen, fuel) from where it is stored or gathered (again by specialised cells), to where it is needed. At the same time, the circulatory system removes the by-products produced by the active cells and transports them to where they can be disposed of.

By this process, it’s possible, despite functioning at a very intense level, despite needing vast quantities of fuel and producing vast quantities of waste, for the cells to keep themselves biochemically in the zone where they can continue to function; this is called homoeostasis. And homoeostasis does not mean keeping things at precisely the same level. Instead, it means keeping things in a range that is compatible with cell function, aka, life.

Nothing, in a multicellular organism, is kept at “the same” level! Change defines life itself, and it’s not a lack of change that characterises health, it’s the ability to respond appropriately to change and maintain the internal environment in a range that is compatible with survival. This is what truly defines life. So, we shouldn’t be surprised that the systems maintaining the cellular environment are themselves very changeable. And we should be even less surprised that an animal with such a huge ability to tolerate change (this time, in terms of athletic activity) as a horse should show wide variation in system function.

Cardiovascular Reserve And The Microcirculation

The cardiovascular system of the horse consists of a heart, the arteries that convey cardiac output (blood) to functioning tissues, the microvasculature that moderates the distribution of blood flow to local tissues, and the venous system that collects the blood from the periphery and returns it to the heart. If I were to ask you which part of this system is most important, which part is in charge, you would probably say the heart - but that’s not true. It’s actually the microcirculation. The heart is simply a pump, a very complex and absolutely indispensable piece of equipment, but it doesn’t actually tell anything what to do, it is simply a pump that responds to the demands of tissues and it is essentially controlled by the brainstem.

Why is it important to make this distinction? Because just about everything that affects heart rate and rhythm is a result of what happens in the brain stem, and the brain stem is mostly responding to what happens in peripheral (functioning) tissues. This is a basic mammalian design - all mammals have it, so what’s different about the horse?

Well, let’s discuss size to start with. The heart in a cow might be between 0.6-0.7% of body weight, and in a cold-blooded horse such as a Belgian it might be just the same. But in an elite thoroughbred used for eventing or National Hunt work, the heart may be 1.1% of body weight - that’s almost twice as large! This means much greater pumping capacity.

The horse is also what we call a “bradycardic” species - it has a very low resting heart rate that is almost completely under the control of inhibitory mechanisms - mediated through the parasympathetic division of the autonomic (involuntary) nervous system, with the nerves carrying the signals being called the vagal nerves, hence the term “vagal tone”. The activity or tone in this division at rest rises with training, which contributes to the low heart rate at rest in very fit animals. If you switch off this division - you can do that temporarily with drugs - heart rate will rise to about 120, and stay there until the drugs wear off.

In contrast, as we have discussed, maximum heart rate rises to at least 240 (more of that later) at maximal effort. At this level, the heart is completely under control of the second, excitatory division of the autonomic nervous system, the sympathetic system, and it’s also subject to a barrage of hormones called catecholamines coming from the adrenal glands. At the point of maximum heart rate the parasympathetic system is completely turned off.

This means that by changing heart rate, the horse can achieve a huge increase in cardiac output, and this means greatly increased flow to functioning muscles is possible. This increase is achieved with the essential collaboration of several other mechanisms, as we shall see.

Blood Volume And Cardiac Filling

A large heart with a large stroke volume (the volume of blood pumped by the heart on each contraction), is of no value if there’s not enough blood to adequately prime the pump. Neither is it of much value if the heart is unable to fill effectively between contractions. So we also need an appropriately large blood volume (which the trained horse has), and we need well-developed mechanisms to get the blood back from the peripheral circulation and into the heart in between beats, which of course the horse also has. In addition to the pressure gradient between the periphery (microcirculation) and the central venous space from which blood enters the heart, the horse has the pumping action of the skeletal muscles themselves and of the chest (fluctuations in pressure that follow respiration and stride) to help move blood back to the heart.

