By understanding how horses muscles contract to produce movement, you can formulate training and conditioning strategies for the competition season, rehabilitation protocols following injury, and exercise routines for weight management. Think of a muscle’s structure as a load of telephone poles lying on top of one another on a flatbed truck.
In the horse’s body the truck bed is a bone, and the telephone poles combine to form a single muscle lying along it. These long, straight proteins lie against one another and interdigitate with little finger like projections extending from the action molecule.
Visible to the naked eye, it runs from the pelvis along the length of the back of the femur (beside where the tail lies) and inserts onto the top region of the tibia (the long bone that stretches from the stifle to the hock). At its insertion, the muscle turns into tendon to make a firm, strong attachment to the bone.
When the semitendinosus contracts (shortens, flexes) while weight bearing, the hip, stifle, and hock all extend backward, causing propulsion. Nerves stemming from the spinal cord connect to the muscles via neuromuscular junctions, also called motor end plates.
Once the Na+ channels in the muscle cell membrane at the neuromuscular junction open, a chain reaction starts. Na+ channels located all along the muscle cell membrane (remember the telephone pole analogy) open in rapid gunfire succession, creating an electric charge.
The Ca2+ then stimulates action to start walking along the myosin chains to cause the fibrils, fibers, and entire muscle to contract. When you watch a horse in heavy training or competition, it’s clear that moving those muscles requires a lot of energy.
Conditioning is the process of preparing a horse to meet the physiological requirements of sport and competition. Muscle fibers differ in contraction speed (i.e., slow-twitch, fast-twitch) and whether they primarily generate energy aerobically or anaerobically via the glycogen-lactate system.
“At the other end of the spectrum, fast-twitch fibers are specialized for anaerobic metabolism and are capable of providing high force and power.” “Short duration, high-intensity exercise stimulates the use of fast-twitch fibers and an increase in the enzymes used for anaerobic metabolism,” Clayton explains.
Genetics, nutrition, and training all play important roles in helping horses meet their athletic goals. If the body delivers adequate levels of oxygen and nutrients, muscle will continue to contract without interruption.
Jump to navigationJump to search There are 3 types of muscle, all found within the equine: Muscle fibers have bundles of fibrils, which are all parallel to one another, and are able to contract due to action and myosin.
When they pass over a joint, they are protected in a tendon sheath, which contains synovial fluid as a lubricant. The tendon pulls upward to extend the carpal, pastern, and coffin joints.
However, unlike the flexor tendons, a horse with a damaged or non-functional “extensor unit” (i.e. tendon and musculature) is not lame, but rapidly learns to compensate by “flicking” the lower limb using the carpal or tarsal extensor units. The tendon continues down the front of the leg and inserts into the proximal portion of the first phalanx.
Extends the carpal, pastern, and coffin joints Deep digital flexor : 3 tendons of the deep digital flexor muscle travel distally and join at the carpus, where they pass through the carpal canal, and travel distally along the back of the leg, finally inserting into the Palmer side of the third phalanx. Fairly commonly injured by horses doing fast work, the DDT is round in cross-section.
Superficial digital flexor : Runs down the back of the leg, behind the carpus and cannon, branches below the fetlock and inserts into the distal side of the 1st phalanx and proximal side of the 2nd phalanx. Additionally, the superior check ligament inserts into this tendon from the caudal side of the radius.
The Soft is the most commonly injured tendon, and appears oval or flattened in cross-section. Brachiocephalic: originates from the temporal bone, atlas, and 3rd and 4th cervical vertebrae, and inserts on the humerus.
Cervical is ascend ens: originates at the transverse process of the final 3-4 cervical vertebrae, inserts into the first rib. Cutaneous cold: originates from the cruciform cartilage and inserts into the cervical fascia.
Latissimus Doris: originates at the supraspinatus ligament & thoracolumbar fascia, inserts in the humerus. Longissimus cost arum: originates on lumbar dorsal fascia, insert on caudal side of ribs, and the cervical vertebrae.
Masseter: cheek muscle, moves the jaw open and closed and allows for chewing Multitudes cervices: originates on last 4-5 cervical vertebrae and first thoracic, insert into the spinors and articular processes of the cervical vertebrae. Obliques wapitis cranial is: originate on ventral side of wing of atlas, inserts on occipital bone.
