Copyright David Marlin 2014. All rights reserved.
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FOOD FOR FUEL! Understanding how what we feed, when we feed it and how we manage and ride our horses can affect their performance Dr David Marlin
The foods that we eat or feed to our horses are usually complex mixtures of many different types of substances. A large proportion of horse feeds are often energy sources such as carbohydrates (simple sugars or monosaccharides e.g. glucose and complex sugars or polysaccharides e.g. starch, cellulose and glycogen), fats (fats, oils, lipids) and proteins, but feeds also contain vitamins (e.g. A, B, C, D, and E), electrolytes (e.g. sodium, potassium, chloride, calcium) and trace elements (e.g. copper, zinc, manganese). The most common sources of energy diet are carbohydrates and fats (protein is only usually used as an energy source in extreme circumstances (e.g. illness or starvation), however at the level of individual cells within the body it is not carbohydrate or fat or even protein that is used as the energy source but a compound called adenosine tri-phosphate (ATP). It is not important whether the cell is a cardiac cell, a muscle cell, a kidney cell, a white blood cell or any other cell in the body. It does not matter what the function is that needs energy (e.g. growth, transmission of a nerve impulse, contraction, protein synthesis, reproduction, contraction). The only form of energy that a cell can use for a process or activity that requires energy is ATP. It will therefore not be surprising to know that the body contains significant stores of ATP. In fact, all living cells within the body have a small store of ATP. Cells or tissues (collections of specialised cells) that are effectively dead and therefore do not contain ATP include certain bone cells, hair and the upper layer of skin cells.
ATP provides energy when the energy stored in the third phosphate bond is broken. ATP is essentially three phosphate molecules (tri = three, phosphate) bonded to an adenosine molecule. The energy to bond a third phosphate to a molecule of adenosine with two phosphate molecules (adenosine diphosphate (di = two) or ADP) comes from carbohydrates or fats or proteins from the diet. This process is known as metabolism. Of course, the energy in the food that we or our horse consumes can be stored in times of plenty for times of scarcity. For some animals this may mean days or weeks between meals. For others it may be hours.
So we now appreciate that energy for life (at least for mammals) can only come from energy stored in ATP. As our cells use or “split” ATP to liberate energy, reactions catalysed (speeded up) by enzymes known as ATPases, ADP and phosphate are formed. Whilst the body stores of ATP are not insignificant, if we were to undertake explosive exercise such as running for 2-3 seconds we would use all the ATP stored within the muscles and convert it to ADP (unfortunately it is not possible to break the second phosphate bond to release energy, although an ADP plus another ADP can be = one) converted to one ATP and one AMP molecule (adenosine monophosphate – mono -) by an enzyme known as myokinase). This is where other forms of energy stored within the body come into play as these can be used to regenerate ATP from ADP. An interesting concept concerning energy is that energy can neither be created or destroyed, only changed from one form to another!
At rest, the rate of ATP breakdown (often referred to as ATP turnover) is quite slow in most cells in the body, at least compared with in muscle cells during exercise. However, apart from exercise, the rate of ATP turnover (usage) may dramatically increased in tissues that are said to be very metabolically active. This could include the brain when we are thinking hard when trying to work out a problem, in a damaged tissue trying to repair or during an infection. When the body temperature drops very low, so the rate of ATP use also falls. In fact, this is one of the reasons why people can often survive in cold water, despite breathing and the heart being stopped for prolonged periods. The cold reduces the rate of ATP turnover and even though there is no breathing or circulation, the ATP stores are not exhausted. After death (when the breathing and heart both stop), this does not mean death occurs at the cellular level. In fact, the cells can carry on regenerating ATP (i.e. energy) from stored energy sources such as carbohydrate and fat for many hours. However, eventually, the lack of oxygen and accumulation of lactic acid (making the cells very acidic) halts the conversion of stored fat and carbohydrate energy sources and the cells themselves die. The time after death at which ADP can no longer be regenerated to ATP is illustrated by the time at which rigor mortis occurs as ADP prevents relaxation of the muscles.
After the onset of exercise, in fact within the first few muscle contractions, large amounts of ATP have been converted to ADP and phosphate. If muscle contraction (and indeed muscle relaxation followed by contraction) are to continue then ADP must be regenerated to ATP. Cells have a very quick way of doing this which relies on transferring the energy in a phosphate bond from a substance known as phosphocreatine or creatine phosphate PCr (not to be confused with creatinine which is entirely different) to ADP. The ADP “steals” the phosphate from the creatine (phosphate) and this reaction is catalysed by an enzyme called phosphocreatine kinase (CPK) or creatine kinase (CK). [In fact CK (or CPK) is one of the enzymes measured in blood to assess muscle damage. Normally the concentration (or more correctly, the activity) of CK in the blood is very low (30-300 units/litre of plasma). However, following a severe bout of tying-up the activity may increase to 500,000 units/litre or even higher)]. The transfer of the phosphate from PCr to ADP to regenerate ATP is very rapid, but stores of PCr are still only 2-3 times higher than those of ATP itself and can only provide energy for a few more seconds of intense exercise. This is the point at which energy from the diet comes into play.