The horse has an additional adaptation, present in only a few other species, in which the spleen stores just about half of the body’s total red cells at rest. When the horse exercises the spleen contracts and all of those red cells are delivered into the circulation, which has two impacts. It raises total blood volume, making more blood available to fill the heart and perfuse the muscles, and it also increases the blood’s oxygen carrying capacity. The result is a circulation filled with blood that fully charges what is essentially a hydraulic system, a pump that is able to maintain a very high output and the delivery of large volumes of oxygen to peripheral tissues. It’s very important to remember the numerous components that participate in this delivery!

Control Mechanisms - Who Is in Control?

Of course, none of this explains why heart rate and rhythm can be so variable, it just describes the system. What we need to explore now is how all of these things are controlled and coordinated, because that’s where the explanations for changes in rate and rhythm mostly lie, plus it’s here and it’s in failure to effectively maintain homoeostasis that we find much of the explanation for the disturbances in rhythm that might be of clinical significance, a.k.a., a problem.

To understand control mechanisms there is actually another little piece of physiology we need to appreciate. As explained earlier, the cardiovascular system exists for no reason other than to meet the needs of peripheral tissues, and in this regard the heart is a rather essential but nonetheless relatively dumb bag of muscle, a pump. It goes like this: blood flows from an area of high pressure to an area of low pressure. The highest pressure is at the left ventricle of the heart during systole, where the pressure is generated, and it’s lowest in the right ventricle in diastole, when the right ventricle is filling, That is, blood flows around the body from the left ventricle to the right ventricle.

In the middle of the circulation, between those two ends, lies the microcirculation, which supplies the functioning tissue, and, as we have seen, the microcirculation is actually in charge! With the exception of extreme circumstances (like severe shock, which isn’t exactly compatible with athletic activity), the peripheral circulation functions entirely autonomously - without any reference whatsoever to what is going on centrally. Flow through a local tissue is determined entirely by the metabolic needs of that tissue. Small arteries called arterioles lying at the beginning of the microcirculation are controlled almost exclusively by local factors such as potassium levels, oxygen tension and acidity, and these are determined by local metabolic activity. So long as there is adequate pressure to drive flow, local arterioles will ensure tissues get what they need. The role of the heart is simply to maintain that pressure.

If maintaining pressure, and thus flow, is the primary role of the heart, then how might pressure change, and how is that change monitored? Moment to moment control of blood pressure is determined by pressure sensitive tissues distributed throughout the vascular system. If pressure falls these sensors send a message to the brainstem that results in an increase in heart rate. In the horse, this is initially achieved by reducing tone or activity in the parasympathetic nervous system, which reduces inhibition of the heart. The resulting rise in heart rate increases cardiac output.

There are at the same time adjustments in the return of blood from the periphery, in pressures in the central venous reservoir - the large venous capacitance vessels leading to the heart - and in contractility of the heart itself, the force with which it contracts. These mechanisms conspire to promote an increase in filling of the heart so filling will be efficient at higher heart rates, and an increased force of ejection.


Progressive increase in the volume of functioning muscle tissue as exercise intensity increases will be associated with progressive dilation of all associated arterioles and filling of the muscle capillary bed. This shift in blood from the centre to the periphery, and the fall in peripheral resistance, if not properly managed, could result in a precipitous fall in blood pressure. After all, the circulation can be likened to a leaking bicycle tyre - the more those peripheral resistance vessels (the arterioles) dilate the more leaky the system and the harder the heart has to pump to maintain pressure.

As demand continues to increase, there is a progressive withdrawal of parasympathetic nervous inhibition and a simultaneous progressive increase in sympathetic nervous activity. Progressive introduction of sympathetic tone has numerous effects, all of them associated with increasing heart rate, increasing myocardial contractility, optimising venous return and cardiac filling, and redistributing blood flow through tone in major muscular arteries to favour flow to functioning tissues.

The Sabre-toothed Tiger

Of course, if the horse suddenly realised that a sabre-toothed tiger was about to leap on its back, there would hardly be the time for all of these highly tuned mechanisms to be fully recruited, let alone fully switching on metabolic machinery - something else would have to give things a kick start. This would of course come from the brain and it would be initially involuntary, i.e., sabre-toothed tiger = bad news = get out of here. Messages would come from the high brainstem followed rapidly by cerebrocortical activity, intense stimulation of the sympathetic nervous system, and a huge kick from the adrenal medulla with release of catecholamines, the fear, fight or flight hormones. All the same, it would still take 20-30 seconds for everything to be fully switched on. And of course, when the tiger has given up and the horse has stopped running, everything has to return to normal, and that is a story in itself!