Omohyoideus: originates from the subscapular fascia of the scapulohumeral joint, inserts in the hold. Omotransversarius: originates in the atlas and the cervical vertebrae (C2-C4), continues down dorsal to the brachiocephalic to the point of the shoulder, then combines with the trapezium and inserts into the humerus.
The pectoralis descend ens (cranial superficial pectoral) originates from the cruciform cartilage of the sternum, and inserts into the humerus. The pectoralis transverses (transverse superficial pectoral) originates from the ventral side of the sternum and inserts on the proximal third of the horse's forearm.
Rectus wapitis dorsal is major and rectus wapitis dorsal is minor: originate on spinors process of axis and dorsal side of the atlas, respectively, both insert into occipital bone. Rhomboids: originates from the nuclei and supraspinatus ligaments, inserts on the medial scapular cartilage, is under the trapezium.
Scale nus: originates on the cranial and lateral side of the first rib, inserts into the transverse process of the cervical vertebrae (C4-C7). Serrated dorsal is cranial and caudal: originates on the lumbar dorsal fascia, inserts into the lateral side of the 5-12 or 10-18th rib respectively.
Sternocephalicus: originates from the cruciform cartilage of the sternum, inserts into the caudal side of the mandible. Sternothyroideus and sternohyoideus: originate from cartilage of the sternum, insert on caudal side of the lamina of the larynx and on the hold bone.
Trapezium: originates along the dorsal side of the neck near the poll, inserts on the spine of the scapula. Helps to raise the shoulder, also involved in moving the scapulohumeral joint.
Biceps brachial: originates from the caudal side of the scapula and inserts into the radial tuberosity. Raises the joint capsule to help prevent it from undue pressure during extension.
Tensor fascia antebrachial: originates from the tendon of the latissimus Doris and the caudal side of the scapula, inserts on the olecranal. Extensor carpi radials: originates from the humerus, continues distally along the dorsal side of the radius, and inserts on the metacarpal tuberosity.
The other part originates from the lateral tuberosity of the radius, and inserts into the tendon. Extensor carpi obliques: originates from the radius and inserts into the top of the second metacarpal.
Flexor carpi radials: originates from the humerus and inserts into the proximal side of the second metacarpal. Flexes the carpus and lower joints, Deep digital flexor: has three heads.
Adductor: originates from the ventral side of the pubis and schism, inserts into the caudal side of the femur (near the third trochanteral) and the medial epicondyle of the femur (including the medial ligament of the femoropatellar joint). Addicts the limb, rotates the femur towards the medial plane, flexes the hip.
Biceps memoirs: originates from lateral sacroiliac ligaments, the coccyges fascia and gluteal fascia, the intermuscular septum between the biceps memoirs muscle and semitendinosus. Allows the leg to extend, for movement as well as kicking and rearing, and allows for abduction of the limb.
Gluteus superficial is: originates from the gluteal fascia and tuber come, inserts into the femur. Gluteus medium: originates from the ilium, from the aponeurosis of the longissimus Doris muscle, from the gluteal fascia, and from the dorsal, lateral, and sacroiliac ligaments.
Gluteus prefunds: originates from the superior sciatic spine and shaft of the ilium, inserts into the femur. Operator external: originates from the ventral side of the pubis ad schism, inserts into the trochanteric fossa.
Operator interns: originates on pelvic surface of the pubis, schism, and ilium, and the wing of the sacrum, inserts into the trochanteral fossa. Pettiness: originates from the republic tendon, the accessory ligament, and the cranial side of the pubis.
Sons minor: originates from first 4-5 lumbar and last 3 thoracic vertebrae, inserts into ilium. Quadrats lumber: originates on the side of the final 2 ribs, inserts into the wing of the sacrum.
Additionally, the vasts intermedia raises the femoropatellar capsule, and the rectus memoirs flexes the hip. Sartorius: originates from the Iliad fascia and the tendon of the sons minor, inserts into the medial patellar ligament and tuberosity of the tibia.
Semitendinosus: originates from transverse processes of 1st and 2nd coccyges vertebrae and ventral side of tuber schism. Flexes the femoropatellar joint, causes inward rotation of the leg, and extends the tarsus and hip.
