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Equine Exercise Physiology

David MarlinAnimal Health Trust

Kathryn NankervisHartpury College

BlackwellScience

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First published 2002Reprinted 2003

Library of CongressCataloging-in-Publication DataMarlin, David.

Equine exercise philisophy/David Marlin, KathrynNankervis.

p. cm.ISBN 0-632-05552-91. Horses–Training. 2. Horses–Exercise. I. Nankervis,

K.J. II. Title.SF287 .M34 2003636.1¢0835–dc21

2002026041

ISBN 0-632-05552-9

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Foreword v

Acknowledgements vii

Part I The Raw Materials 1

1 Introduction 32 Energetics of exercise 73 Muscles 214 Connective tissue 355 The respiratory system 426 The cardiovascular system 55

Part II Exercise and Training Responses 73

7 Muscular responses 758 Skeletal responses 869 Respiratory responses 94

10 Cardiovascular responses 11311 Aspects of physiological stress and fatigue 12712 Thermoregulation 13313 Introduction to biomechanics 151

Part III Applications of Exercise Physiology 165

14 The demands of equestrian sport 16715 Training principles 18016 Training facilities 18917 Practical training 19818 Exercise testing 21119 Indicators of performance 24520 Feeding performance horses 26121 Transport 276

References 285

Further reading 290

Index 291

Contents

Foreword

The training of competition horses has changed a great deal over the last few decades,for example with the introduction of the all weather gallop and the ‘interval’ methodof training for staying horses.

This book explains the scientific reasoning behind the training of horses for com-petition in a manner that those working with horses will comprehend. It explains whytraining methods succeed and, just as importantly, if your horse is over stressed whythose methods might fail.

The trainer of today’s horse is presented with a different set of problems from thoseof yesteryear. Arguably the competition is now tougher, which puts a horse undergreater stress, and trainers are presented with ever more information about the con-dition of their horses – blood tests, food analysis and so on. We need to have at thevery least a basic understanding of these factors if we are to make rational decisionsabout what is best for our horses. This book will help you understand how to manageyour competition horse in today’s environment.

Equine Exercise Physiology is a readable, up-to-date account of how to achieve thehighest standards in your competition horses. It will suit all horse enthusiasts and stu-dents, as well as experienced trainers.

Peter Scudamore

The authors would like to thank the following friends and colleagues for commentson various chapters within this book: Rachel Neville (Chapters 2 and 20), Dr StephanieValberg (Chapters 3 and 7), Dr Rachel Murray (Chapters 4 and 8), Dr Bob Colborne(Chapters 4, 8 and 13), Dr Colin Roberts (Chapters 5, 9 and 18), Dr Lesley Young (Chapters 6 and 10), John Robertson and Rod Fisher (Chapter 14), Dr CatherineDunnett (Chapter 20), Matthew French at Hartpury College for assistance in the pro-duction of the figures and Dr David Evans, Equine Performance Laboratory, Univer-sity of Sydney, for providing Fig. 18.10.

Cover photo: Courtesy of Dr D.J. Marlin.

To Roma and George (DM)

To Tom (KN)

Acknowledgements

Part I

The Raw Materials

Chapter 1

Introduction

Much of what we currently understand aboutequine exercise physiology has been established inthe last 20 to 30 years, largely as a result of anincreased scientific and veterinary interest in exer-cise physiology, improvements in technology, andavailability of equipment such as high speed tread-mills. High speed treadmills enable vets and scien-tists to study the horse in controlled situationswhere the speed, distance, slope, going and envi-ronmental conditions can all be closely regulated.In addition, with a horse exercising on a treadmillit is a very simple matter to collect a blood samplefrom a catheter in an artery or vein, or to measurehow much oxygen the horse is using. Proceduressuch as these are either difficult or at present not possible to undertake in the field. Inevitably,running on treadmills is not the same as runninground a racetrack or a cross-country course, but ithas enabled scientists to make great advances in the study of the horse’s responses to exercise andtraining. Many of these advances can now easily beapplied to the management and training pro-grammes of our own competition horses with agood degree of success. Whilst science cannot guar-antee a winner, it may well shorten the odds in ourfavour.

What are the aims of a training programme?

What exactly are we trying to achieve as a result oftraining? The fundamental purposes of any trainingprogramme are to:

(1) Increase the horse’s exercise capacity(2) Increase the time to the onset of fatigue(3) Improve overall performance, by increasing:

— Skill— Strength

Why train?

In theory and in practice, the horse must surely beconsidered the best all round athlete of the animalkingdom. Horses are not great thinkers or fighters,they are runners. Whatever the breed or type ofhorse, they are all blessed with the same basic structure and the same basic physiological mecha-nisms; therefore they all have the potential torespond favourably to training. A horse’s perfor-mance, i.e. how fast it runs, how high it jumps, islargely determined by its natural ability, and to alesser extent by its level of training. Natural abilityis determined mainly by the genes the horse inher-its from its parents (Fig. 1.1). We can’t do anythingabout the genes an individual horse has once it hasbeen born, but we can do something about thetraining. To reach a horse’s genetic potential forperformance, whether it is aimed at local riding clubevents or the Derby, it must be fit! From the unfitto fit state the horse undergoes a metamorphosisand its shape, its gaits, its looks, often even its attitude to life, are altered. Whatever we strive toachieve with our horses, there is much to be gainedby making sure that they are fit enough for the task. To compete on an unfit horse puts both you and your horse at risk, quite apart fromdecreasing your chances of success and also thelikelihood of the two of you going on to competeyear after year.

Horses are always huge investments in terms ofboth time and money. If you aim to compete at anylevel, it pays to improve the horse’s chances of com-pleting the work goals without risking mechanicalbreakdown and so incurring large veterinary bills,long periods of rehabilitation at best and destruc-tion at worst. There is no doubt that training is anart, but a little understanding of the physiology ofthe horse can help anyone perfect their own art.

— Speed— Enduranceor all four of these

(4) Decrease the risk of injury.

By analysing the adaptations the horse makes in theshort term (during exercise) and in the long term(throughout training) we can begin to understandhow to design the horse’s work programme toachieve these aims (Fig. 1.2).

Exercise, work, training, fitnessand performance

First of all, let’s tackle the vocabulary of ‘exercisephysiology’. Being associated with horses entitlesyou to become a member of a club that has its ownlanguage, a language which is only understood bythose ‘in the know’. Consider some of our expres-sions: we talk about grey when we mean white; we‘break’ horses when we are introducing them tobeing ridden; a three-day event can be held over 4

days. What chance do outsiders have? Scientistsalso have their own language, one that is universalamongst all sorts of them, such as biochemists,geneticists, physiologists, etc. To be able to translatethe results of scientific studies and apply them to real-life training situations we need to becomefamiliar with the scientific vocabulary associatedwith equine exercise physiology.