Normal Rhythm - How Normal Is Normal?

Now, at last we can start talking about arrhythmias. Firstly, there is no such thing as a steady heart rate. An absolutely steady, metronome-like rhythm is totally incompatible with normal life, which as we have seen, involves constant change and readjustment. If you monitor the ECG of a horse at complete rest and you measure, with suitably high resolution, the interval between consecutive beats, you get what is called a Heart Rate Variability time series consisting of the instantaneous heart rate for the period monitored. In a normal animal this is anything but a straight line. The amount of variation from beat to beat varies tremendously from horse to horse, circumstance to circumstance, moment to moment.

If you have a mathematical frame of mind, you can analyse this sequence of instantaneous heart rates to learn about underlying control mechanisms, which tend to vary in a cyclic or periodic manner. With a little faith and a suitable measure of scepticism, you can relate the cycles to underlying autonomic (parasympathetic and sympathetic) control. This is because control mechanisms such as the blood pressure control loop don’t simply turn on or off when necessary, they cycle all the time at fairly stable frequencies. What changes when they have something different to say is the amplitude of the signal, not its frequency. Among other things therefore, looking at the amount of activity in different frequencies inside HRV signal provides insights on whether sympathetic or parasympathetic tone predominates, as well as on other biological functions such as respiration, and even temperature regulation.

Back to the mare the veterinary students were examining at the start. She is quiet and relaxed, almost sleeping. She has very little sympathetic activity and lots of parasympathetic activity. This means she will have lots of high-frequency changes in instantaneous heart rate - she will be making adjustments with every beat. Occasionally this will result in her dropping a beat completely, at other times the interval between beats will be variably long. You would imagine that if everything was completely stable, she ought to maintain the same slow basic rate, but it’s not that simple, because blood pressure is not the only thing stimulating her parasympathetic nervous system.

She is also breathing, very slowly (maybe 6-8 times a minute), and these breathing cycles are also adjusting both BP and parasympathetic activity. As a result, the actual effect on heart rate (beat-to-beat) sometimes is additive and sometimes subtracts. Since the input of the parasympathetic nervous system to the heart actually has a left and right branch, and since they tend to innervate different parts of the heart, she can also slow down the heart and reduce cardiac output by slowing down the primary pacemaker (the sinus node), the AV node, which lies between the atrium and the ventricles in the middle of the heart’s conduction system, or she can use both! The result is wide variation in instantaneous heart rate, and thus rhythm.

There’s also another consideration, which I like to call “playing catch-up”. If the heart is only beating 30 times a minute (once every two seconds), and if control signals arrive in “clumps”, there’s going to be a delay between the signal to slow down and response. It’s even possible at very low heart rates that by the time the signal to slow down arrives, there may be a signal to speed up on its way will stop This means the feedback loop is going to be unstable, and may wobble. This problem is well known to engineers, and it’s an entirely predictable consequence of what you have to work with.

Another example might be that fit event horse with several years of aerobic training. At rest, it sometimes drops 2 beats at a time, and it’s resting heart rate is 16 beats a minute! Yes, the horse is very relaxed, but it also has a large heart both by virtue of genetic selection and prolonged training. It can perhaps put out enough blood in three consecutive beats to take the next two off. The result - huge variation in resting heart rate, AND IT’S ALL NORMAL! It is basically an example of instability in feedback loops.

Can such low heart rates at rest ever be abnormal? Yes, certainly, but your instinct would tell you something isn’t right. Some horses suffer from a condition called third degree heart block, in which none of the signals from the top of the heart get to the bottom, and the heart starts beating on its own from the AV node. This results in a very low resting rate, lethargy, and even a tendency to fainting (syncope). The signs would tell you something was wrong, plus such a low rate in an animal lacking either the breeding or the exercise history of our event horse would be very suspicious. An ECG will give you the answer in seconds.