For simplicity it is best to only consider carbohydrates and fats (tryglycerides, cholesterol, oils, lipids, fats, free fatty acids, volatile fatty acids). Food from the diet in its complex form is digested into simpler components and used immediately or stored within the body. In plants, the storage form of carbohydrate is starch. Starch is a polysaccharide – simply a chain of many (poly) sugars (saccharide). In animals, the stored form of carbohydrates is glycogen. In simple terms glycogen is chain of many thousands of glucose molecules – i.e. a polysaccharide. They are not actually linked in one long chain but more like the branches of a tree. Glycogen molecules are usually so large that they can often be seen with a microscope within cells. Because of their size they also remain inside the cell unless its cell wall is damaged. However, glucose itself is relatively small and can diffuse into and out of cells passively or can be pumped into cells by specialised glucose transporter pumps within the walls of cells. It is worth noting that very little ATP is present in blood or fluid surrounding cells as ATP cannot cross cell membranes (walls) unless they have been damaged. Therefore whilst feeding ATP itself is possible and might seem a great way to cut out all those indirect steps of metabolism, it would not be taken up from the gastro-intestinal tract.
Glycogen granules occur within the main body of the cell (known as the cytoplasm) and not in the nucleus (where the genetic material [DNA] is held) or within the mitochondria (a specialised structure within cells also related to a particular way of regenerating ATP). In fact, it is possible to use special “stains” on small and thin sections of muscle cells to show how much glycogen they contain. A large difference in glycogen content can be seen in muscle biopsy samples taken before and after either intense, short duration exercise (e.g. after a Thoroughbred flat race) or after prolonged, low-moderate intensity exercise (e.g. after a 100 mile endurance ride).
The body stores of glycogen are considerably greater than those of PCr. The majority of the glycogen stored in a horses’ body, around 90%, is stored within the muscle cells themselves. The remainder, around 10%, is stored within the liver. This is used to maintain the blood glucose level (often referred to as the “blood sugar” level. In fact, glucose is often measured in terms of its plasma concentration and not blood level) within a fairly narrow range, primarily under the control of the hormones insulin, cortisol, glucagon, adrenaline and noradrenaline. Maintenance of an adequate blood or plasma glucose concentration is essential for the health of one organ in particular, which can only use glucose (as opposed to glycogen or fats) – the brain. Similarly, red blood cells do not contain mitochondria and can also only utilise glucose to regenerate ATP. Whilst much of a hangover is caused by dehydration, a low blood sugar (hypoglycaemia) can contribute significantly to the feeling of illness – just ask a diabetic. Hyperglycaemia (high blood sugar) is not necessarily a pleasant alternative either. However, despite the fact that blood glucose concentration is usually maintained within a range of 4-6 mmol/litre, it can increase quite dramatically as a result of intense, short-term exercise (e.g. Thoroughbred racing) and may fall very low after prolonged endurance exercise. For example, it is not uncommon to measure blood glucose as low as 2 mmol/l following a 100 mile competitive ride. The loss of interest, fatigue, ataxia (unsteadiness), unwillingness and decreased responsiveness sometimes seen in these animals may often be related to a low blood glucose. Tremor, fits and coma may occur when the blood glucose concentration falls much below 2 mmol/l.
The process of getting energy from glycogen to regenerate ATP from ADP is also relatively rapid and can be accelerated from “standing” within a matter of seconds and can provide significant energy for ATP regeneration in intense exercise lasting for around 3-4 minutes. This source of energy is also used for acceleration during a period of exercise and also for other explosive muscular activity during exercise i.e. jumping. The breakdown of glycogen is triggered by a number of factors, including increase in adrenaline. The breakdown of glycogen to yield individual “glucose units” is controlled (catalysed) by the enzyme glycogen phosphorylase. This enzyme literally passes along each branch of the glycogen tree chopping off glucose molecules. For accuracy, this is slightly more complicated, in that the glycogen is broken down into some free glucose molecules, but the majority is in the form of glucose with a phosphate linked to it – known as glucose-1-phosphate (G1P). In fact although free glucose is produced during the breakdown of glycogen and can also be taken up from the blood, it can only be used in the phosphorylated form of glucose-1-phosphate. This means that any free glucose in the cell from either glycogen breakdown or uptake from the blood must have a phosphate added to it by the enzyme hexokinase. During high-intensity exercise when glycogen breakdown is rapid, glucose-1- phosphate actually inhibits the enzyme hexokinase and so the glucose concentration of the muscle rises and much passes out into the circulation, increasing the blood concentration.
G1P is then metabolised by a special linked sequence of chemical reactions catalysed by a number of different enzymes to regenerate ADP to ATP. This is the process known as glycolysis and is the pathway whereby lactic acid is formed. Glycolysis is also sometimes referred to as anaerobic glycolysis or anaerobic metabolism because of the fact that oxygen is not required in any of the steps forming ATP from ADP. This does not mean that oxygen is in short supply. There may well be plenty of oxygen around when there is a high rate of glycolysis.
The good news about glycolysis is that it can be accelerated immediately and it doesn’t have to wait for an increase in breathing and heart rate to deliver oxygen to the muscles. In fact, its the bodies equivalent of 0-60 mph in under 2 seconds. In fact, the 100 metre runner or the acceleration of the racehorse out of the starting stalls or flat out gallops would not be possible without glycolysis. There must be a downside? Nothing can be this good can it? Sadly, no. The problem with glycolysis is that firstly, its not very efficient. It only produces a small amount of ATP from the potential energy locked in the glucose or glucose-1-phosphate resulting from the breakdown of glycogen to lactic acid. It’s also self-limiting. The body has an in built safety mechanism – its called fatigue. Of course we usually view fatigue as an annoyance, especially if it occurs too early! However, fatigue is the body’s way of saying “I’ve had enough”. For human athletes, going beyond the pain barrier really means pushing your body beyond the normal point of fatigue and of course this can sometimes have dire consequences in terms of the occurrence of injury.