Tensor fascia late: originates from the tuber come, inserts into the lateral patellar ligament, the cranial side of the tibia, and the broad aponeurosis of the patella. Illustrated Atlas of Clinical Equine Anatomy and Common Disorders of the Horse Vol.
^ Hirohito Yamazaki, Molokai Got, Toyohiko YOSHIHARA, Marko SEKIGUCHI, Mutsuhito Kongo, Suzuki MO MOI and Shiloh Kawasaki. “Exercise-Induced Superficial Digital Flexor Tendon Hyperthermia and the Effect of Cooling Sheets on Thoroughbreds”.
Bones provide rigid structure to the body and shield internal organs from damage. They also house bone marrow, where blood cells are formed, and they maintain the body’s reservoir of calcium.
The type of joint formed determines the degree and direction of motion. Smooth muscle helps facilitate many involuntary processes in the body, such as the flow of blood (by surrounding arteries) and the movement of food along the digestive tract.
Tendons are tough bands of connective tissue made up mostly of a protein called collagen. At selected points, they are located within sheaths that allow them to move easily.
Ligaments are also tough cords formed of connective tissue. Ligaments surround joints and help to support and stabilize them.
This way we can influence and shape the whole body of the horse, not only the head and neck. Since there are approximately 700 skeletal muscles in the horse, which produce movement, create stability and maintain the posture, it’s quite a complex territory to dive into.
First you want a nice ‘wind’ blowing from behind, this is the energy you generate from engaging the hind legs to step forward and under the center of mass, so they can carry. This ‘wind’ needs to blow forward over his back, through his spine, into the contact of the reins which are your ‘sails’.
You do so with a combination of aids: your inner picture, inner feeling, energy, body language, whip and reins: You start with influencing the hind legs and then you catch and canalize the energy in front of your reins. In this round, connected posture, the horse uses isometric muscle activity in the area of head and neck so his nose doesn’t get in front of the vertical.
During the work, the muscle length doesn’t change, because when it does, when the isometric contraction disappears, the horse ends up in a long ‘cucumber shape’, poking the nose far in front of the vertical. In the beginning you will train with light weights so you can focus mainly on the technique in order to create precise movement and posture, so you won’t ruin your back once you start to lift more heavy weights.
But only loosening the muscles won’t help the horse, because stiffness provides in a way some core stability, and when you remove all stiffness and there’s no other muscle activity, the horse will move like a drunken sailor. Plus we focus on developing the LFS, where the horse learns to stretch his body to both sides (Lateral bend), starts to stretch his towline (Forward down) and starts to use his hind legs to support his body (Stepping under), so his balance and coordination improve.
Once the horse is more supple, balanced and coordinated in body and limbs, we start to work on the isometric muscle activity : we make a start with developing the connected ‘tomato shape’ by using ‘the wind in the sails’ and the ‘arrow in a bow’ concepts. To compare it to a branch of a tree, a twig, when you use too much force on both sides, it will break.
After the yielding you encourage the horse to searches towards the hand, keeping a long, arched neck. If not, if they collapse as soft pudding after you take away the frame, you have to change your approach a bit in your lab….
Without them, the horse would be unable to walk, chew and digest food, or even swish his tail. In this article, we’ll take a look at how equine muscles function and are nourished, as well as examine some problems that have surfaced, such as hyperkalemic periodic paralysis (Hype) and tying-up.
Much of the information concerning description of muscle structure comes from a paper authored by Craig H. Wood, PhD, coordinator of Distance Learning at the University of Kentucky, and published in the Horse Industry Handbook. When we discuss Hype, the work of Sharon Spear, DVD, Dial Achim, PhD, associate professor at the University of California, Davis, becomes a source of information.
No discussion on tying-up should be conducted without drawing on the research of Stephanie Val berg, DVD, PhD, professor of large animal medicine and director of the Equine Center at the University of Minnesota. These filaments are large polymerized protein molecules that are responsible for muscle contraction.
He also tells us that skeletal muscle contains a sarcoplasmic reticulum (calcium pump) and a tubular system. The slow-contracting or slow-twitch Type 1 fibers do not oxidize the muscle fuels rapidly and, as a result, are fatigue resistant.