Are there other variations on normal that you will encounter at rest? Yes, many, but few represent a problem of any clinical significance. All mammals throw occasional extra beats, for example, which may come from the atria or the ventricles. So long as every extra beat comes from the same place in the heart, up to one every minute is regarded by some as normal and not worthy of concern.

So, the story at this point is that benign rhythm variations are extremely common in horses and that they are largely a result of the animal’s basic design, represent instability in feedback loops, and, most importantly, disappear with the even the lightest of stimulation. Also, virtually all of the rhythm disturbances to which we have made reference so far occur in the upper part of the heart, at or above the AV node (supraventricular). Of these, there is some thought that they might be abnormal if they are present in very pronounced degree, but whether that is in fact the case is far from clear.

What IS Abnormal?

What is clear is the small group of supraventricular rhythm disturbances that everyone agrees are a problem. These are third-degree heart block (referred to above), atrial fibrillation, atrial flutter/tachycardia, and frequent atrial ectopic beats arising from multiple foci and with random timing. Stimulation will not cause the horse to come out of any of these disturbances, and all will have a performance impact, but it is very unlikely that they would lead to death, and with the exception of atrial fibrillation, equally unlikely that they would be a cause of sudden performance deterioration during work. In fact, some of these may not be noticed unless the horse is examined by a veterinarian or is asked for a maximal performance. Third degree heart block is thankfully very uncommon, and usually untreatable. Atrial fibrillation is quite common and can be treated in most cases. Atrial flutter is also very uncommon, as is complex atrial ectopy, but in horses they can often be managed.

Ventricular Rhythms

Rhythm disturbances involving the ventricles, in contrast, always generate a great deal of anxiety, and because some can indeed be fatal and are often associated with systemic disease, there is cause for some concern. It might help if we try to clarify the role and significance of these disturbances by adopting a loose categorisation. We can talk about probably benign variations on normal, we can talk about problems associated with systemic disease, and we can look at issues associated with intense exercise.

Benign Variations

Benign variations come mostly in one shade, occasional single ventricular ectopic beats. These are benign especially if they are always the same shape and especially if they are always consistently linked to the preceding normal beat, and are probably nothing to worry about, especially if they only appear in very limited heart rate ranges. You need an ECG to confirm all of this, and admittedly it can be very disconcerting when you hear the extra beat, but with a light exercise, these extra beats usually disappear. Research shows that these same single extra beats can occur even at maximal heart rates, without having any visible impact on performance. The issue here is abnormal impulse generation.

Rhythms In Systemic Disease

Ventricular rhythm abnormalities that are not so benign consist of problems with impulse generation and impulse conduction in various combinations. These are quite common in severe systemic disturbances, and they don’t necessarily indicate primary problems with the heart, but problems with homoeostasis. Yes, in situations in which there are major systemic disturbances of homoeostasis, the heart is very vulnerable because it is simultaneously working harder yet exposed to the same disturbances.

What sorts of disturbances? Acidosis, dehydration, toxaemia, and major electrolyte imbalance will all contribute to disturbed ventricular electrical activity, and can be responsible for both abnormal impulse generation and abnormal conduction. The resulting rhythm disturbances most often involve the atria and the ventricles beating independently (that is, no normal conduction between the two), with the ventricles beating from some location within ventricular muscle mass. Another characteristic in these cases is that the ventricular rate is almost invariably higher than the atrial rate.

This sort of rhythm disturbance is usually classified according to strict electrocardiographic criteria, but clinically that classification it is not particularly important. What is important is to realise the impact systemic disturbances are having on the heart, and to appreciate the strong need to correct those imbalances. What you don’t do is to reach for antiarrhythmic medication, except in the most severe cases.

Instead, you fix the homeostatic disturbance and the rhythm disturbance simply goes away! One of the clinical ironies in managing these cases, is that before correction, the heart rate will usually be high, but the rhythm may actually be very regular! Also, part way through treatment, as normal balance starts to reappear, the heart almost invariably goes through a period of extreme irregularity, which sounds as though things are getting worse when they are actually getting better. This sort of situation is very common in cases of severe diarrhoea. Again, this is primarily indicative of the horse’s systemic state, not of the status of the heart.

