STRUCTURE. FUNCTION. Two completely ordinary, simple, everyday words. But when you are able to apply them to the way a horse moves, it will take you to a level of understanding that will empower you to increase his performance, resilience to injury and provide him with a pain free, active life.
A single word can indeed be substituted for structure and function: posture. But now you are probably thinking ‘What has my horse’s posture got to do with anything?’ The answer is that it has everything to do with the way he stands, moves and performs. But even more importantly poor posture is significantly implicated in primary injury and secondary dysfunction in the horse.
For the horse, sound and lame are two ends of a very wide spectrum and, in the absence of trauma, a series of small compensatory postural changes can take place over several days, weeks or even months. By the time that clinical lameness manifests, a number of small, sub-clinical anatomical pressures have been created. Without an appreciation of this phenomenon, treatment of the primary lameness, whilst ignoring the compensatory changes that led to it, will simply lead to a relapsing or evolving condition. Further, in the absence of physical trauma, escalating subtle postural compensations can eventually result in lameness in anatomical structures far away from the original source of pain.
Why should this be so? The answer lies in the fact that the horse evolved primarily as a prey animal. His major means of defence is to outrun a predator. Therefore, the predator will select as its target that which it perceives as the sick, lame or lazy animal from the herd. Consequently it is in the interests of the horse to disguise that he is in any way impaired from running because of pain. Horses, more so than any other animal, have developed strategies to conceal injury, and therefore by the time that lameness is expressed, the animal is already in significant pain and may have been so for some time. Further if postural compensations have been longstanding, he may be experiencing pain in many areas of his body and the particular lameness that he is exhibiting may be completely disassociated with the original painful area. So if only the presenting lameness is addressed, the mechanisms which created that lameness are still likely to be present.
It takes a very experienced and critical eye to perceive pre-lameness postural compensations in the horse. It is what veterinary surgeons will refer to as a sub-clinical lameness, as there is dysfunctional movement but nothing that would classify it as clinically ‘lame’. New advances in gait analysis with horses have shown the remarkable extent by which the horse can imperceptibly transfer his body weight to compensate for pain. An original postural compensation can result in a minor overload of another anatomical structure, which in turn becomes painful and the horse must shift his weight again and again. This leads to a downward spiral of complex compensatory mechanisms which inexorably result in observable lameness when the horse is unable to disguise his pain further.
The basis of this book is functional anatomy, which is an important scientific discipline. Not only is it necessary for an understanding of the correct movement of the horse, but it is vitally important to understand the anatomical pressures associated with riding, competition, training, overtraining, injury, disease and rehabilitation. There are welfare implications to also consider, not just for the leisure horse but particularly in the sport horse. Injury is an unfortunate effect of sporting life and brings with it pain, and incapacity. For the owner it also brings the inevitable emotional and economic costs. It is a sad fact that 70 per cent of horses involved in sport will sustain at least one lame episode in each competitive season. Some of these will, of course, be as a result of direct trauma such as a fall, striking a solid fence etc., but many of them will be as a result of compensatory gait patterns which have gone unnoticed by the rider/trainer/owner. How many times has the veterinary surgeon or veterinary physiotherapist heard the plaintive cry of ‘He was fine when I rode him yesterday, but he’s come out of the stable lame today’?
The other possible scenario which is frequently encountered by the vet or physiotherapist is the horse that has developed the so-called ‘poor performance syndrome’, i.e. he is no longer able to undertake a movement that he has been able to do previously, such as refusing jumps, he shows an inability to perform lateral movements one way or another, or his temperament has changed in some way. Very often the history given by the rider will be of their horse apparently ‘resisting’ or ‘refusing to go forwards’. Whatever the history, the primary factor is one in which the horse is not doing what is wanted of him. Unfortunately some riders and trainers will not even consider pain as a possible cause for temperament changes or athletic resistance, and will use strong aids such as the use of a whip or spurs to ‘overcome’ his problems. The word ‘his’ has been emphasised because it is automatically assumed by these riders/trainers that the problem is with the horse.
However, if you learn anything from this book at all, in the interests of equine welfare make it the following.