It is estimated that 80-90% of the muscle fibers in Thoroughbreds and Quarter Horses are of the fast-twitch or Type 2 variety. For example, the number of Type 2A muscles fibers will increase in Thoroughbreds and Standardized as they are trained to race at longer distances.
The amount of adenosine triphosphate (called ATP, supplier of energy to cells in the body) required by a working muscle is dependent on the effort being expended. For example, when a horse is just ambling across the pasture at a slow walk, very little energy is required, and Type 1 fibers are utilized.
This involves the breaking down of glucose or glycogen into energy (ATP) without oxygen and, thus, is an anaerobic reaction. Glucose is the end product of carbohydrate metabolism and is the chief source of energy for living organisms.
Excess glucose is converted to glycogen and is stored in the liver and muscles for future use. Thoroughbreds travel at a high rate of speed during a race, with Type 2 muscle fibers being recruited along the way.
Because this relatively high rate of speed requires a continued burst of energy, it isn’t long before the utilization of fat and glycogen stores by the muscles is unable to supply all the energy required and anaerobic glycolysis (without the presence of oxygen) occurs with its more rapid burning of glycogen. The lactic acid that accumulates as the result of glycolysis can bring with it an early onset of fatigue.
The gasoline engine must emit the exhaust in order to continue functioning properly. Likewise, the horse’s muscles must rid themselves of lactic acid for optimal functionality.
When lactic acid accumulates faster than it can be dissipated, the working muscles are compromised, and the horse is fatigued. It normally travels at slower speeds where muscles can rely heavily on aerobic energy generation.
It quickly becomes apparent that the most important commodity for the equine muscles to function appropriately is oxygen, even though a portion of its energy might be produced anaerobically during strenuous exercise. Researchers have conducted countless experiments using treadmills to measure the amount of oxygen the exercising horse inspires.
These studies have revealed that the strenuously exercising horse might be required to inspire up to 90 liters of oxygen per minute. We have already indicated that the thickness and massiveness of the draft horse’s muscle structure adapt it for power at the walk.
Within these respective groupings, however, conformation differences can have a strong bearing on how efficiently the muscles function. This means that the muscles must work harder via more frequent strides for this horse to reach a particular rate of speed.
Its counterpart, with appropriate conformation, will have a fluid stride that will cover more ground and reach the same rate of speed with much less effort. This is a muscular affliction that has been traced to a genetic defect in the Quarter Horse stallion Impressive.
Proper functioning of the sodium channel is vital for electrical stimulation and contraction of the muscle fibers. In severe cases, the horse might suffer an episode of paralysis that could cause its death through cardiac arrest or respiratory failure.
Minus the energy that the glycogen is designed to supply, these horses develop muscle cramps and stiffness. There are more types of tying-up, some of which show up in excitable young racing Thoroughbred fillies and might be genetic in origin.
Identify individuals at risk for developing muscle disease prior to the onset of clinical signs, allowing early intervention and informed breeding decisions; and Identify the functional alleles underlying these diseases, allowing for a deeper understanding of how these mutations disrupt normal muscle function, which will eventually allow us to develop specific targeted therapies. Because the value of these horses depends on their athletic performance, health problems such as muscle diseases that affect their ability to train and race can have large economic consequences.
The importance of these athletic phenotypes has motivated horse breeding for centuries as horses are the only domesticated species that have been highly selected for athletic phenotypes, such as an ability to sprint short distances, pull heavy loads, or compete in endurance races 9. The intense selection for these performance traits has resulted in positive selection for alleles that enhance muscle mass and performance, such as a misstating SINE insertion that leads to increased muscle mass and improved sprinting ability 10,11,12.
Intense selection for muscle phenotypes may also underlie the surprisingly large number of heritable muscle diseases in horses, including Hype, PSSM1 and PSSM2, RER, MH, Mm, MFM, dystrophic and non-dystrophic myotonic, and mitochondrial myopathy 4,6,13–18. In other words, our understanding of the basic causes of muscle disease in the horse is still evolving.
The other fraction of unexplained muscle disease constitutes a category of complex conditions; some combined into catch-all names (such as RER and PSSM2) with multiple alleles and environmental influences both contributing to the development of clinical muscle disease. Recently, a private company, Equine, has marketed a group of single-gene genetic tests to diagnose PSSM2/MFM and RER.