Myocardial Damage

In this group of ventricular rhythm disturbances that are not immediately associated with exercise, there’s also another set of circumstances to consider. These are situations in which, whether or not there is disturbance of homoeostasis, there is also actual damage to the myocardium, the heart muscle itself. When might this be the case?

Well, the horse with colitis and toxaemia could develop heart muscle damage if the toxaemia and the homoeostasis are untreated and the heart is left to beat at a high rate, well beyond what the body actually needs, for a day or two. This is one of the reasons why you’d get in there and treat rather than wait with your fingers crossed. There can also be direct damage to the myocardium if the horse passes through episodes of bacteraemia - with bacteria circulating in the blood stream. If these bacteria happen to set up house in the heart muscle they will cause localised bacterial myocarditis or inflammation of the heart muscle, and the cells in the area of damage will become electrically unstable and prone to firing off spontaneously on their own.

You can also get localised damage to the heart muscle in viral infections, particularly influenza caused by the A-equi-2 variant. Horses with this temporary problem that are rested can come through without any permanent damage, but if the horse is worked, all bets are off. Yet another situation would be the exhausted horse, where combinations of disturbances in homoeostasis, low oxygen supply, and high catecholamine levels combine to cause damage to heart muscle cells. Damage caused under this circumstance is not reversible and can be fatal, and may be so severe as to involve not only microscopic areas of muscle, but sometimes whole blocks of muscle in a manner indistinguishable from the coronary occlusion and infarcts seen in human heart attack

There’s also the example of specific myocardial damage in such things as ionophore poisoning and blister beetle toxicity. Once again, the damage can be fatal, and even if not, will be associated with reduced performance and a long term tendency to ventricular rhythm disturbances.

When there is localised heart muscle damage there’s a much greater tendency to abnormal impulse generation rather than problems with impulse conduction, and this manifests as frequent ectopic beats, sometimes in groups, and with varying shape and timing. Because these rogue signals can occur without any reference to the normal beats, they are particularly likely to cause even more serious arrhythmias, possibly even ventricular fibrillation, which obviously is fatal. Additionally, one or more of these damaged areas can develop accelerated automaticity, in which they discharge rapidly (more rapidly than the normal pacemaker) and essentially take over ventricular rhythm. This can also be fatal.

In all these cases you would still try to address the underlying disturbance directly first - the inflammation and tissue damage - but there is a greater chance you may need also to use specific antiarrhythmic medication to stabilise the patient and improve prognosis. It’s also clear that in all of these cases, even if the patient survives, there is likely to be an impact on athletic ability, a potential impact on safety, and a significant reduction in value of the animal.

Exercise and Arrhythmia

Which brings us to the question of ventricular rhythm disturbances associated with exercise, and here the water gets very muddy indeed! Although in humans individuals experiencing serious rhythm disturbances during exercise, and possibly even succumbing, are often found to have some predisposing, often genetic abnormality, such has not been shown to be the case in the horse, at least at this time.

There are two underlying themes here that are worth noting. The first is that virtually all the homeostatic disturbances that naturally occur with exercise are potentially arrhythmogenic. The fact exercise is not consistently associated with arrhythmias is assumed to mean these factors essentially cancel each other out, plus the characteristics of basic membrane function may change with exercise. The second is that, at present, the more we learn about rhythm disturbances and exercise in the horse the less we seem to understand! In particular, we don’t really know what to expect with exercise.

There is only one arrhythmia that has been consistently observed in association with exercise in the horse. This has been variously called sinus arrhythmia of exercise or punctuated deceleration. The last term best describes what happens. After exercise, usually but not always of at least moderate intensity, heart rate decelerates in a stepwise fashion in which there will be a sudden deceleration followed by a gradual acceleration to a rate just below that at which the heart initially decelerated. This cycle will repeat several times before the heart again assumes a gradual deceleration. In the period of deceleration there is usually evidence that the slowing has occurred at the sinus node, but occasionally it takes place at the AV node, with clear dropping of a beat (a P wave with no QRS). The more fit the horse and the more intense the exercise the more likely you are to see this rhythm change on deceleration.