Physiology is the study of the function of cells,tissues, organs and whole systems. Exercise physi-ology is thus the study of all systems involved inexercise. Exercise is a good example of a word com-monly used in completely different contexts by scientists and horse people. Horse people often dif-ferentiate between lungeing a horse either for exer-cise or for work. The horse person’s interpretationof this is that by lungeing for exercise you aremerely allowing the horse to ‘stretch its legs’ on theend of the lunge line, but it is not asked to do any-thing too taxing. Lungeing a horse for work meansthat it would probably wear side reins or maybe a ‘gadget’, e.g. a pessoa, and would be asked toengage its hindquarters and carry itself in a correctoutline. To a scientist, work refers to the energyused up when an object moves a known or fixed dis-tance; the amount of work done is described interms of the energy used and is commonly mea-sured in units such as joules (J) or kilojoules (kJ),or calories (cal) or kilocalories (kcal). A force hasto be applied in order to perform work, and thisforce requires energy to be expended. Thereforethe horse is doing work simply by moving from Ato B. In scientific circles, ‘work’ does not infer any-

4 Equine Exercise Physiology

Fig. 1.1 A horse’s performance is largely determined by thegenes the horse inherits from its parents.

SpeedQuarter horse

Eventer

Showjumper

Strength

DressageEnduranceracing

Endurance(stamina)

‘Stayer’12 furlongs

‘Sprinter’5 furlongs

Fig. 1.2 Requirements for speed, strength and endurance ina range of equestrian sports.

thing about the quality of the movement (i.e. speed,distance or direction), simply that something hasmoved. In fact, in strict scientific terms, it takes thesame amount of energy to move a horse from A toB at a walk as it does at the gallop: the differenceis in the rate at which energy is used. The sameamount of energy is required to move from A to B,regardless of the speed, but when the horse movesat the gallop, the rate of energy utilisation must begreater. The rate of energy usage is referred to interms of power. Power is measured in terms of therate of work done (units of energy per unit time),e.g. in joules per second or watts. In galloping fromA to B, the horse must generate more power thanif he walks from A to B. Exercise refers to anymovement or activity, so as soon as the horse movesoff from a standstill, it is performing exercise. Touse our scientific terms, if the horse is exercising,work is being done.

Training is another term that may have differentinterpretations depending upon the context inwhich it is used. To horse people, ‘training’ oftenimplies that the horse is learning: its ‘basic training’is its basic education. To an exercise physiologist,training is a long-term process of repeated bouts ofexercise, which results in an improvement in fitness,where fitness refers to a certain capacity for exer-cise. Training for improvement in fitness is some-times also referred to as ‘conditioning’, particularlyin the USA.

Throughout exercise and training, the horse’sbody should make certain physiological adjust-ments, adaptations or responses. An exercise re-sponse is any short-term physiological adaptationthat is made as a result of an increase in the levelof muscular activity, whilst a training response is along-term physiological adaptation to repeatedbouts of increased muscular activity. Exercise re-sponses tend to return to baseline levels after thework is done. For example, during exercise there is an increase in heart rate, corresponding to theintensity of the work done. When the horse stopsexercising, the heart rate will gradually return toresting levels. Training responses are more longlasting and are maintained as long as the horse con-tinues to regularly undertake a certain volume ofwork. For example, a training response may be anincrease in heart mass (weight) or an increase in the

number of capillaries (small blood vessels) aroundeach muscle fibre. Changes such as these occur overa period of time as the horse responds to a gradualincrease in workload, but they do not changethroughout the course of an exercise bout. Trainingchanges are mainly mediated through activation ofgenes that may then ‘code’ for greater productionof an enzyme in an aerobic energy pathway, forexample.

The type of work undertaken is particularly im-portant in determining whether or not a trainingresponse is induced. For example, walking a horse16km (10 miles) a day, 3 days a week for a monthmay produce a noticeable loss of body mass (body-weight) as the horse will be using up a considerableamount of energy on each of these walks. However,it may do very little in terms of increasing fitness,i.e. producing a training response. When we thinkabout training it is therefore not simply how muchenergy we use, i.e. the volume of work, that countsbut the way in which that work is done, i.e. thequality of work, to induce appropriate trainingresponses.

In summary, if we want to improve our horse’sperformance, we would do well to increase theirfitness (Fig. 1.3). This can be done by carrying outregular exercise, of progressively increasing workloads, to bring about the necessary trainingresponses. The key is knowing what is the rightwork for what sport and when to settle for less than100% fitness to reduce the risk of injury that mightcome from training very hard for a long time.

Introduction 5

Performance

Fitness

Training

Fig. 1.3 Training leads to an increase in fitness and animprovement in performance.

• Horses are natural athletes.• Probably the biggest impact we can have on how

well a horse performs is through training.• The aims of training are to increase the time to

the onset of fatigue, improve performance anddecrease the risk of injury.

• Physiology is the study of the function of cells,tissues, organs or whole systems.

• Exercise means that work is done and so by definition energy is used.

• Exercise responses, e.g. an increase in heart rate,are short term.

• Training is a longer process of many repeatedbouts of exercise that brings about an increase infitness.

• Training responses, e.g. an increase in heart size,occur over a relatively long period of time.


KEY POINTS

Chapter 2

Energetics of exercise

the majority are more likely to be converted to fuelstores within the liver, muscle and adipose tissue(fat) to be used at a later date. Regardless of thetype of feed we put into the horse, all the nutrientscapable of releasing energy for work (glucose, fattyacids and amino acids) are ultimately converted tojust one vital ingredient – ATP or adenosinetriphosphate. ATP is our energy ‘currency’ that isrequired for normal functioning of all cells both atrest and during exercise.

The resting horse

A certain amount of fuel must be provided withinthe diet to support the horse’s energy requirementsat rest and to do so whilst maintaining its bodymass. Within 1 or 2 hours of a meal, particularly acereal meal, the levels of glucose in the horse’sblood rise from about 5 millimoles per litre(mmol/l) of blood to about 7mmol/l of blood. Inresponse to this increase, the pancreas increases thesecretion of insulin, a hormone that acts to decreaseblood glucose, and several hours later the bloodglucose levels are restored to 5mmol/l. Insulinbrings about a lowering of blood glucose by increas-ing the uptake of glucose into the muscle and liver.In other words, in times of plenty the emphasis ison accumulation of potential fuel sources withinthe liver and muscle. This ensures that muscle hassufficient fuel stores should there be an increase inmuscle activity, and also that the liver has sufficientfuel stores to ‘buffer’ fluctuations in blood glucosearising as a result of exercise. Whilst glucose has avery important role in providing energy for muscu-lar contraction, it is far more important from aphysiological ‘housekeeping’ perspective to ensurethat the brain and the heart are provided withglucose, because glucose is the primary fuel sourcefor these vital organs. One of the most important

Introduction

A little knowledge of biochemistry is a powerfulthing! When you first become aware of the cellularprocesses involved in the conversion of nutrientsinto mechanical energy for muscle contraction it islike an enormous penny dropping, making so muchof what the nutritionists tell us fall into place. Forperformance horses, one of the most important considerations is the energy content of the diet.To make sure our horse has enough energy forexercise, it helps to understand something aboutthe way the horse’s muscles obtain energy fromnutrients within the diet, and this forms the basis ofthe study of the energetics of exercise. Awarenessof the energetics of exercise can help us formulatea diet to achieve a specific result. As far as inter-pretation of energetics is concerned, the horse isnot dissimilar to a car: we input fuel at greatexpense and we expect a certain performance interms of mechanical output. The horse, like thepetrol engine in a car, is required to performmechanical work. Unlike cars, however, the horsecan run on a variety of fuels, and we can expect tosee a difference in performance depending uponthe type of fuel we put in.