Therefore, we have initiated a study to confirm or refute the role of the mutations that are part of Equine’s muscle disease panel. Sources Occur ME, Val berg SJ, Miller MB, et al. Glycogen synthase (GYS1) mutation causes a novel skeletal muscle glycogenosis.
Alemán M, Riel J, Eldridge BM, Lecturer RA, Stott Jr, Essay IN. Finn CJ, Gaining G, Perumbakkam S, et al. A misses mutation in MYH1 is associated with susceptibility to immune-mediated myositis in Quarter Horses.
Rudolph JA, Spear SJ, Burns G, Rojas C V, Bernice D, Hoffman EP. Periodic paralysis in quarter horses : a sodium channel mutation disseminated by selective breeding.
Occur ME, Val berg SJ, Lucio M, Michelson JR. Glycogen synthase 1 (GYS1) mutation in diverse breeds with polysaccharide storage myopathy. Val berg SJ, McKenzie EC, Erich L V., Shivers J, Barnes NE, Finn CJ.
Suspected fibrillar myopathy in Arabian horses with a history of exertional rhabdomyolysis. Fritz KL, Occur ME, Val berg SJ, Rental AK, Michelson JR. Genetic mapping of recurrent exertional rhabdomyolysis in a population of North American Thoroughbreds.
Petersen Jr, Michelson JR, Rental AK, et al. Genome-Wide Analysis Reveals Selection for Important Traits in Domestic Horse Breeds. Identification of the misstating locus (MSN) as having a major effect on optimum racing distance in the Thoroughbred horse in the USA.
Petersen Jr, Michelson JR, Rental AK, et al. Genome-Wide Analysis Reveals Selection for Important Traits in Domestic Horse Breeds. All’Ohio S, Wang Y, Satori C, Fontanel L, Antoni R. Association of misstating (MSN) gene polymorphisms with morphological traits in the Italian heavy draft horse breed.
Occur ME, Val berg SJ, Miller MB, et al. Glycogen synthase (GYS1) mutation causes a novel skeletal muscle glycogenosis. Taylor RJ, Lives L, Schumacher J, et al. Allele copy number and underlying pathology are associated with subclinical severity in equine type 1 polysaccharide storage myopathy (PSSM1).
Abnormal regulation of muscle contraction in horses with recurrent exertional rhabdomyolysis. Val berg SJ, Carlson GP, Cabinet III GH, et al. Skeletal muscle mitochondrial myopathy as a cause of exercise intolerance in a horse.
Occur ME, Val berg SJ, Lucio M, Michelson JR. Glycogen synthase 1 (GYS1) mutation in diverse breeds with polysaccharide storage myopathy. Val berg SJ, Maclean JM, Bistro JA, Hower-Moritz MA, Michelson JR. Skeletal muscle metabolic response to exercise in horses with “tying-up” due to polysaccharide storage myopathy.
They may be present at birth (congenital) or occur due to nutritional imbalances, injury, or ingestion of a poisonous substance. The most common signs are muscle pain, stiffness, and reluctance to move due to rhabdomyolysis, which may or may not be related to exercise.
Muscle weakness or damage can also occur as a sign of many disorders (such as nerve trauma or influenza). Disorders related to vitamin E, selenium (an element required in small amounts for normal nutrition), and fat metabolism can all affect the muscles, leading to inflammation and degeneration.
Degeneration of muscle is sometimes associated with a deficiency of selenium or vitamin E. The condition may cause rapid, unexpected death in adult horses. Blood tests are used to confirm a selenium or vitamin E deficiency and muscle damage (indicated by increases of muscle-associated enzymes).
In foals, this nutritional myopathy may be seen at birth or shortly thereafter and may be accompanied by inflammation of fatty tissue or “yellow fat disease.” Stiffness and pain are noticeable when feeling for the firm, fat masses below the skin, and severely affected foals may be unable to suckle. Exertional myopathies in horses involve muscle fatigue, pain, or cramping associated with exercise.
Once considered a single disease, it is now understood that there are several conditions that appear similar but have different causes. Excessive sweating, increased breathing rate, rapid heartbeat, reluctance or refusal to move, and firm, painful hindquarters are common.