Hearing this arrhythmia after exercise during a physical examination (for example, as part of a pre-purchase examination), can be quite disconcerting, since it is reasonably assumed that something bad is going on. In fact, it appears to be perfectly normal, and simply part of being a horse. More on the possible underlying mechanisms a little later.

With the exception of this rhythm disturbance and occasional premature contractions, exercise is infrequently associated with arrhythmia in the horse. However, recent work we performed in racing Standardbreds in which horses were monitored from first harnessing in the paddock to the end of the race and return to the paddock revealed about 16% of horses to have arrhythmias during deceleration after the race. These disturbances would have been regarded as very serious indeed if noted in the resting horse, yet all of the affected horses spontaneously returned to normal sinus rhythm, and went on to race in subsequent events without problem, raising questions about what is normal or “usual”.

Sudden Deaths

Despite the lack of consequences, the disturbances took place at a point in persons as well as horses when there tends to be a peak in sudden deaths. None of the horses in the study described died, but the fact that the disturbances were potentially fatal raises obvious questions. One obvious interpretation is that this is a normal manifestation, another that despite this interpretation, some horses might not spontaneously recover. Since this study we have performed the same investigation in thoroughbred horses during normal racing with similar, though less frequent findings. A clue to possible underlying mechanisms is provided by the fact that these disturbances almost always took place during episodes of punctuated deceleration, implying contributions from autonomic turbulence and sudden introduction of parasympathetic tone.

Although there is a much longer history in humans of following rhythm disturbances at rest to see whether they were warning signals for exercise in human athletes, the type of study performed in these racehorses has never been performed in humans. However, there is as of yet no reliable indication in humans that rhythm disturbances identified at rest provide any predictive value for exercise, with the exception of abnormalities of repolarisation such as long and short QT syndrome. These have been clearly associated with an exercise risk and affected persons are advised not to undertake intense athletic exercise.

In the horse, the appearance of a rhythm disturbance at rest is usually seen as a contraindication for exercise, but there is little evidence to support this, and this may not always be appropriate advice. If the disturbance is of the type described above in which there is possible myocardial damage, and obviously if there is evidence of a systemic disturbance of any type, the horse should most certainly not be working. However, identifying more benign forms of ectopic activity at rest, and even observing episodes of ventricular tachyarrhythmia at low or intermediate heart rates does not necessarily mean the horse will have problems at exercise - each horse needs to be assessed individually.

One of the particularly interesting features of the rhythm disturbances identified in the two track studies to which reference is made above, is the clear evidence that psychological factors and instability in the autonomic nervous system are probable predisposing causes. Extreme emotional disturbance is accepted as a possible cause of cardiac arrhythmia in people, while the horse, as an animal experiencing marked autonomic turbulence during cardiac deceleration may be a suitable model for investigation of possible contributions to arrhythmia in sudden death in human athletes.

Heart Rate Responses

One of the especially interesting findings in the track studies has been a wide range of maximum heart rates in horses undertaking maximal or sometimes supra-maximal effort. Although maximum heart rate is supposed to be about 240, rates as high as 270 have been observed in intensely contested competitions. Equally, maximum rates as low as 210 have been seen in other races that also appeared to be competitive. It is very surprising to discover that we can’t even be sure of what might constitute a maximum heart rate response, because of the presence of huge variation.


We are currently investigating the evidence for a greater burden of cardiovascular disease in exercise-associated performance problems, all the way from poor performance and exercise induced pulmonary haemorrhage to sudden death in the horse. Evidence from our track studies, from post-mortem studies, and from comparative investigations in other species, and supporting data from studies of equine cardiopulmonary exercise physiology suggest that the cardiovascular system in general, and disturbances of rhythm in particular, might be worthy of much greater and closer study as contributing factors in a range of equine performance problems. Perhaps the clearest conclusion to draw from what has been discovered to date, is that we really do not known very much about the relationship between exercise, disease, and cardiac rhythm in horses. In particular, at the present time, we really do not know for sure what is normal!