The precise factor or combination of factors causing fatigue does differ depending on the type of exercise being undertaken and other circumstances, such as climatic conditions (heat, cold), fitness, hydration status, etc. Fatigue can also be defined in different ways. For example, fatigue in a sprinting race may be defined as the point a which the athlete cannot maintain the same speed and begins to slow down, even if this is hardly detectable to those watching. In the case of prolonged exercise, such as a human marathon or equine endurance ride, fatigue may mean a complete inability to continue to exercise at all, even just walking. In the case of short-term, intense exercise fuelled by glycolysis, fatigue occurs due to a combination of different factors, but partly due to the accumulation of lactic acid within the muscle, which in turn dissociates (splits) into lactate and a hydrogen ion. Hydrogen ions lower the muscle pH and make the conditions inside the muscle cell acidic, which in turn slows glycolysis.
The role of lactic acid in fatigue in short-term, intense exercise has lead to it being labelled the bad guy in many general text books dealing with exercise. The truth is very different. Glycolysis could not continue if the natural end-point, a substance called pyruvate, was not continually removed. The muscle cell’s solution to keeping the concentration of pyruvate low is to convert it to lactic acid immediately that it is formed. This reaction is catalysed by the enzyme lactate dehydrogenase, and it should not be surprised to learn that this is present in large amounts within the cytoplasm of muscle cells. If it were not for glycolysis and lactic acid production, we could not sprint, accelerate or maybe even manage more than one jump without a long rest in between. In fact, there are people with a genetic defect known as McArdles Syndrome in which the enzyme glycogen phosphorylase is missing and so glycolysis cannot take place. These people are unable to sprint or run fast and often experience severe pain. So glycolysis and lactic acid production are good if you want to be fast, but will limit how far you go. Horses or human athletes that produce the most lactic acid are almost always the fastest e.g. the 100 metre sprinter, the Quarter-horse, the polo pony, the 5 furlong sprinter. By comparison, the human marathon runner produces very little lactic acid, even when running a maximum speed to fatigue. Similarly, whilst the 5 furlong Thoroughbred sprinter may have a blood lactate of 30 mmol/l after a race, it may be hard to push the blood lactate concentration of an elite 100 mile endurance horse above 5 mmol/l, even at a flat out gallop. The difference, the endurance horse may be able to go for 100 miles at 10mph, but will come in way behind the 5 furlong sprinter and vice versa.
So we have learned that glycolysis (anaerobic glycolysis – where no oxygen is used) is good if we want to be fast for a short time. What if we want to go further? We know that glycolysis is inefficient and self-limiting when it is running flat-out. The option is to run at a lower speed, well below our maximum, and instead of converting the pyruvate to lactic acid (glycolysis), to metabolise the pyruvate to regenerate ATP from ADP in the presence of oxygen. This is referred to as aerobic …. and takes place within specialised structures known as mitochondria. The great advantage of mitochondrial oxidative phosphorylation (phosphorylation = addition of phosphate to ADP, in the presence of oxygen = oxidative) is that it is extremely efficient and produces x times as much ATP from ADP as glycolysis. The end products are water and carbon dioxide, which do not contribute to fatigue and so exercise based on aerobic (in the presence of oxygen) metabolism can be sustained for much longer. The downside is that an adequate delivery of oxygen to the mitochondria must be maintained for oxidative phosphorylation to continue. This involves expending energy to ventilate the lungs and to pump the blood through the lungs and to the muscles. So efficient, but not as fast.
Almost all equestrian disciplines rely on a combination of glycolysis (often referred to as anaerobic) and oxidative phosphorylation (often referred to as aerobic) sources of ATP regeneration from ADP. In disciplines involving short, term high-intensity exercise (e.g. Quarterhorse racing), the greater contribution will come from anaerobic energy production. With increasing duration, the contribution will shift more towards aerobic energy production. In many disciplines the underlying exercise may be supported mainly by aerobic sources with the energy for sprinting, acceleration and jumping efforts coming from surges in glycolysis.
Where does fat fit in?
There is one more fuel source that we have not discussed up to this point – fat. Whereas glycogen and or glucose can be metabolised through glycolysis (anaerobically) or through mitochondrial oxidative phosphorylation (aerobically), fat can only be metabolised to regenerate ATP from ADP within the mitochondria and requires oxygen (i.e. another form of aerobic metabolism). The disadvantages of aerobic metabolism of fat are that large amounts of oxygen are required, it takes maybe 20-30 minutes to get up to speed and the rate of ATP regeneration is very slow (in terms of numbers of ATP regenerated per second). The advantage of fat is that per gram it contains considerably more potential energy than glucose or glycogen. Exercise is almost never, if ever limited by running out of fat. Even a thin endurance horse with only 3-4% of its bodyweight as fat, would have enough energy stored in fat to complete 5, 100 mile rides. By contrast, many different types of exercise, ranging from high-intensity disciplines such as steeplechasing to 100 mile endurance race rides are limited by low or exhausted glycogen stores within individual muscle cells. Once the glycogen has been exhausted, these cells can only continue to work obtaining their energy for regeneration of ATP from either metabolism of blood glucose (which will also likely be in short supply after 10 or more hours of exercise) or from aerobic metabolism of fat. The implication is that at this point, the ability to sprint, accelerate or jump may be lost. In man, studies have also shown a direct correlation between the glycogen concentration at the start of exercise and time to exhaustion. The more glycogen you have, the longer you can exercise for. Even for short-duration, very high-intensity exercise where complete glycogen depletion will not occur, it has been shown that the rate of glycogen breakdown is related to the glycogen concentration. To be fast you need to use glycogen and the more you have, the faster you can use it.