Severe episodes may involve muscle damage with kidney failure and reluctance to stand. The most common cause of sporadic exertional rhabdomyolysis is exercise that exceeds the horse’s physical condition (level of training, health, etc.).
Respiratory disease and deficiencies of sodium, calcium, vitamin E, or selenium in the diet may also play a role. As soon as the condition is diagnosed, exercise should stop and the horse should be moved to a stall with comfortable bedding and access to fresh water.
Treatment should aim to relieve anxiety and muscle pain and to correct dehydration and metabolic imbalances. In severely affected animals, regular blood and urine tests are advised to assess the kidney damage.
The horse should continue to rest with regular access to a paddock until the blood muscle enzyme levels are normal. Because the cause is generally temporary, most horses recover with rest, a gradual return to normal training levels, and dietary changes.
They should be watched especially closely in hot, humid weather for signs of dehydration or muscle cramping. It is caused by a dominantly inherited gene mutation and can be diagnosed with genetic testing of blood or hair samples.
Signs include a tucked-up abdomen, a camped-out stance, muscle twitching, sweating, abnormal gait, stiffness in hind limbs, and reluctance to move. Draft horses may have more dramatic signs that include loss of muscle mass, progressive weakness, and lying down.
Type 2 polysaccharide storage myopathy occurs in light breeds such as Arabians, Morgans, Thoroughbreds, a variety of Warm bloods, and some Quarter horses. Signs may be noticed as a gait abnormality, exercise intolerance, and loss of muscle mass during periods of rest.
Malignant hyperthermia is caused by a different dominantly inherited gene than Type 1 polysaccharide storage myopathy and can also be diagnosed with a genetic test performed on hair roots or blood. Exertional rhabdomyolysis in Quarter horses with the mutation can result in sudden death preceded by excessive sweating and the signs described for anethesia-related events.
Recurrent exertional rhabdomyolysis is most often seen in Thoroughbreds (in which it may be an inherited condition), Standardized, and Arabian horses. Determining the severity of the condition during mild exercise is helpful in deciding how quickly to resume training.
Management of this condition is best done by minimizing the factors that lead to an episode and regulating calcium within muscle cells through the use of medication. Simply adding vegetable oil or rice bran cannot supply enough calories for athletes in intense training.
About 4% of Quarter Horses are affected by this condition, which results from an abnormally high level of potassium in the blood. Horses descended from the stallion named Impressive with signs of this condition are strongly suggestive.
A brief period in which muscles stay contracted for much longer than normal and have difficulty in relaxing is often the first sign. Muscle spasms begin on the flanks, neck, and shoulders and may spread to other parts of the body.
Most horses remain standing during mild attacks, but weakness with swaying, staggering, dog sitting, or lying down may be seen. Lack of food, anesthesia or heavy sedation, trailer rides, and stress may also cause an episode.
Owners may treat early mild episodes with light exercise or feeding of grain or corn syrup. Grains such as oats, corn, wheat, and barley; beet pulp; and late cuts of timothy and Bermuda grass should be fed in small meals several times a day.
Pasture is ideal for horses with this condition, because the high water content of live grass reduces potassium intake. Diagnosis of sarcocystosis requires history, clinical signs, laboratory tests, and muscle biopsies.
Ana plasma phagocytophilum is a parasite that infects cells in the bloodstream and is passed to horses and other animals by tick bites. In rare cases, horses develop clinical signs that may include severe muscle stiffness, fever, malaise, and limb swelling from fluid accumulation (edema).
A stiff gait is the first clinical sign, which progresses rapidly to severely painful, firm, swollen muscles along the back and hind limbs. Flushing infected guttural pouches and draining abscessed lymph nodes will diminish the amount of bacteria that are producing toxins.
Anti-inflammatory drugs and possibly high doses of short-acting corticosteroids may diminish the inflammatory response and reduce the clinical signs. A variety of clostridia bacteria can potentially infect the site of an injection or deep wound, causing local muscle swelling and body-wide toxic effects in horses.
Clostridia spores may lie dormant in muscles, or be deposited directly into tissue during trauma. If suitable conditions exist, the spores begin to grow and release powerful toxins.
Within 2 days, horses show depression, fever, fast breathing, and swelling at the site of injury. Tremors, unsteadiness, difficulty breathing, incumbency, coma, and death may occur in the next 12–24 hours.