Horse diets usually vary from being 100%forage-based to about 80% cereal-based. Weshould never feed a 100% cereal-based diet tohorses, because they need a certain minimumamount of forage for effective functioning of thedigestive tract. Consequently, most horses are fed acombination of forage and cereals which has to bebroken down by a combination of mechanical,chemical and microbial digestive processes. Theproducts of digestion are then absorbed into thebloodstream mainly from the small and large intes-tine. Some of these products may be used immedi-ately to supply energy for muscular contraction, but

functions of the liver, aided by a number of hor-mones, is to act as a ‘glucostat’, i.e. a regulator ofblood glucose, ensuring that blood glucose does notsignificantly decrease or increase, thereby guaran-teeing a constant supply of glucose for the brainand heart, regardless of whether the horse is fed,starved, exercised or rested.

The energy for muscle contraction

Energy cannot be created or destroyed: it is merelyconverted from one form into another. All animalsconvert chemical energy from food into mechani-cal energy of work and heat is given off as a by-product. No process of converting stored orpotential energy into work or movement is 100%efficient. In fact, animals (including humans) arerather inefficient energy converters, with onlyaround 20% of the energy obtainable from foodbeing converted into useful work, i.e. used formovement by muscle, and the rest (about 80%)being released as heat. To put this in context ofmechanical engines, modern car engines would beable to convert around 20–30% of the potentialenergy in petrol into movement.

Adenosine triphosphate (ATP) is the universalfuel source: it has to be produced and stored withinall cells in the body, whether muscle cells or anyother cell, because it cannot be transported aroundthe body. ATP is stored throughout the muscle cell.The structure of ATP is shown in Fig. 2.1. It is madeup of adenosine attached to ribose and three phos-phate groups. Only a certain amount of ATP canexist within the muscle: this is approximately 6mmol/kg wet muscle (equivalent to 24mmol/kgdry muscle) or approximately 700g throughout allthe skeletal muscle in the body of a 500kg horse.

ATP provides a chemical energy source that isused by all cells, in all animals. Muscles cannot con-tract or even relax without ATP being present.When muscle cells contract, ATP is broken downinto adenosine diphosphate (ADP) and phosphate(see Fig. 2.1), a reaction that is triggered by anenzyme within the muscle cell called adenosinetriphosphatase (ATPase). The breakdown of ATPto ADP releases a fixed amount of energy – exactly1.8kJ per mole of ATP. To give some idea of the

enormous rate of ATP regeneration, consider thatthe average person turns over (breaks down andrestores) more than half their own bodyweight inATP in a day, just at rest. An active horse may actu-ally turn over four times their own bodyweight inATP per day. The chemical breakdown of fuelstored within the muscle ensures that this enor-mous demand for ATP is met.

The main fuels used to provide energy areglucose, glycogen (both glucose and glycogen areforms of carbohydrate) and fatty acids (fat).Protein is only used to provide energy in cases ofextreme exhaustion, starvation or disease. Glucoseand fatty acids both circulate in the bloodstreamand can also be easily taken up or released bymuscles. Glycogen is the animal equivalent ofstarch in plants and is simply a long string ofglucose units joined together. Because of its struc-ture and size, glycogen in cells cannot leave andenter the bloodstream. The main sites of glycogenstorage are within liver and muscle.

The conversion of food intouseful energy for exercise

Muscle contractions can only be produced usingATP. Because only a small amount of ATP existswithin the muscle and this is rapidly used up during


ATPase

P P P

adenine

ribose

P P P

adenine

ribose

Energy

Fig. 2.1 Adenosine triphosphate breakdown to adenosinediphosphate.

exercise (in fact within one or two muscle contrac-tions), to continue working the muscle must con-stantly regenerate ATP by phosphorylating ADP toensure a constant release of energy. The phospho-rylation of ADP is achieved by several differentbiochemical processes or energy pathways withinthe muscle cell, all of which require the input ofnutrients or fuels. One way to look at this would beto think about electricity and gas which are two dif-ferent forms of energy or fuel. Electricity could beproduced from a gas turbine generating station, butwe can only light a bulb using electricity not gas.ATP is the equivalent of electricity, whereas gas isthe equivalent of all the other potential fuels suchas glucose, glycogen and fat. You may wonder whywe cannot simply stick the phosphate back on tothe ADP to regenerate ATP. To do so would be liketrying to send the reaction uphill against an energygradient: if it were possible to recycle ATP in thisfashion, there would be no need to obtain energyfrom our diet and exercise could continue indefi-nitely. Simple recycling is not an option, and if wedo not want to deplete our stores of ATP, we mustutilise fuel supplies. Ideally, we should aim to regen-erate ATP as fast as it is being used up by muscu-lar contractions. The faster an animal travels, thegreater the rate of ATP consumption by themuscles and the more quickly it needs to regener-ate ATP from ADP to match demand to supply.Whilst regeneration of ATP from ADP is importantto maintain a high ATP concentration, it is alsoimportant to keep the ADP concentration lowbecause an increase in free ADP may contribute tomuscle fatigue.

The energy demands of a single bout of exercisecan significantly deplete a horse’s fuel stores;however, on a day-to-day basis, the food providedin the horse’s diet should keep the main carbohy-drate and fat stores stocked up. Carbohydrates andfats are stored within the liver, skeletal muscle andadipose tissue. Glucose (a carbohydrate) is storedas glycogen within the liver and skeletal muscle,whilst fatty acids (fat) are stored as triglycerideswithin liver, muscle and adipose tissue, e.g. aroundthe withers, crest, loins and around internal organs.A certain amount of fuel is available within thebloodstream, in the form of glucose and free fattyacids. The primary fuel supplies for any given pieceof exercise are normally provided by glycogen

within the muscle and free fatty acids from thebloodstream. Fuel stores within the liver andadipose tissue are used to top up the muscle storeswhen demand for energy is substantially increasedas a result of exercise of either high intensity orlong duration.