If a horse is not doing what you want him to do there are usually three main causes:
He doesn’t understand what you want him to do.
He is not physically capable of doing what you want him to do.
It hurts him to do what you want him to do.
And guess what? None of those are his fault, so before you start aggressively using your whip or spurs, make sure that you have ruled those three factors out.
By the time you have read this book, you will be in a much better position to assess your horse physically and functionally, and you will be equipped with a number of skills to help your horse become the very best that he can possibly be. Not only that, you will be able to identify and resolve any physical or functional problems before they result in significant pain and lameness. Nonetheless it is emphasised that the information given here is not a substitute for direct professional involvement from your vet or from a fully qualified veterinary physiotherapist such as a member of ASSVAP (Association for the Scientific Study of Veterinary and Animal Physiotherapy). If in any doubt at all, you should consult one of these professionals.
What is functional anatomy?
Functional anatomy is essentially the study of movement and physical activity. Whilst the latter is basically a physiological subject, physiology and anatomy are close bedfellows and cannot be easily separated. However, functional anatomy is the fundamental building block of biomechanics and is therefore generally considered to be a mechanical system. Therefore, as a visual science, the unaided eye is used to examine the structure and movement of the equine body. Also palpation (using the senses of touch and pressure) skills are utilised to provide further information beyond surface visualisation. For the animal healthcare professional, particularly vets and veterinary physiotherapists, eyes and hands are their most important tools. Eyes can appreciate the surface anatomy, both static and dynamic, whilst palpation can provide an appreciation of the condition and mass of deeper anatomical structures. Effectively hands are used as substitute eyes to add information from the deeper anatomy that cannot be viewed to the information gleaned from the surface visualisation.
Horses are vertebrate animals, which means they have a vertebral column (axial skeleton) attached to which are limbs (appendicular skeleton). Bones are usually joined together by means of arthroses (joints). Muscles are attached to bone by way of tendons. Muscles contract and relax and transmit the forces they generate via the tendons to the bones, to either change joint angles to produce locomotion, or to stabilise joints when stationary, enabling standing. In basic biomechanical terms we can think of joints, particularly in the appendicular skeleton, as levers. As in all mechanics theory, the more efficient the levers, the greater the power produced and the more effective the movement generated.
In the equine body, if the levers are malfunctioning because of musculoskeletal pain, then the static and dynamic posture of the horse is altered, and the smooth operation of the whole system is impaired. As outlined earlier in this chapter, this may not be immediately evident to the rider/trainer. It can be a long road from sound to lame. Sound and lame are the black and white of the situation, in the absence of trauma it can be a very long journey between the two, with movement compensations being piled on top of each other. To begin to appreciate how important static and dynamic posture is in the horse, we must start to think not in terms of sound and lame, but in terms of functional and dysfunctional movement.
The majority of injuries leading to pain and dysfunction have mechanical causes. Forces and force-related factors not only lead to injury but have an effect on its severity. We must therefore have a definition of ‘injury’. Injury is the damage caused by physical trauma to musculoskeletal tissues. Such trauma may be sub-clinical and induce subtle postural adaptations, or it may be major and immediately give rise to observable injury. But these major traumas in themselves produce postural compensations.
Figure 1.1 Illustration of transfer of weight in lame horse trotting. If the left fore is lame, the horse compensates by throwing his weight back onto the diagonal hind limb by lifting his head and neck.
For example, in quadrupeds, such as the horse, body weight is transferred away from an injured limb to its diagonal. Therefore if the left forelimb is painful, the horse will throw as much of his weight off that limb to the right hind limb, increasing the forces of locomotion to that diagonal limb. Imagine trotting this lame horse, his head will nod up and down. He will lift his head up high when the left forelimb is on the ground and throw his weight off that limb and back onto the right hind limb. When the right forelimb comes into stance phase, he drops his head low to prepare to throw it up again when the painful left forelimb it put to the ground. By doing this he automatically transfers an abnormally high force off his left hind limb onto the right forelimb (Figure 1.1). Therefore every limb is experiencing a compensatory mechanism, not just the lame one.