Fat stores within the body are almost the opposite to glycogen. The majority of fat (correctly referred to as tryglyceride: three fatty acids linked to one glycerol) is stored outside the muscles within special types of tissue known as adipose tissue – e.g. under the skin, between organs within the body cavity. Only around 5-10% of the bodies fat stores are within the muscle cells themselves where they can often be seen as droplets.
Why does it take so long to start using fat as a fuel?
The main reason is that the stored tryglycerides must be broken down by enzymes known as lipases. This releases the free fatty acids (FFA) which are then transported by the blood to the muscles where they are taken up.
Can we tell what fuel an animal is using during exercise?
There are a number of different ways to measure what fuels are being used. Complex methods involve using radioactively labelled food sources. A simpler and more widely used approach is to measure the ratio of oxygen used to carbon dioxide produced. For example, if the horse was consuming 50 litres of oxygen per minute and producing 50 litres of carbon dioxide per minute, this would be equivalent to a respiratory exchange ratio (or RER) of carbon dioxide/oxygen = 50/50 = 1.0. An RER or 1.0 indicates that the animal is using only carbohydrate and no fat. If the animal was exercising slowly and had been doing so for some time (perhaps an hour) we might find that the oxygen consumption was higher than the carbon dioxide production such that the RER was now 21/30 = 0.7, this would indicate that all the energy production was coming from fat. Values in between 0.7 and 1.0 indicate different proportions of fat and carbohydrate metabolism as shown below. This method does make some assumptions and has some limitations, but is useful in many circumstances, for example to measure the effect of different dietary formulations. Table 1. Proportions of energy coming from metabolism of fat and or carbohydrate for different values of RER. RER %Carbohydrate %Fat 0.71 0.0 100.0 0.75 15.6 84.4 0.80 33.4 66.6 0.85 50.7 49.3 0.90 67.5 32.5 0.95 84.0 16.0 1.00 100.0 0.0 If the carbon dioxide production increases to 100 l/min and the oxygen to 75 l/min, as would happen during very intense exercise, the RER would now be 1.33. The horse is still using carbohydrate, but the fact the RER is greater than 1.0 indicates an increasing contribution from glycolysis resulting in lactic acid formation and accumulation.
It is of particular interest that whilst people at rest may have low RER values (0.7-0.8), suggesting that they we obtain a significant amount of energy for basal metabolic needs from fat, the horse tends to have RER values closer to 1.0. This suggests that even the resting horse obtains most of its energy from carbohydrate sources. Should we be surprised by this? Lets look at the differences in diet, body composition, digestive system and behaviour or evolutionary niche between us and horses, as these may help us understand the basis for this difference.
The horse is a herbivore. How much fat and oil would a horse get from its diet in the wild? The answer is very little. Even when we feed a horse a “high fat” diet, this may only equate to 15% of the total dietary energy coming from fat. In fact if we increase the fat content of a horse’s diet too much above 15% we are likely to induce loose droppings or even diarrhoea. This is because fat/oils speed up the passage of food through the digestive tract and also upset the bacterial flora of the hindgut. Digestibility is reduced and the water content of the faeces is also increased. This is very different from us. We are omnivores – basically we eat anything!! Meat, fish, high fat, high carbohydrate. The structure of our gastro-intestinal tract is very different and we don’t rely on bacterial fermentation. The fibre we eat goes in as fibre and comes out as fibre. Very different to the horse. Whereas the horse can only tolerate slight variations in diet composition in respect to the proportions of protein, fibre, carbohydrate and fat, we can eat and tolerate dramatic changes in diet from one day to another. On a Monday we can eat lean steak and fish (high protein meal), the next day we may eat pasta and potatoes (high carbohydrate meal) and next day we could eat eggs, cheese, cream and fried bread (high fat meal). We could cope with this, the horse would not.
There is considerable evidence to suggest that being overweight is bad for people. When we are overweight we have excess bodyfat, not excess muscle or excess bone or excess skin – it’s excess skin. Typical % bodyfat for a person is x% for a man and x% for a woman. The racehorse in training is around 5% bodyfat. Much lower than the average human, but nearer to the serious athlete. Even horses in the wild do not usually carry excess fat. The horses that are overweight are often show animals, dressage horses and sometimes ponies. Why are they overweight? Genetics? No, we overfeed and under exercise them. Is this good for their health? No!! It’s the same for people. Being overweight carries an increased risk for many conditions, such as diabetes and heart disease. Overweight for a horse is not nicely covered or ideal or desirable – it’s bad!! Sorry!
Role of Hormones in Controlling Use of Different Energy Sources
The concentration of many different hormones in the circulation changes with exercise. For example, adrenaline and noradrenaline, ACTH-cortisol and glucagon (all involved in control of blood glucose) increase, as do other hormones like growth hormone, testosterone and renin-angiotensin- aldosterone, whereas insulin decreases.