Cut tissue from the affected area may reveal abundant fluid with an odor of rancid butter. Opening the wound and removing infected tissues over the entire affected area is required for successful treatment.
Extensive skin loss over the affected area is common in surviving horses and will require long term care. Staphylococcus aureus, Streptococcus equip, and Corynebacterium pseudo tuberculosis are bacteria that commonly cause muscle abscesses.
An abscess may heal, expand, or open to the skin surface with potential for a chronic glaucoma with intermittent discharge. The effect of an abscess on the horse’s gait depends on its location and can vary from mild stiffness to severe lameness.
Certain additives (of a type called ionospheres) that are often added to feeds for poultry or livestock other than horses may cause muscle disease. Signs include colic, persistent loss of appetite, heart failure with rapid heartbeat, difficulty breathing, diarrhea, stiffness, muscle weakness, and reluctance to stand.
Diagnosis requires history of exposure to these drugs and physical signs, along with appropriate laboratory tests. Degeneration of skeletal and heart muscles results when some animals consume the toxic portions (often the leaves, fruit, or beans) of certain plants.
Treatment consists of supplemental feeding and removal of animals from the area in which they ingested the toxic plants. This condition is seen primarily in working Quarter Horses as a result of injury to the inner thigh muscles after exercise that requires abrupt turns and sliding stops.
Usually, it affects one leg at a time and involves thickening and scarring of connective tissue that progressively worsens. Immune-mediated myositis is characterized by rapid decay of back and hind limb muscles following injury to blood vessels.
This may be an immune-mediated consequence of equine respiratory diseases associated with Streptococcus equip (the bacteria that cause strangles in horses). Horses have lived on Earth for more than 50 million years, according the American Museum of Natural History.
According to Scientific American, the first horses originated in North America and then spread to Asia and Europe. The horses left in North America became extinct about 10,000 years ago and were re-introduced by colonizing Europeans.
It is believed that horses were first domesticated in Asia between 3000 and 4000 B.C., according to Oklahoma State University. Eventually, horses joined oxen as a form of animal transportation.
Horses can be as big as 69 inches (175 centimeters) from hoof to shoulder and weigh as much as 2,200 lbs. The smallest breeds of horses can be as small as 30 inches (76 centimeters) from hoof to shoulder and weigh only 120 lbs.
Horses are found in almost every country in the world and every continent except Antarctica. For example, the Abyssinian is found in Ethiopia, the Buoyancy comes from Russia, Delibes is from Georgia and Armenia, the Egyptian came from Egypt and the Colorado Ranger bred comes from the Colorado plains, according to Oklahoma State University.
In the wild, horses will live in herds that consist of three to 20 animals and are lead by a mature male, which is called a stallion, according to National Geographic. A well-fed horse eats 1 to 2 percent of its body weight in roughage, such as grass or hay, every day, according to The Humane Society.
This wallpaper shows Assateague Island in Maryland and Virginia. (Image credit: National Park Service) Horses have live births after around 11 months of gestation.
Some people mistakenly call baby horses ponies. Ponies are adult horses that are shorter than 56 inches (147 cm), according to Encyclopedia Britannica.
Populations have been reintroduced to China, Mongolia and Kazakhstan, according to the San Diego Zoo. The Hungarian Warm blood was bred to be a sport horse breed.
Skeletal anatomy of a horseshoe limbs of the horse are structures made of dozens of bones, joints, muscles, tendons, and ligaments that support the weight of the equine body. The limbs play a major part in the movement of the horse, with the legs performing the functions of absorbing impact, bearing weight, and providing thrust.
As the horse developed as a curatorial animal, with a primary defense mechanism of running over hard ground, its legs evolved to the long, sturdy, light-weight, one-toed form seen today. Good conformation in the limbs leads to improved movement and decreased likelihood of injuries.
Structural defects, as well as other problems such as injuries and infections, can cause lameness, or movement at an abnormal gait. Injuries to and problems with horse legs can be relatively minor, such as stocking up, which causes swelling without lameness, or quite serious.
This is in contrast to even-toed ungulates, members of the order Artiodactyla, which walk on cloven hooves, or two toes. According to evolutionary theory, equine hooves and legs have evolved over millions of years to the form in which they are found today.