This is a very simple explanation for what is, in its sub-clinical form, a complex process. It is purely to demonstrate how compensatory postural changes as a result of pain can affect the whole body in terms of forces on musculoskeletal tissues which may result in secondary pathology elsewhere in the body.
Elastic energy in equine locomotion
Another important aspect of equine locomotion is the heavy reliance on elastic energy for forwards movement. As a prey animal, whose major means of defence is to outrun a predator, the horse has evolved to make greatest use of movements that do not require direct energy derived from food (ATP [adenosine triphosphate]derived from glycogen, fat, proteins etc.) which would drain energy levels on any activity that is not actually propelling the horse away from that predator. These movements are primarily those which involve movements of the limbs whilst they are non-weight bearing, such as flexion and protraction.
In physics elasticity is a physical property of materials which return to their original shape after they are deformed. When an elastic material is deformed due to an external force, it experiences internal forces that oppose the deformation and restore it to its original state if the external force is no longer applied. Put very simply, imagine an elastic band. If you stretch it you are applying an external force, but when you release it, it will return to its original length. So returning to its original length did not require any additional energy input, the elastic band simply stored the energy as part of the stretching process and released it to return the band to the original dimensions when you let it go.
All musculoskeletal tissues exhibit varying degrees of viscoelastic behaviour (i.e. time and rate dependent), but for the horse it is mainly the viscoelasticity of tendons in the distal (lower) limb, or tendinous tissue running through muscles that protract the fore and hind limb, that have highly evolved to display maximal elastic energy utilisation. In the biceps brachii, biomechanical studies have shown that the significant tendinous tissue that runs through the muscle from origin to insertion not only significantly contributes to the passive (lacking active energetic input) protraction of the forelimb, but increases the power over 100 times.
Figure 1.2 Iliopsoas muscle which acts elastically to aid hind limb protraction.
The major hind limb protractor is the iliopsoas, which has two parts – the iliacus and the psoas major. The iliacus origin covers the ventral surface of the ilium, whilst the psoas major origin arises along the ventral surfaces of the lumbar vertebrae transverse processes. They fuse to have a common insertion on the lesser trochanter on the medial aspect of the femur (Figure 1.2).
These muscles are primarily tendinous in structure so think of them as large straps of strong elastic. As the hip joint extends whilst the limb is on the floor undergoing retraction, these strong elastic bands stretch. As soon as the weight is taken off the hind limb, these elastic bands ‘spring’ back to bring the hip into flexion without any additional energetic input from vital energy stores and the rest of the hind limb follows passively.
In the distal limb the long tendons of the flexor muscles similarly store elastic energy as the limb is loaded and the fetlock extends towards the floor during weight bearing, and those tendons are stretched. As soon as the limb is lifted from the floor, the distal limb joints flex passively due to the release of elastic energy.
Watch a racehorse come out of a starting gate; his first movement is to drop the hindquarters to flex the hocks and stifles. The fore and hind toes are driven deep into the surface to create something akin to the effect of human athletes’ starting blocks. For the first few strides, both his hind limbs move together in a bunny-hopping movement, with the toes digging into the surface until the elastic energy system can begin to function, at which time he will settle into the traditional transverse gallop. Until the elastic energy system begins to function he is in danger of stumbling and going down on his knees, or his hind feet can cut into the back of the front legs.
This elastic energy system is wonderful when the horse’s dynamic posture is good. But if there is pain or muscular asymmetry or poor foot balance then it can become a liability. Also ‘fine tuning’ of this elastic energy system is provided by the antagonists, which are the muscle(s) acting in opposition to the muscle(s) providing the desired movement working eccentrically (lengthening whilst developing tension) whilst the elastic structures release energy. Pain in these antagonists can lead to erratic protraction or flexion of the limbs. For example, the main antagonist to the iliopsoas is the middle gluteal muscle. Pain in the gluteal muscle will lead to impaired retraction and decreased weight bearing in the affected hind limb. This in turn leads to inappropriate loading of the elastic structures required for efficient flexion and protraction of the limb. Similarly, changes in posture due to chronic, sub-clinical pain produce erratic behaviour in elastic structures resulting in less than optimal gait patterns.