Effect of Environmental Conditions – Cold
Many people exercise their horses early in the morning in the Winter months when air temperatures may be close to 0°C. In addition, some horses undertake strenuous exercise in competition on very cold days (e.g. point-to-pointers). In cold conditions, it may take longer to “warm-up” physically (increasing body and muscle temperatures) and physiologically. Decreases in skin temperature lead to decreases in blood temperature and body temperatures (hypothermia). Decreases in skin or blood temperature cause the hypothalamus (the region of the brain involved in thermoregulation) to activate a number of mechanisms to restore body temperature. These include shivering and non-shivering thermogenesis (thermo – heat, production – genesis) and peripheral vasoconstriction (blood vessels in the skin narrow or close in order to limit further heat loss. Shivering (rapid, but small and relatively uncontrolled muscle contractions) can increase heat production by 5 times. Remember that muscle contraction during exercise is only 20% efficient with 4 times as much energy being released as heat for every unit of energy that is converted directly into movement. However, shivering uses up muscle glycogen. Non-shivering thermogenesis is an increase in metabolic rate driven by increases in adrenaline. This also shifts metabolism towards using glycogen. Decreases in body temperature in a cold environment (in an animal) occurs primarily from the blood circulation in the skin. The blood enters the skin warm and returns to the heart cooler. The cooler blood then warms by passing through muscle and other tissues. However, these then become cooler. A fall in central body or blood temperature of only 1°C can be enough to turn on these mechanisms of heat production. In contrast, skin temperatures may fall very low indeed. This is due to constriction (narrowing or in some cases, closure) of the blood vessels in the skin (particularly the extremities) to reduce heat loss and to try and maintain core body temperature.
When the temperature of a muscle is lowered it becomes weaker and so performance may be reduced and fatigue occurs earlier in exercise. In cold conditions, if the horse is not sufficiently well rugged and without adequate warm-up before exercise, increased amounts of adrenaline are released. This pushes the muscles towards using glycogen. In relatively prolonged exercise such as racing, eventing or endurance, fatigue may occur earlier due to greater production of lactic acid or depletion of glycogen in certain populations of muscle fibres. In the horse exercising intensely for short periods (e.g. showjumping, polo), muscle strength, and therefore performance, may be decreased.
The answer to dealing with cold environmental conditions is to ensure horses are well rugged and warm-enough during travelling (as good ventilation should still be maintained even in cold weather), that horses are kept well rugged on arrival prior to competition, that horses are walked with rugs for perhaps at least 20-30 min before exercise and that a rug is kept on until the last possible moment before the start of exercise in the case of competition. Furthermore, it is Ó Copyright David Marlin 2007. All rights reserved. important to keep horses moving by walking if there is some delay until being able to start. There is also some evidence from studies in man that acclimatisation to cold does occur after repeated exposure.
Effect of Environmental Conditions – Heat
Just as the hypothalamus monitors skin and body temperature and responds to cold, it is also responsible for responding when body temperature increases (hyperthermia). The body temperature of a horse can increase 2-3°C when intense exercise (e.g. racing, eventing, polo) is performed in a cold, neutral or hot environment. However, in a hot or hot humid climate, the horse may become hot even before the start of exercise. This may happen during transport, in the stables or during warm-up before starting exercise or competition. Prior to exercise, increases in body temperature can cause an increase in fluid and electrolyte loss through sweating, increased heart rate and increases in adrenaline (interestingly, the same response as in hypothermia). This shifts metabolism towards glycogen breakdown and lactic acid production. Fine for very short exercise (e.g. show-jumping) not good for prolonged exercise. As well as elevations in adrenaline from the increase in body temperature, dehydration may also increase adrenaline concentrations.
In hot or hot humid environmental conditions, a greater proportion of the blood flow may have to be directed to the skin, This blood flow is then not available to the muscles. This means for a given exercise intensity, there is a greater stress on the cardiovascular system and heart rates will be higher than in a neutral or cool environment. There is some evidence that increasing muscle temperatures 1-2°C prior to exercise improves muscle function (i.e. warm-up) but that increases above this amount may lead to decreased muscle strength.
How can we deal with hot environments? When travelling, make sure there is good ventilation. Allow horses access to water at all times during travelling by hanging buckets in the trailer or lorry. A rubber tire can be used over the top to prevent spillage. Make sure you avoid travelling in the hottest part of the day. Travel early morning or late evening. Arrive well enough in advance to allow your horse to drink and recover. Reduce the amount of warm-up you do with your horse. This can be a reduction in time and or a reduction in the intensity of warm-up. Your horse will get hotter (i.e. “warm-up”) much quicker when its hot. Whereas in cold you want to extend the warmup period, in the heat you want the opposite. If you really need to warm your horse up for an hour, do it in the shade if possible, or break it up into three 20 minute periods. Between each period let your horse drink and try and cool him down by washing with cool water.
Excitement (anticipation, anxiety, pain) causes increases in adrenaline. Fine for the human sprinter in advance of a short, explosive effort. Not good if you are going to have to do a three-day event speed and endurance test when you are at the start of the roads and tracks. Might be ok for the showjumper. However, repeated show-jumping rounds will decrease muscle glycogen stores. Whilst the horses “skill” may improve from round to round, its physiological ability to jump will almost certainly decrease, even if not obviously so.