Energy pathways

There are several biochemical routes for phospho-rylation of ADP, otherwise known as ‘energy path-ways’, and one or more of these pathways will beautomatically selected within any particular periodof exercise. However, it is important to understandthat the pathways available are not used on an allor nothing basis and that a number of differentpathways may be used simultaneously for generat-ing energy. The different pathways vary in their fueleconomy, i.e. in how much ATP is released per gramof fuel broken down, and also in their ‘perfor-mance’, i.e. how quickly ATP is made available forcontraction. There is no one energy pathway thathas both a high ATP yield, i.e. is economic, and ahigh rate of ATP production, i.e. a high perfor-mance. The horse will therefore select a particularcombination of energy pathways depending on thenature of the exercise and the state of its fuel stores.There are four basic energy pathways, two requir-ing oxygen (aerobic energy pathways) and two thatdo not require oxygen (anaerobic energy path-ways). It is important to understand that the twoanaerobic pathways are not only used in situationswhen there is no oxygen around. They are calledanaerobic because they do not need oxygen, butthey may be used when there is a plentiful supplyof oxygen to the muscle.

Pathway 1: anaerobic phosphorylation of ADP using high energy phosphatestores in muscle

High energy phosphates include molecules such asphosphocreatine (PCr) that have high energy phos-phate bonds. In other words, the energy is boundup in their structure. If these molecules can bebroken down, the energy stored within their bondsbecomes available for the regeneration of ATPfrom ADP. The production of ATP from ADP using

Energetics of Exercise 9

PCr is catalysed by creatine phosphokinase (CK orCPK), and is described by the chemical equation

PCr + ADP Æ Cr + ATP

Phosphocreatine thus provides a quick method ofregenerating ATP for use by the muscle. By ‘steal-ing’ a phosphate from PCr, ATP is very quicklyregenerated within the muscle cell. Phosphocrea-tine stores can be used in this way to regenerateenough ATP rapidly, but there is only enoughstored PCr to last for several seconds’ exercise.Earlier we learned that the concentration of ATPin the horse’s muscle is around 6mmol/kg wetmuscle, but the amount of stored PCr is around15–20mmol/kg wet muscle. However, it is impor-tant to emphasise again that the muscle cells cannotuse the energy bound in the phosphate bond in PCrdirectly, but only after it has been transferred toATP.

In certain circumstances, another reaction knownas the myokinase reaction (named after the enzymecatalysing the reaction) may take place. This reac-tion occurs when the rate of breakdown of ATP isvery fast, such as during acceleration or galloping,and the concentration of free ADP within themuscle fibres (cells) starts to increase. In thisinstance, ADP is the high energy phosphate, butalso like PCr, it cannot be used directly by themuscle cells. However, when two ADP moleculesare combined, one ADP effectively loses a phos-phate (producing a molecule of adenosinemonophosphate, AMP) whilst the other ADP gainsa phosphate to become ATP. The chemical equationfor this reaction is

ADP + ADP Æ ATP + AMP

The myokinase reaction normally only occursduring high intensity exercise and then primarily inthose muscle fibres which are recruited during highspeed exercise, acceleration and jumping. Reac-tions such as this are often self-limiting in that ifthere is a build up of, in this case, AMP, the reac-tion from left to right will slow down. Becauseincreases in ADP may be related to the fatigueprocess in high intensity exercise, the aim would beto try and keep the ADP low by removing it as fastas it appears. To do this, the muscle also needs a wayto remove the AMP: this is carried out by theenzyme AMP deaminase. AMP deaminase con-

verts AMP to inosine monophosphate (IMP) andammonia.

All these reactions regenerate ATP quickly andwithout the use of oxygen. High energy phosphatessuch as PCr are used at the onset of exercise or foran explosive effort such as in a jump, or wheneverspeed of ATP regeneration is the primary require-ment. The stores of ATP and PCr are small; there-fore to sustain exercise for more than merely a fewseconds, the body must switch to other energy path-ways to regenerate ATP for muscle contraction.Once other forms of energy production have takenover, the high energy phosphate stores will them-selves be replenished if exercise is of low tomedium intensity. During higher intensity exercisethe muscle ATP and PCr concentrations may bereduced by 50–70% by the end of the exercise boutas a result of decreases in muscle pH consequent tolactic acid production (see later).

The following two energy pathways (see path-ways 2 and 3) involve the breakdown of fuel storesto support exercise lasting from several minutes tomany hours. Fuel stored in the form of fat and car-bohydrate can be broken down aerobically, i.e. inthe presence of and requiring oxygen, to producesignificant amounts of energy in the form of ATP.Glycogen (a carbohydrate) is a very large polymer(many strings of glucose molecules) of glucoseresidues and is the animal storage form of glucose(equivalent to starch in plants). By storing glucosein the form of glycogen, energy from glucose isavailable between meals. The glycogen moleculesthemselves vary enormously in size, existing in cellsin the form of glycogen granules that cannot passout of the cell into the bloodstream.

Pathway 2: aerobic (oxidative)phosphorylation of ADP usingcarbohydrate stores

The breakdown of glycogen within the muscle usingoxygen involves several stages, with oxygen playinga part only in the final stage. The first stage of thebreakdown involves the conversion of glycogen topyruvate, which occurs in the cytoplasm of themuscle cell and without the involvement of oxygen.The conversion of glycogen to pyruvate involves a specific sequence of phosphorylating reactionsknown as glycolysis (see Fig. 2.2). Glycolysis itselftakes place rapidly but only yields a small amount


of ATP directly (three ATP molecules per glucoseunit broken down from carbohydrate stored withinthe muscle, i.e. from glycogen). However, moreimportantly, glycolysis produces two molecules ofpyruvate that are used to feed into the next stageof the aerobic energy pathway, ultimately yieldingconsiderably more ATP. Up to this stage, all reac-tions have taken place in the cytoplasm of themuscle cell.

The next stage in the aerobic breakdown ofglycogen is the conversion of pyruvate to anotherthree-carbon structure known as acetyl coenzymeA (acetyl CoA). This reaction only occurs insidemitochondria and is catalysed by an enzyme calledpyruvate dehydrogenase (PDH). Mitochondria arefound throughout the muscle cell, but particularlyaround the myofibrils (see Chapter 3). Mitochon-dria are specialised structures with an outer mem-

brane and an inner folded membrane on which theenzymes of oxidative phosphorylation are located.The folding of the membrane increases the surfacearea available for reactions to take place. Thenumber of mitochondria within a cell or tissue is anindication of its activity. Hence, the density of mito-chondria is high in both locomotory muscle andcardiac muscle cells. Acetyl CoA then enters thethird stage of the aerobic breakdown of glycogenthat occurs within the mitochondria. Acetyl CoAinitiates a series of reactions known as the tricar-boxylic acid (TCA) cycle (see Fig. 2.3), also some-times referred to as the Krebs cycle.

The net result of the TCA cycle is the productionof two molecules of ATP and two hydrogen ions.Two hydrogen ions are also produced by glycolysisand these hydrogen ions combine with the twocoenzymes nicotinamide adenine dinucleotide


ATP consumed

2 NAD+ consumed

ATP consumed

2ATP produced

2ATP produced

Hexokinase

Glycogenphosphorylase

Phosphofructokinase

Pyruvate kinase

Fructose 6-phosphate

Fructose 1,6 diphosphate

1,3-diphosphoglycerate ¥ 2

3-phosphoglycerate ¥ 2

2-phosphoglycerate ¥ 2

Phosphoenolpyruvate ¥ 2

Pyruvate ¥ 2

Dihydroxyacetonephosphate

Glyceraldehyde3-phosphate

Glucose 6-phosphate Glycogen

Glucose (from, blood)

Fig. 2.2 Glycolysis.