Effects of forces on musculoskeletal tissues
These changes to the normal functioning of limb dynamics places abnormal stress and strain on other limb structures such as joints and ligaments. During normal, functional movement, all musculoskeletal tissues will acquire, via normal physiological responses, the mass and density required for the particular sporting/leisure requirements. Inappropriate loading leads to inappropriate physiological response leading to the potential for tissue damage which post-injury needs an intricate understanding of how to rehabilitate the horse to ensure a repair that will lead to the tissue recovering as much of its biomechanical function as possible.
Bone, particularly, is a remarkably adaptive tissue, and its response to stress and strain is to remodel very quickly, to lay down more bone tissue in areas of the skeleton that are experiencing the greatest loading challenges. This phenomenon was first described in the nineteenth century by Charles Darwin in his book The Origin of Species where he stated:
With animals the increased use or disuse of parts has a marked influence; thus in the domestic duck the bones of the wing weigh less and the bones of the leg more, in proportion to the whole skeleton, than do the same bones in the wild duck; and this may be safely attributed to the domestic duck flying less and walking more than its wild parents.
Essentially, wild ducks fly more (and so have increased bone density in their wing bones) than domestic ducks that walk more (and so have increased density in their leg bones)
This observation found its way into the nineteenth century scientific literature in the form of ‘Wolff’s Law’ which stated:
Every change in the form and function of a bone or of their function alone is followed by certain definite changes in their internal architecture and equally definite secondary alterations in their external conformation, in accordance with mathematical laws.
Very simply this means that bone adapts to the stresses and strains put upon it by remodelling by reducing bone density in skeletal areas that are experiencing reduced loading, and increasing the bone density in skeletal areas that are experiencing increased loading.
Immobilisation leads to disuse osteoporosis in the bones that are immobilised. Post-injury, because of the body’s immediate response to forces, recovery of bone density and strength can be made within weeks.
Ligaments and tendons
Ligaments, which generally serve to stabilise joints by joining bone to bone, and tendons, which attach the muscle to the bone, also respond to stress and strain and are very sensitive to training and disuse. Exercise leads not only to hypertrophy (increased diameter of fibres) but also an increase in strength. Normal exercise can increase ligament strength by over 20 per cent, whilst immobilisation can lead to a rapid deterioration in strength and stiffness as well as loss of important tissue constituents such as glycosaminoglycans. The site of the insertion of the tendon or ligament into the bone is particularly vulnerable, and whilst recovery of strength within the body of the ligament may only take weeks after immobilisation, the insertion site can take many months. Without a proper understanding of how tissues adapt to exercise and recover from injury, the insertion site can be stripped from the bone in an avulsion fracture, which is a particularly serious injury. An injury within the body of the ligament, if not rehabilitated satisfactorily, can lead to persistent joint instability, prolonged pain and progressive degeneration. Likewise tendon injury not rehabilitated appropriately will lead to significantly altered mechanics and will be prone to re-injury.
Ligaments also possess elastic qualities and contain special receptors known as mechanoreceptors which react when the ligament is stretched to the limit and the joint is near to its maximum movement and in danger of injury. They send ‘help’ signals to the surrounding muscles which react to act as dynamic stabilisers to protect the joint. Therefore ligaments are an important part of functional anatomy which, if loaded properly, can act as strong stabilisers protecting the joint from injury, but any impairment to loading due to postural changes or immobilisation leads to loss of strength and potentially permanent joint injury.
The tendons in the equine distal limb have a sophisticated and complex reaction to normal and abnormal forces which this book is not designed to address, but injury to these tendons can be some of the most devastating and economically significant injuries in equine sport. Healing is lengthy in time and requires highly skilled post-injury rehabilitation. We know that tendon failure can be the result of long-term postural compensation. Indeed in a retrospective study using force plates to study the forces generated by equine movement, scientists at Bristol Veterinary School demonstrated that changes in movement patterns could be detected up to two weeks prior to the actual injury.
Each joint has a range of motion (ROM) through which it normally operates and which determines the joint’s mobility. ROM is joint specific and relative to individual conformation. Joints with more than one movement plane have a ROM for each plane.