Age & Training
Training Young, untrained horses have a very high capacity to break down glycogen to lactic acid to produce energy for running. The horse is born as a sprinter. In the wild the horse uses short, fast sprints to get out of trouble. Horses very rarely exercise in the wild or even in the field for the durations that we expect from them in competitions. With increasing age, the untrained horse does become more aerobic. This is mainly due to changes in muscle fibre composition (see below). Nearly all the training programs we use with horses shift the muscles to become more aerobic. The exception may be training the show-jumper or quarter-horse. We sometimes confuse training horses with training people. A human 100m sprinter trains to develop large, powerful muscles. They don’t rely much on oxygen in a 100m race as they hold their breath from start to finish!! Although you may have heard it said that a 5f (1000m) equine “sprinter” can hold its breath for the entire race (around 55 seconds), we know this is a slight exaggeration. However, we have seen horses hold their breath for 10-15 seconds when accelerating to maximal speed on the treadmill. A human sprinter does almost no “aerobic” work (prolonged exercise at heart rates around 170 b.p.m.). Its either short, explosive, near maximal efforts on the track for 2-10 seconds or strength work in the gym. This makes the muscle fibres larger, the muscles themselves increase in size, the blood supply to the individual muscle fibres decreases (because they don’t need it) and the enzymes involved in glycogen breakdown to lactic acid (i.e. anaerobic energy production) increase. We very rarely see this in horses with training. Most horse training programmes in the UK produce some improvement in the ability of the muscles to use oxygen. Thus, after training, when exercising at the same speed, a fit horse will rely less on anaerobic glycogen metabolism and more on aerobic glycogen metabolism. The result, at least at a speed that before training was high enough to produce lactate, will be that lactate production will be lower. This is the basis behind the shift in the lactate speed curve to the right after training. Figure 1. Effect of training on the blood lactate response to exercise. After training, for a given speed pre-training, the horse produces less lactate. Earlier on, the effect of initial glycogen concentration on the rate of glycogen breakdown during near-maximal exercise and the time to exhaustion in prolonged exercise was highlighted (high initial muscle glycogen concentration = high rate of breakdown or longer time to exhaustion). The muscle glycogen concentration can be dramatically affected by exercise during training. So if you give your racehorse or eventer a short, hard gallop the day before an event or race, it is likely that the muscle glycogen concentration will not have recovered fully by the day of competition. The same applies to prolonged exercise. It would be unwise to do any fast exercise with an endurance horse in the 3-4 days prior to a competition. Whilst it is not possible to glycogen load horses by a combination of diet and exercise as practised by human athletes, reducing the amount and intensity of exercise in the last week before competition should ensure muscle glycogen concentrations at the start of competition are as high as possible.
Breed & Muscle Fibre Type
Muscle Fibre Type To a large extent, the type of fuel or fuels a horse will use for a given intensity (speed) of exercise is governed by the horses’ muscle fibre type. Thoroughbred horses and Quarter horses are fast because they have high proportions of type II muscle fibres (also known as fast twitch fibres) and low proportions of type I fibres (also known as slow twitch fibres). Type II fibres are further subdivided into IIA fibres and IIB fibres. The type I fibre relies mainly on aerobic metabolism of fat and glycogen and has a low capacity for anaerobic metabolism (i.e. to produce lactic acid). If you want to cover a long distance at a slow speed, lots of type I fibres are ideal. If you want to be faster, you need type II fibres. The IIA fibre is a fast twitch fibre, which has a high capacity to metabolise glycogen and fat aerobically to produce energy, and some capacity to produce lactic acid. The IIB fibre has a very high capacity for anaerobic metabolism of glycogen to lactic acid and a relatively low capacity for aerobic energy production (compared to type IIA & type I fibres).
In general terms, at walk the horse will use mainly type I and some IIA fibres, with increasing speed up to medium canter, more and more type I and IIA fibres will be used or recruited. However, once the type I and IIA fibres that can be recruited have been, the horse can only increase its speed or jump by recruiting IIB fibres. However, not all breeds of horses or even horses of the same breed, have the same fibre composition. For example, some Thoroughbreds may have 15% type I fibres, 75% IIA fibres and only 10% IIB fibres. These type of horses will be better suited to longer races (e.g. 2 miles or further). Some Thoroughbreds may have 5% type I fibres, 30% IIA fibres and 65% IIB fibres. A horse like this would be fast but for only a short distance (e.g. 5 furlongs). The difference is that although we said recruitment of fibres is generally type I to type IIA to type IIB, if we exercise these two very different horses at canter (where they might be using around half their muscle fibres), the 75% IIA fibre horse will probably not be recruiting any of its 10% IIB fibres and producing very little lactic acid (i.e. it is relying almost entirely on aerobic metabolism of glycogen and possibly some fat). In contrast, the other horse has no option to use some of its IIB fibres because only 35% of its fibres are NOT IIB’s. That means at this speed it will be relying more heavily on anaerobic metabolism than the other horse. So where each horse gets its energy from to regenerate ATP to some extent is also determined by fibre type which in turn is determined by genetic makeup. Figure 2. Principle of pattern of recruitment of different muscle fibre types with increasing speed.