(NAD) and flavin adenine dinucleotide (FAD) toproduce NADH and FADH2. NADH and FADH2

enter the ‘electron transport chain’ (see Fig. 2.4) onthe inner mitochondrial membrane.

The hydrogen ions are then split into electronsand protons, and through a series of chemical reac-tions (‘electron transport’) ADP is regenerated toyield 34 molecules of ATP and the hydrogen ionsare eventually combined with oxygen to producewater. Because this process requires oxygen it canbe termed aerobic or oxidative phosphorylation.The production of water at the end of the chain has the advantage of ‘removing’ hydrogen ionsfrom the cell because these would make the insideof the cell acidic. Both glycogen and glucose can be

used in glycolysis. Glycogen would be obtainedfrom the muscles’ own glycogen stores whilstglucose would be obtained from the bloodstream.The process of glycogen breakdown is known asglycogenolysis and results in the formation ofglucose-1-phosphate. The breakdown of glycogen iscontrolled by an enzyme called glycogen phospho-rylase which has both inactive and active forms,termed a and b. Whilst glucose units from glycogenbreakdown end up as glucose-1-phosphate andafter conversion to glucose-6-phosphate can enterdirectly into the glycolytic pathway, glucose takenup into the muscle from the blood must first bephosphorylated, i.e. have a phosphate added tomake it into glucose-6-phosphate. This reaction iscatalysed by an enzyme called hexokinase andrequires a molecule of ATP to ‘donate’ a phosphate.The fact that glucose-1-phosphate is produceddirectly from glycogen breakdown saves an ATPbeing expended in the initial stages of glycolysis,and prevents leakage out of the muscle cell,because phosphorylated compounds, includingATP, ADP and AMP, cannot normally cross cellmembranes unless these have been damaged.Whether the glucose units come from blood glucoseor muscle glycogen, the first stage of glycolysis istherefore considered to be the production ofglucose-6-phosphate.

Complete aerobic metabolism (breakdown) ofone glucose unit from glycogen to water and carbondioxide (formed from the TCA cycle) yields 39 mol-ecules of ATP (three ATP from glycolysis, two ATPfrom the TCA cycle and 34 ATP from the electrontransport chain). The complete aerobic breakdownof glucose taken up by the muscle cell from the


CO2

CO2

Pyruvate

Acetyl CoA (2 carbon)

(6C) Citrate

Succinyl CoA (4C)

(4C) Oxaloacetate NADH

NADH

ATP

FADH2

NADH

Fig. 2.3 Tricarboxylic acid (TCA) cycle.

NADH/H+

NAD+

H2O

1/2O2

Oxidisedcarrier

Reducedcarrier

Reducedcarrier

Oxidisedcarrier

Reducedcarrier

Oxidisedcarrier

etc.

ATPATPATP

Fig. 2.4 Electron transport chain.

bloodstream yields one less ATP because one ATPmolecule is required to convert glucose to glucose-6-phosphate in the first stage of glycolysis. There-fore the net ATP yield from the aerobic breakdownof glucose is 39 - 1 = 38.

Pathway 3: aerobic phosphorylation ofADP using fatty acids

The aerobic breakdown of fat in the form of fattyacids begins with the conversion of 2-carbonchunks of fatty acid being converted to acetyl CoAby a process called beta-oxidation. In the break-down of fat, acetyl CoA is therefore not producedby glycolysis but by beta-oxidation. The mitochon-

drial stages of the breakdown of fat, i.e. the TCA(Krebs) cycle and the electron transport chain, arethus identical to those of glycogen, but the stepsleading to acetyl CoA formation are different. Aschematic overview of the stages of glycogen andfat breakdown is shown in Fig. 2.5.

The individual stages involved in the aerobicbreakdown of fat (as for carbohydrate) are alsoknown collectively as oxidative phosphorylation.The yield of ATP from fat is always higher than forthe same mass of carbohydrate (whether glucose orglycogen) but also varies between different types offat source. The fats stored within the body are in aform known as triglycerides that consist of one mol-ecule of glycerol and three fatty acid molecules. The


Glycogen Glucose

Glycolysis

Pyruvate

Acetyl CoA

CYTOPLASM

TCA cycle

CO2

NADH andFADH2

Electron transport chain

MITOCHONDRION

ATP H2O

b-oxidationof fatty acids

Fig. 2.5 Schematic overview of the stages ofglycogen and fat breakdown.

triglycerides are broken down by enzymes knownas lipases and the process is referred to as lipolysis.Once the fatty acids have been separated from theirglycerol ‘backbone’, they are free to move into thebloodstream and be taken up by muscle. In thisstate they are known as free fatty acids (FFA).Muscle itself also contains small triglyceride storesthat can also be broken down to liberate FFA thatcan be used inside the muscle cell. There are anumber of different FFAs found in the body whichdiffer primarily in the number of carbon atoms theycontain. Volatile fatty acids (VFAs) are anothervery important source of fuel, being produced fromthe fermentation of carbohydrates in the largeintestine. Once in the circulation VFAs can betaken up and used immediately to fuel muscle con-traction after conversion to ATP; if not, they arestored in adipose tissue as triglycerides.

The complete aerobic metabolism of palmiticacid (a typical 16-carbon fatty acid) with the mole-cular formula C16H32O2 yields 129 molecules ofATP net per molecule of fatty acid. The total pro-duction is 131 molecules of ATP, but two ATPs areused to ‘activate’ (prepare) the FFA before theycan enter the TCA cycle. Activation of FFA takesplace on the outer mitochondrial membrane beforeoxidative phosphorylation within the mitochondriathat results in a total of 35 ATP. Every time the fatty acid chain is shortened by two carbons, oneFADH2 and one NADH are formed, resulting inthe production of five ATP molecules by oxidativephosphorylation. In a 16-carbon fatty acid, the

chain is shortened by two carbons seven times toleave eight two-carbon pieces; hence 5 ¥ 7 = 35 ATP.The TCA cycle yields eight ATP molecules directlyand 88 by oxidative phosphorylation, totalling 131ATP minus two ATP for fatty acid activation, giving129 ATPs.

The fact that oxidative phosphorylation of fatyields about three times as much ATP as the oxida-tive phosphorylation of carbohydrate explains whyfat is referred to as an ‘energy-dense’ food source.With one molecule of fat yielding three times asmuch energy as one molecule of carbohydrate, youcan begin to see why exercising to lose fat oftenseems like an uphill struggle as you have to expendconsiderable amounts of energy at a relatively lowintensity, i.e. exercise over a longer time in order tobreak down excess adipose tissue. On the positiveside, the fact that fat is energy-dense is great newsfor endurance athletes, as a little bit of fat goes along way. Even a thin horse will only use a smallproportion of stored body fat to complete a 100-mile endurance race.