The stability of the joint is directly related to its ROM because it is the ability of a joint to maintain an appropriate functional position throughout its range of motion. ROM is determined by the combined effects of the degree of bony fit, restraint provided by the joint capsule, ligaments and other periarticular surfaces, and the action of the muscles surrounding the joint. Injury to joints occurs when the joint exceeds its normal ROM, the tissues are violated and experience injury-producing forces.
The forces experienced by horses can be of considerable magnitude, especially in the speed or jumping horse, and injury-producing forces lead to tears in the menisci and/or articular cartilage degeneration. Of all types of connective tissue, articular cartilage (AC) is the most severely exposed to stress leading to wear and tear as it has a role in control of motion, transmission of load and maintenance of stability. It decreases the load by increasing the load-bearing surface because AC is plastic and capable of deformation.
During locomotion, the limb joints in the horse are constantly moving through their ROM. The short term effects of that movement are that the synovial fluid that lubricates the joint increases, which improves the nutrient supply to the AC and the removal of waste products. In the long term, with the application of appropriate forces and training within the joint’s capacity the AC thickens, thus providing greater resistance to forces. Injury to the AC occurs (in the absence of fracture) due to overuse from excessive training, and repeated trauma causes a fracture of the cartilage matrix.
The final tissue that bears discussion in terms of functional anatomy is fasciae. Scientific investigation into this particular tissue is in its infancy, but research is now demonstrating that it has a marked role as a force transmitter in animal posture and movement regulation.
Fasciae are dense connective tissues that surround muscles, groups of muscles, blood vessels, nerves and internal organs. It binds some structures together whilst allowing others to slide smoothly over each other. The definition of fasciae was only finally determined in 2007 as ‘All collagenous connective tissues whose morphology is dominantly shaped by tensional loading and which can be seen to be part of an interconnected tensional network throughout the whole body.’
The fascial body appears to be one large networking organ, with many bags and hundreds of rope-like local densifications, and thousands of pockets within pockets, all interconnected by sturdy septa as well as by looser connective tissue layers1. It extends uninterrupted from the head to the toes encapsulating all tissue structures and joint/organ capsules.
Under the microscope it is seen as numerous layers of collagen fibre bundles with each layer showing different orientations and separated by a thin layer of adipose tissue. They are typically punctured by nerve/artery/vein bundles which interestingly equate very well with traditional Chinese acupuncture points. Fasciae contract in a smooth muscle-like manner and influence musculoskeletal dynamics. However, the contractures of fasciae occur over a time frame of minutes to hours but can be strong enough to influence low-back stability and general biomechanics.
Fascial tissues are commonly utilised in dynamic energy storage for postural stability during movement. During movement, the supporting skeletal muscles contract more isometrically whilst the fascial elements lengthen and shorten like elastic springs, which clearly has a particular relevance to the horse because of his heavy reliance upon elastic energy for movement.
A very important factor in efficient static and dynamic posture is proprioception. Proprioception is the ability of an animal to know where his limbs/joints are in space and time without looking at them. For example, if you put your hand behind your back, you don’t have to look to know where it is or what orientation your joints are in. Proprioception is such an important part of posture that is has been termed the sixth sense. We know that the fascial network serves as a sensory organ because it is densely innervated by myelinated sensory nerve endings including very specialist neural tissues such as Pacini corpuscles, Golgi tendon organs and Ruffini endings. In fact, the extent of the fascial system makes it the largest sensory organ in the body.
Its full biomechanical role, response to training and injury, however, are little understood at this time, but many physiotherapists have anecdotal evidence as to marked effect of fascial contraction on locomotion, and use myofascial release techniques as part of their treatment protocol.
The equine locomotor system is therefore a complex, multifactorial system in which not only do individual structures have individual effects, but they can also work in any number of combinations with other musculoskeletal structures. It is this individual and combined effect which produces movement. Injury or pain can have a profound effect on how these systems work and we must therefore take a journey through the functional anatomy of the horse to demonstrate these phenomena, and how to utilise this knowledge in your management, training and rehabilitation of the horse.
1 Robert Schleip, Heike Jager, Werner Klingler. ‘What is ‘fascia’? A review of different nomenclatures.’ Journal of Bodywork & Movement Therapies (2012) 16, 496–502