Exercise Intensity, Duration and Pattern
The proportions of fat and carbohydrate used during exercise are affected by the transition from rest to exercise, the intensity of exercise and the way in which a horse is ridden. At rest, in general horses have a higher RER than people i.e. the horse relies more on glucose and glycogen at rest than we do. In the transition from rest to exercise the rate of ATP turnover (breakdown & regeneration) increases. We have already leaned that it may take several minutes to accelerate aerobic metabolism. So in the very early stages of exercise, there is generally reliance on anaerobic glycogen breakdown, even if the exercise is of low intensity. Thus at the onset of exercise there is usually an increase in RER and a strong reliance on carbohydrate (glucose/glycogen). If exercise continues to be maintained at a low intensity (e.g. at a heart rate below 140-150 b.p.m.), then the RER will fall so that there is a gradual change towards using more fat. However, this may take 20-30 minutes before a stable and lower RER is reached. If at the onset of exercise the intensity if moderate or high, the RER will likely rise to around 1.0 and not fall and may even increase. This means the horse is relying almost completely on glucose and glycogen.
In general, walking, trotting and slow cantering exercise (heart rates of around 70-140 b.p.m.) will result in significant utilisation of fat. If your horse is overweight and you want to get rid of excess fat, do lots of walking and trotting. If you work your horse hard, it will not “burn-off” the fat. At heart rates around 140-190 b.p.m., the horse will be using a mixture of fat and carbohydrate aerobically at the lower heart rates and aerobic glycogen breakdown at the upper end. Above heart rates of around 200 b.p.m., the horse will get the majority of energy from aerobic glycogen breakdown and with increasing speed, the proportion of energy coming from anaerobic breakdown of glycogen to lactate will increase. Of course, these are generalisations as the fuel sources and the relative importance proportions of aerobic/anaerobic glycogen breakdown will be related to other factors such as breed, age and muscle fibre composition.
Another factor that determines the balance between the aerobic utilisation of fat, aerobic utilisation of glucose/glycogen and anaerobic utilisation of glycogen is the pattern of exercise. If the horse is maintained at a constant pace.
Remember, the reason we are interested in optimising the utilisation of fat or aerobic utilisation of glycogen is that in many forms of exercise it is glycogen depletion that is a significant factor in fatigue and performance. If we can use as much fat as possible, then this spares glycogen. If we are exercising our horse at a faster speed which means that we cannot avoid using glycogen, then it is better to try and ensure that the glycogen breakdown is mainly aerobic. Remember that aerobic glycogen breakdown is more efficient but slower than anaerobic glycogen breakdown. Finally, of course we cannot avoid anaerobic glycogen breakdown if we want to exercise our horse very fast or accelerate. However, this gives us a clue how to minimise unnecessary anaerobic glycogen breakdown to lactate by using an appropriate rising strategy.
If we need to get from A to B on our horse at an average speed of lets say 600 metres/min or 10 m/s (perhaps as when jumping a cross-country course), we can achieve this in a number of ways. Firstly, we could ride the first half of the course at 300 metres/minute and the second half at 1200 metres/min. Or we could vary our pace up and down, for example, between jumps we might go quite fast, and around the jumps we might slow right down. Another way we could ride is to try and keep our horse in a regular pace. The last strategy is the one that will result in the most efficient utilisation of glycogen (i.e. at this intensity of exercise, primarily aerobically). Accelerations and decelerations in pace demand anaerobic glycogen breakdown to lactic acid and as this is fast but relatively inefficient, if we ride this way then we run the risk of limiting our Ó Copyright David Marlin 2007. All rights reserved. horses performance by depletion of glycogen stores. This could well be important during moderate-high intensity, moderate duration exercise (5-15 min) and will certainly be important during prolonged exercise (e.g. endurance).
Thus, in summary, if we maintain a slow-medium pace we can optimise utilisation of fat. Faster speeds require aerobic utilisation of glycogen and even faster speeds and accelerations require additional breakdown on glycogen to lactate. The difference between aerobic and anaerobic glycogen breakdown are that the switching on and off of anaerobic production is rapid. At a medium speed canter, acceleration to gallop causes a surge in glycogen breakdown to lactate. If the speed is fast enough, lactate will still continue to be produced to supplement aerobic glycogen breakdown. If the pace is slowed back to canter, there is a rapid response and if this intensity does not require anaerobic glycogen breakdown to lactate, then this will be turned off within a matter of seconds. The switch between aerobic metabolism of fat and aerobic metabolism of glycogen is much different situation. If a horse has been exercising at trot for 30-40 min, the rate of ATP regeneration from fat will probably be at its maximum. If the horse accelerates, resulting in an increase in the contributing from glycogen and then slows back to a trot, the return to utilisation of fat at the previous rate may take 10-20 minutes or longer. Therefore to preserve glycogen stores as much as possible in prolonged exercise, particularly in sports such as endurance, it is essential to avoid too many sudden and dramatic changes in pace. Of course it may not be possible to maintain exactly the same pace for say 10 hours or even 10 min, but one should aim for as regular and steady rhythm as possible.
Effect of Diet & Time of Feeding
There is evidence from both human and horse studies that eating a diet high in fat increases the ability to use fat during exercise. In human athletes, a high fat diet has also been shown to have a detrimental effect on the ability to perform moderate to high intensity exercise. This should not be a surprise as of course moderate to high intensity exercise relies on a combination of aerobic and anaerobic glucose and glycogen breakdown. If the RER is 1.0 or above, very little or probably even no energy for regeneration of ATP is coming from fat. However, it is interesting to note that no human athlete would choose a high fat diet, even a marathon runner consumes a diet rich in mainly carbohydrate with very little fat. Perhaps the only exception are Sumo wrestlers!!!!
