Download FOOD FOR FUEL!

 Copyright David Marlin 2007. All rights reserved.
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
 Copyright David Marlin 2007. All rights reserved.
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
 Copyright David Marlin 2007. All rights reserved.
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-1phosphate 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
 Copyright David Marlin 2007. All rights reserved.
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.
 Copyright David Marlin 2007. All rights reserved.
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 mitochodrial
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
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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
0.71
0.75
0.80
0.85
0.90
0.95
1.00
% Carbohydrate
0
15.6
33.4
50.7
67.5
84.0
100.0
% Fat
100
84.4
66.6
49.3
32.5
16.0
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
 Copyright David Marlin 2007. All rights reserved.
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 reninangiotensin-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
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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
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
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).
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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.
Blood Lactate (mmol/l)
8
Unfit (Un-trained)
VLA4 = 6 m/s
6
Fit (Trained)
VLA4 = 10 m/s
4
2
0
2
6
10
14
Speed (m/s)
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
 Copyright David Marlin 2007. All rights reserved.
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
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.
% Fibres Recruited
100
80
IIB
60
IIA
40
20
I
0
Stand
Trot
Canter
Gallop
 Copyright David Marlin 2007. All rights reserved.
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
 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.
 Copyright David Marlin 2007. All rights reserved.
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.
Summary
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.
 Copyright David Marlin 2007. All rights reserved.
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.