On a mass for mass basis, 1 gram of fat is betterthan 1 gram of carbohydrate when it comes to ATPyield, but the disadvantages of fat as a fuel are that,firstly, it requires far more oxygen to break downone molecule of fatty acid than it does to breakdown one molecule of glycogen. Secondly, thespeed (rate) of energy release from fat is muchslower than from carbohydrate (see Table 2.1).Exercise using fat as the main fuel source is there-fore limited to trotting and slow–medium speed


Table 2.1 Power, acceleration, oxygen requirement and capacity of the different sources of energy available to mammals(adapted from Sahlin (1985))

Maximum power Time to reach O2 requirement Work time (mmol ATP/kg/s) maximum power (mmol O2/ATP) to fatigue

AnaerobicATPa 11.2 <1s 0 secondsPCrb 8.6 <1s 0 secondsCHOc Æ lactate 5.2 <5s 0 minutes

AerobicCHOc Æ CO2 + H2O 2.7

2–3min0.167 hours

FFAd Æ CO2 + H2O 1.430min

0.177 days!!

a Adenosine triphosphate.b Phosphocreatine.c Carbohydrate.d Free fatty acid.

cantering. At speeds above this the body must grad-ually switch to using more and more carbohydrateto match the increased rate of ATP usage by themuscles with the rate of rephosphorylation of ADP.The faster a horse runs the less it is able to use fatas an energy source.

Pathway 4: anaerobic phosphorylation ofADP using carbohydrate

Technically, the conversion of ADP back to ATPusing phosphocreatine (pathway 1, describedabove) is an anaerobic energy pathway, but theoverall contribution of this energy pathway to thetotal energy cost of a bout of exercise is not usuallysignificant because most exercise bouts last morethan a few seconds. The most significant anaerobicenergy pathway involves the conversion of glyco-gen or glucose to lactic acid to yield ATP. Onlyglycogen or glucose can be used to produce energyanaerobically via the glycolytic pathway. The glycolytic pathway involves the production of pyru-vate from glucose or glycogen as in aerobic energyproduction, but this time, instead of the pyruvatebeing converted to acetyl CoA and entering themitochondria, the pyruvate is converted to lacticacid by the enzyme lactate dehydrogenase (LDH).Lactic acid immediately dissociates into a freehydrogen ion (with a positive charge) and a lactateion (with a negative charge). The two terms lacticacid and lactate are often used interchangeably,for example when referring to blood or plasma concentrations. Thus, the reactions involved in the aerobic and anaerobic productions of ATP areidentical up to the point at which pyruvate isformed. The net result of the anaerobic breakdownof carbohydrate is the production of a small amountof ATP (three ATP molecules if glycogen is theglucose source and only two ATP molecules ifblood glucose is used) and the conversion of NADto NADH. NADH is an important intermediary inglycolysis and one that would normally be regener-ated to NAD following the completion of the elec-tron transport chain in oxidative phosphorylation.Because there is no electron transport chain in theanaerobic pathway, the only way of regeneratingNAD from NADH to allow continued productionof ATP by glycolysis is as a by-product of the con-version of pyruvate to lactic acid. If all the NAD in

a muscle cell were converted to NADH then gly-colysis would stop. The production of lactic acidenables NADH to be regenerated to NAD andallows glycolysis to proceed beyond glyceraldehyde3-phosphate.

Pyruvate + NADH Æ Lactate + H+ + NAD

The anaerobic energy yield from one molecule of‘glucose’ from glycogen is three ATP molecules,whereas it is two ATP molecules for one moleculeof glucose from blood. Two molecules of lactate arealso formed which can be converted back to pyru-vate and eventually to glucose by a process knownas the Cori cycle. Because the anaerobic productionof energy involves the conversion of pyruvate tolactate, it can be seen that it would be impossible tobreak down fat anaerobically.

Anaerobic energy production isinefficient but fast

When you need energy fast, such as during accel-eration, when galloping or jumping, glycogen isbroken down anaerobically to lactic acid. A majordisadvantage of anaerobic energy production is thelow ATP yield per molecule of glycogen or glucose;therefore substantial reliance on anaerobic energyproduction leads to significant depletion of muscleglycogen stores (Fig. 2.6). Resting muscle glycogenconcentrations in the horse are in the region of 100mmol/kg wet muscle, and up to around 150mmol/kg wet muscle (600mmol/kg dry muscle)or more in trained horses. Muscle glycogen con-


Speed (m/s)

100

50

0

200

150

4 8 12 16Gly

coge

n ut

ilisa

tion

(mm

ol/k

gdm

/min

)

Fig. 2.6 Glycogen utilisation as a function of running speed.

centrations can be reduced by one-third after just a single bout of high intensity exercise. Fine! Gofast, use lots of glycogen, but if you want to do itagain in a few hours’ time, or tomorrow, and the dayafter, and the day after that, you may run intotrouble. The muscle needs a certain amount of timeto restore the glycogen levels to those before exer-cise. In man, it has been shown that by manipulat-ing the diet it is possible to both increase glycogenstorage before exercise (glycogen loading) and tospeed up glycogen repletion after exercise. So far,no one has managed to achieve the same in horsesand it doesn’t matter if after exercise you feed yourhorse hay, or hay and cereals, or even pure glucosepowder, the rate of glycogen repletion appears tobe the same.

The duration of exercise that you can undertakewhen using glycogen alone as the energy source islimited because fatigue is partly related to the acid-ification of the muscle cells by the free hydrogenions produced in the conversion of pyruvate tolactic acid. At the sort of rates of glycogen break-down seen during maximal all-out sprints, muscleglycogen stores can be reduced by around 50%.Even more glycogen can be used by carrying outrepeated bouts of short, fast exercise with recoveryperiods in between (often termed intermittent,high intensity exercise or intermittent, maximalexercise). However, as more and more lactic acid isproduced and the muscle pH becomes lower (moreacid), a feedback mechanism takes over to preventcomplete exhaustion of muscle glycogen stores. Therate of glycolysis slows and therefore so does therate of glycogen breakdown and lactic acid pro-duction. This process of fatigue is actually protec-tive. Whilst it is possible to completely use up allthe muscle glycogen present in those cells used themost during high intensity exercise, it is not possibleto deplete all cells in a muscle. Glycogen depletioncan also occur in endurance exercise, affectingthose cells used predominantly during low tomedium intensity exercise (see Chapter 3).

Energy partitioning

At the onset of maximal exercise the demand forenergy is high, but there is a lag time in reachingmaximal aerobic energy production. In otherwords, anaerobic pathways are often necessary to

supply energy for the early stages of exercise (eventhough there may be no shortage of oxygen in themuscle) whilst the aerobic pathways get up tospeed. It can take up to at least a minute to reachmaximal aerobic energy production at the start ofmaximal exercise. Thus the intensity of the exerciseand the nature of the onset of the high intensityexercise (gradual increase in speed to maximum orflat out from a standing start) have a bearing on theextent to which aerobic and anaerobic pathwayscontribute to the overall energy requirement.