However, there is a problem in using the term high-fat diet. If we wanted to feed a person a high fat diet, we could choose to eat foods like cream, chocolate, cheese and corned-beef. We might be able to reach a point where around 75% of our calories were coming from fat. Because we are omnivores, we can tolerate quite wide variations in dietary energy source. A meal for a human athlete during training might consist of around 75% or more carbohydrate. In contrast, the horse being a herbivore with a small-stomach and relying heavily on bacterial fermentation for the digestion of fibre, is much less tolerant of changes in dietary composition. So a normal fat content in a horse diet might be 7-8% and a high fat diet might be considered to be 15-20%. Above this the horse may suffer from digestive disturbance (e.g. diarrhoea, colic). We should therefore not be surprised that the horse has and can only tolerate a relatively low fat diet, that the horse normally has quite a low % bodyfat and that they rely primarily on carbohydrate at rest and during most types of exercise. However, there is evidence that feeding a horse an increased amount of dietary fat (up to around 15%) can improve the utilisation of fat during exercise, provided that the exercise in question is of low enough intensity. Once heart rates increase to above around 180 b.p.m. and RER rises above 1.0, even a horse that has been fed a high fat diet for many months during training cannot continue to use fat. Fat is high in energy, but the release of the energy is slow. This is why it will only support low-moderate intensity exercise to any appreciable extent.
One of the things to avoid as far as diet is concerned is to start exercise with a high blood glucose. For a human athlete, eating something high in sugar 10-15 min before exercise would have a negative effect on performance. If exercise is started with a high blood glucose, insulin is released and blood glucose drops. A second effect is that adrenaline will be released, causing a shift towards glycogen utilisation, even during low-intensity exercise. The same is true for horses.
What and when should horses be fed in relation to the start of exercise? If the concentration of free fatty acids (FFA) in the blood can be elevated by dietary means (e.g. fasting or feeding hay only), this may cause a shift towards utilisation of fat. However, there appears to be tremendous variation between horses in their ability to use fat during exercise. In one study, the horses that produced the highest amounts of lactate and had the highest proportion of type IIB fibres showed almost no change in RER during low-moderate intensity exercise when plasma FFA concentration was increased before exercise. However, horses with a high proportion of type I and IIA fibres and few IIB fibres did show an increased utilisation of FFA (lower RER).
In most circumstances we would want to avoid starting exercise with an elevated blood glucose concentration for reasons explained previously. One way of achieving this is overnight fasting after a final feed of hay (i.e. no hay or grain on the morning of exercise). Of course we may decide that fasting a horse is not a good option because of the possible risk of gastric ulcers or colic. Feeding hay only has little effect on blood glucose concentration. In contrast, feeding grain only can cause a marked increase in blood glucose concentration for 2-4 hours after feeding. Feeding grain with hay is better than grain alone, provided the grain is given either after or at the same time as the hay and 4-6 hours before the onset of any exercise. However, grain and grain and hay (whether restricted or ad libitum) all increase plasma glucose in the post-feeding period more than hay or fasting and may affect other responses to exercise, including elevated heart rate and or lactate.
Therefore to avoid increasing plasma glucose prior to exercise and considering that fasting may induce anxiety/excitement or colic or gastric ulcers, the most favourable management strategy would be to provide a restricted volume of hay (i.e. normal or reduced volume as opposed to ad libitum access) around 4-6 hours before the start of exercise. During this period the horse should have ad libitum access to water.
Exercise in the horse is almost never, if ever, limited by the bodies stores of fat. In contrast, prolonged low-moderate intensity and high-intensity exercise can frequently be limited by muscle glycogen stores. The horse, both at rest and during exercise, relies more on glycogen than we do. The horse’s natural diet (grass!!!) contains very small amounts of fat. Even the traditional hay/grain diet is low in fats and high fat diets for horses may only result in a total fat intake of 15%. Higher amounts than this are poorly tolerated. Ensuring optimal glycogen stores before exercise and riding in a way that does not “waste” glycogen, especially in moderate to prolonged duration exercise, may contribute to acceptable or expected performance. Factors such as breed, age, muscle fibre composition, training, diet, feeding practices prior to competition, riding strategy, fitness and competitive demand can all interact to determine the balance between fat (aerobic) and glycogen utilisation (aerobic & anaerobic). This knowledge should help us understand how what we feed, when we feed it and how we manage and ride our horses can affect their performance.
Suggested Reading Marlin and Nankervis, Equine Exercise Physiology, Blackwell Wilmore, J.H. and Costill, D.L. Physiology of Sport and Exercise. Human Kinetics, PO BOX IW14, Leeds, LS16 6TR, UK Lawrence, L. Nutrition and the Athletic Horse in: The Athletic Horse, Hodgson, D.R. and Rose, R.J. (eds), W.B. Saunders Company. Duren, S.E., Pagan, J.D., Harris, P.A. and Crandell, K.G. (1999) Time of feeding and fat supplementation affect plasma concentrations of insulin and metabolites during exercise. Equine Vet J Suppl. 30, 479-484 Pagan, J.D. and Harris, P.A., (1999) The effects of timing and amount of forage and grain on exercise response in Thoroughbred horses. Equine Vet J Suppl. 30, 451-457 Pagan, J.D. (1997) Gastric ulcers in horses: A widespread but manageable disease. World Equine Vet Review, 2 28-30.