During low intensity exercise of long duration(exercise producing heart rates up to around 160beats/min), energy is provided largely by aerobicpathways because these can produce ATP at a suf-ficient rate and offer the greatest fuel economy.During high intensity exercise of short durationenergy is provided by anaerobic pathways offeringhigh rates of ATP production but low fuel economy.However, there is not a point at which a directswitch from one source to the other occurs. At anypoint in time, some muscle fibres will be function-ing aerobically and some anaerobically, but there isa general increase in the reliance on anaerobicpathways as speed increases. At speeds greater than8–10m/s, i.e. 500–600m/min (around 20mph), themitochondria tend to back-up with substrate andthere is neither sufficient area of mitochondrialmembrane nor aerobic enzymes available to copewith demand. Latterly it was thought that theswitch was due to lack of oxygen availability, butthis is not usually the case. Oxygen delivery to theworking muscles is usually sufficient; the main driveto begin to recruit anaerobic pathways is the pointat which the aerobic energy pathways are workingat maximum, but demand for ATP is still rising, i.e.the horse is being asked to go faster. The resultantshortfall in ATP supply must be addressed usinganaerobic pathways resulting in an increase inblood lactate levels. The point at which lactatelevels start to rise in often called the ‘anaerobicthreshold’ (AT). This term is widely used among laypeople to describe the point at which anaerobicpathways begin to contribute significantly to totalenergy requirements, but it is a slightly misleadingterm in that it implies there is a switch from oneform of energy pathway to the other, which is nottrue, as described above.

The contribution of each energy pathway to thetotal energy requirement for exercise is known as


energy partitioning. Scientists have been able toestimate how much each pathway contributes to thetotal energy requirements by measuring oxygenuptake and carbon dioxide and lactic acid produc-tion at various speeds of exercise. In the UK, theshortest distance raced is 5 furlongs or 1000 metres.In the USA, Quarter horses run over 2 furlongs or400m: these are the true sprinters of the horseworld, reaching speeds of around 40m.p.h. Duringexercise of this intensity and duration, the horse willobtain approximately 60% of its energy anaerobi-cally and 40% aerobically. Compare this to humansprinters who run 100 metres near 100% anaerobi-cally; only taking one or two breaths in 10 seconds.In contrast, the true equine sprinters, the Quarterhorses, are running for at least double this time. In amiddle distance Thoroughbred horse race such asthe Derby run over 11–2 miles (2.4km), the energypartitioning would be approximately 80% aerobicand 20% anaerobic.The anaerobic portion is mainlyrequired for the acceleration at the start and for thelast furlong or so.

The true endurance athletes of the horse worldare able to complete 100 miles (160km) in a day,travelling at speeds of 10m.p.h. (16km/h). Trueendurance horses will work about 96% aerobicallyat this speed. Even the speed and endurance day ofa three-day event is predominantly aerobic (about90%).

Normally, anaerobic energy production begins ata heart rate of around 150–180 beats/min, but thereis great individual variation. A heart rate of150–180 beats/min is the equivalent of a ‘good’ orthree-quarter speed canter. In other words, as soonas the horse starts to really open up the canterstride, it is likely that it is getting some of its energyby anaerobic means, with the resultant appearanceof lactic acid in the bloodstream.

Although it is possible to give general guidelinesconcerning the onset of anaerobic processes inmuscle, a number of factors can affect the speed atwhich anaerobic energy production starts. Forexample, a horse will start anaerobic energy pro-duction at a lower speed when unfit compared towhen fit. A horse that has a high proportion of fast-twitch high glycolytic (‘sprinting’ or type IIB fibres)in its muscles will produce lactate at a lower speedthan a horse with few of this type of muscle fibre.Health problems that interfere with oxygen trans-fer from atmosphere to mitochondria, such as

upper airway obstruction, cardiovascular disease orlower airway disease will also tend to decrease thespeed at which anaerobic energy production starts.Even excitement, pain, amount and type of warm-up exercise, time of feeding and environmentalconditions can affect the point at which the anaer-obic metabolism becomes significant and the con-centration of lactic acid in blood begins to increase.

How can we tell what fuels are being used forenergy generation? The amounts of oxygen used upand carbon dioxide produced vary according to theenergy substrates being used at any point in time.The respiratory exchange ratio (RER) is the ratioof carbon dioxide production (

.VCO2

, litres/min) tooxygen consumption (

.VO2

, litres/min) measured atthe nostril (p. 94). The ratio of carbon dioxide pro-duction to oxygen consumption or RER is 1.0 whencarbohydrate is the only fuel being used and isbeing fully oxidised. However, when fat is the solefuel source a relatively greater amount of oxygen isrequired and the RER is 0.7. Any RER valuebetween 0.7 and 1.0 either at rest or during exer-cise therefore indicates that both fat and carbohy-drate are being used simultaneously (see Table 2.2).During moderate to intense exercise, the produc-tion of lactic acid within muscles causes an increasein the hydrogen ion concentration of blood (bloodpH decreases). As a consequence of the mechanismwithin the blood for buffering hydrogen ions, thereis an increase in the amount of exhaled carbondioxide. Thus, an RER above 1.0 indicates thatsome of the energy is coming from anaerobic lacticacid production. The higher the RER the greaterthe contribution from lactic acid to total energyproduction, with values as high as 1.4 being reachedin intense exercise. However, once the RER has risen above 1.0 it is not possible to estimate the


Table 2.2 Approximate percentage contribution of energyfrom fat and carbohydrate during exercise in relation to res-piratory exchange ratio (RER)

% Energy from % EnergyRER carbohydrate from fat

0.70 0 1000.80 33 660.90 66 331.0 100 0>1.0 100 0

relative contributions of fat and aerobic and anaerobic carbohydrate metabolism.

RER can be used to determine responses todietary manipulation, exercise and training, andmay also reflect the muscle fibre type compositionin horses with very different muscle types. RER inhumans can be around 0.7–0.8 at rest but is gener-ally around 0.9 in horses. In a study of Standard-bred horses fed different diets for 4 weeks each,RER was about 0.9 on a typical hay and concen-trate diet, but was around 0.75 on a high fat diet(containing 15% soyabean oil), indicating that thehorses were actually using more fat for energy atrest on the high fat compared to the normalhay–concentrate diet (Pagan et al. 1987).

Size of the fuel stores

How much fuel can a 500kg horse carry? The sumof fat, muscle and liver comes to just over 230kg,with muscle weighing about 200kg, liver about 6.5kg and fat about 25kg.

The horse has around 95% of its total bodyglycogen stored in muscle and around 5% in theliver (although the actual concentration of glycogenin the liver is greater than in muscle). In contrast,around 95% of the body’s fat is stored in adiposetissue, with only around 5% stored within themuscles.

Approximately ten times as much energy (eitherin terms of kilojoules or kilocalories) is stored as fatcompared with glycogen (see Table 2.3). This meansthat if you were to oxidise or simply burn (literally

set alight) all the available fuel in the horse’s body,the fat stores would give off ten times as much heatenergy as glycogen. However, if all the availablefuel is respired aerobically, approximately 30 timesas much ATP is produced from the oxidative phos-phorylation of fat as from the oxidative phospho-rylation of glycogen. Remember, in terms of ATPyield, fat is better than glycogen, with over threetimes as much ATP produced per gram of fat compared with a gram of carbohydrate. Fat is anenergy-dense source; literally, a little bit of fat goesa long way. If you were setting out on a day’swalking or trekking and you had to carry all yourfood for the day, you would look to carry thosefoods which gave you lots of energy, but did notweigh very much; in other words, you would lookfor energy-dense foods. If you were a horseembarking upon a 100-mile endurance ride, itwould pay you to use fat as your fuel source as faras possible because it is so energy-dense. Exerciseis rarely, if ever, limited by running out of fat.

Fat is ideal for exercise where the body requires:

• Slow release of energy, i.e. for exercise at lowspeed

• A large energy reserve, i.e. for exercise of longdistance or duration.

Training of low speed and long duration increasesthe number of enzymes involved in the oxidativephosphorylation of fat, so that the body becomesbetter at utilising fat, and will tend to rely more onfat as an energy source. This is good news for thoseof us thinking of training to get rid of unwanted fat:the more you train, the better you are at burning


Table 2.3 Estimated times to exhaust each of the main body energy stores of a 500kg horse if each fuel was used as the only energy source at 60% (endurance),90% (four-star three-day event steeplechase speed) and 120% max (1 mile (1.6km) flat race)

Total body storesaExercise time at

(kJ) 60% max 90% max 120% max

ATP 38 3.3 s 1.8 s 1.1 sPCr 188 16.3 s 9.0 s 5.7 sGlycogen 75300 109min 60min 38minFat 640000 15.4h 8.5h –b

a From McMiken (1983).b No figure has been calculated for 120% max because at this intensity no fat wouldbe used.

V◊O2

V◊O2V◊O2V◊O2

V◊O2

fat, but you must keep the speed and intensity ofthe exercise sessions low. If, as a rider you want tolose weight, i.e. reduce your body mass, there is nobetter way to start than by doing plenty of walkingand slow jogging. Start to run faster and you willstart using more and more carbohydrate up to apoint where you won’t be using any fat. You can getfit but won’t necessarily weigh any less. It is alarm-ing how many people still think that the best wayto reduce a horse’s waistline is to gallop and ‘get asweat on him’. If you gallop a fat horse, all you willdo is:

(1) Risk breakdown of musculoskeletal structures(2) Make it sweat and lose body mass (due to loss

of fluid) in the short term which it will put backon as soon as it can drink

(3) Use up muscle glycogen(4) Give it an appetite!

You will not encourage utilisation of fat stores. It isalso worth being aware that when you train yourhorse, although its shape and appearance maychange, its body mass may not change dramatically.This doesn’t mean that you aren’t working it hardenough. Fat is less dense than muscle. The densityof fat is 0.9007g/cm3 (1cm3 = 1ml), whilst thedensity of muscle is 1.065g/cm3, i.e. 20% moredense than fat. That means that the same volumeof fat weighs less than the same volume of muscle.Therefore, if you replace 1kg of body fat by 1kg ofmuscle, it will take up less space but you will havethe same body mass. This is why dieting combinedwith exercise may mean your shape changes as youlose fat but your body mass may stay the same oreven increase as a result of muscle developmentfrom the exercise.

Running out of energy

Fatigue during exercise is almost never caused byrunning out of fat because the fat stores through-

out the body are so plentiful, but is commonly dueto running out of muscle and/or liver glycogen.Depletion of muscular glycogen leads to muscularfatigue. Depletion of liver glycogen and as a con-sequence low blood glucose may make you feellight headed and tired. Human athletes competingin long duration events use a technique calledglycogen loading or carbohydrate loading to tryand offset fatigue. It involves either exercising tofatigue or fasting in order to deplete the existingglycogen stores, and then eating large quantities of a high carbohydrate meal. Depletion beforeloading seems to increase the amount of glycogenthat it is possible to store. Glycogen loading is notrecommended in horses because it would requirethe feeding of large, high carbohydrate meals, whenwe know that high energy feeds should be split upinto several small meals to avoid conditions such ascolic or azoturia (tying-up).

Whilst we should not attempt to strategicallyglycogen load our horses, it is likely that a horse inhard regular work that is not provided with suffi-cient energy in its diet will be at a disadvantage.Following a hard piece of work that significantlyreduces muscle glycogen, such as a short fast gallop,it may take 2 days for the horse to fully replenishthe glycogen stores. This should be rememberedwhen planning a training programme that involvesfast work. You cannot expect a horse to performintense work, e.g. maximal sprint or interval work,well more than two or three times a week or on con-secutive days, because glycogen stores will not befully replenished before the next bout of intensework. In addition, the rate at which glycogen can bebroken down in glycolysis to yield ATP has beenshown to be dependent on its concentration. If the concentration is high, the rate of breakdownwill be high and vice versa. This is likely to be anadvantage in high intensity sprint or jumpingevents.


KEY POINTS

• Energy that is used each day for exercise must be replaced by energy obtained from the diet.

• Glycogen (the animal form of starch) and fat rep-resent the two main sources and body stores ofenergy.


• Cells cannot use glucose, glycogen or fat directly,only the energy released from the breakdown ofATP to ADP.

• At rest, food is converted via digestion to storesof glycogen (liver and muscle) and fat (adiposetissue).

• Energy cannot be created or destroyed, onlychanged from one form to another.

• The efficiency of conversion of energy intouseful, mechanical work is only around 20%.

• Stores of ATP within the body are only suffi-cient for several seconds of exercise; for con-tinued exercise ADP must be regenerated toATP by two anaerobic (PCr and glycolysis tolactic acid) or aerobic pathways (oxidative phosphorylation of glucose or glycogen or fattyacids).

• PCr and metabolism of glucose or glycogen tolactic acid regenerate ADP fast without the needfor oxygen but inefficiently, i.e. only a smallamount of ADP is regenerated.

• Aerobic oxidation of carbohydrate and fatrequire oxygen and are much more efficient butregenerate ADP to ATP more slowly.

• Energy partitioning describes the relative contri-bution of different pathways of ADP regenera-tion at different stages of exercise and duringdifferent types of activity.

• The respiratory exchange ratio (RER) indicateswhat fuels are being used at any point in time.

• Fat stores almost never limit exercise capacity,but carbohydrate (glycogen) stores can becomesignificantly depleted by repeated bouts of highspeed exercise or prolonged endurance exercise.

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