The original ancestors of horses had shorter legs, terminating in five-toed feet. Over millennia, a single hard hoof evolved from the middle toe, while the other toes gradually disappeared into the tiny vestigial remnants that are found today on the lower leg bones.
Prairie-dwelling equine species developed hooves and longer legs that were both sturdy and light weight to help them evade predators and cover longer distances in search of food. Forest-dwelling species retained shorter legs and three toes, which helped them on softer ground.
Approximately 35 million years ago, a global drop in temperature created a major habitat change, leading to the transition of many forests to grasslands. This led to a die-out among forest-dwelling equine species, eventually leaving the long-legged, one-toed Equus of today, which includes the horse, as the sole surviving genus of the Equidaefamily.
Skeleton of the lower forelimbEach forelimb of the horse runs from the scapula or shoulder blade to the particular bone. Each hind limb of the horse runs from the pelvis to the particular bone.
After the pelvis come the femur (thigh), patella, stifle joint, tibia, fibula, tarsal (hock) bone and joint, large metatarsal (cannon) and small metatarsal (splint) bones. Although having a small range of movement, the proximal interphalangeal joint (pastern joint) is also influential to the movement of the horse, and can change the way that various shoeing techniques affect tendons and ligaments in the legs.
Due to the horse's development as a curatorial animal (one whose main form of defense is running), its bones evolved to facilitate speed in a forward direction over hard ground, without the need for grasping, lifting or swinging. The ulna shrank in size and its top portion became the point of the elbow, while the bottom fused with the radius above the radio carpal (knee) joint, which corresponds to the wrist in humans.
A similar change occurred in the fibula bone of the hind limbs. These changes were first seen in the genus Merychippus, approximately 17 million years ago.
This is the shoulder in which provides the ease of movement as it is connected to various bones surrounding it such as the cervical vertebra (a section of the spine). 55 million years ago when the Phipps existed, the cannon bone used to be the 3rd toe of the foot.
Its fusion took place in order to increase height and power of the limb. The splint bones are also known as the 2nd and 4th metacarpal and fused 25 – 35 million years ago during the time of the Miohippus.
They provide extra strength and support of the cannon bone and used to be the 2nd and 4th toes of the foot. Firstly are the sesamoid bones that act as part of the system that allows the leg to drop as pressure is applied and spring back up as pressure is released.
Forward motion and flexion of the hind legs is achieved through the movement of the quadriceps group of muscles on the front of the femur, while the muscles at the back of the hindquarters, called the hamstring group, provide forward motion of the body and rearward extension of the hind limbs. The fetlock joint is supported by group of lower leg ligaments, tendons and bones known as the suspension apparatus.
During movement, the apparatus stores and releases energy in the manner of a spring: stretching while the joint is extended and contracting (and thus releasing energy) when the joint flexes. This provides a rebound effect, assisting the foot in leaving the ground.
This ability to use stored energy makes horses gaits more efficient than other large animals, including cattle. Horses use a group of ligaments, tendons and muscles known as the stay apparatus to “lock” major joints in the limbs, allowing them to remain standing while relaxed or asleep.
The lower part of the stay apparatus consists of the suspension apparatus, which is the same in both sets of limbs, while the upper portion differs between the fore and hind limbs. The upper portion of the stay apparatus in the forelimbs includes the major attachment, extensor and flexor muscles and tendons.
The same portion in the hind limbs consists of the major muscles, ligaments and tendons, as well as the reciprocal joints of the hock and stifle. The hoof of the horse contains over a dozen different structures, including bones, cartilage, tendons and tissues.
At the top of the hoof wall is the cerium, tissue which continually produces the horn of the outer hoof shell, which is in turn protected by the people, a thin outer layer which prevents the interior structures from drying out. The impact zone on the bottom of the hoof includes the sole, which has an outer, insensitive layer and a sensitive inner layer, and the frog, which lies between the heels and assists in shock absorption and blood flow.
The final structures are the lateral cartilages, connected to the upper coffin bone, which act as the flexible heels, allowing hoof expansion. It acts as a support and traction point, shock absorber and system for pumping blood back through the lower limb.
The pastern absorbing shock sequence of movements in which a horse takes a step with all four legs is called a stride. During each step, with each leg, a horse completes four movements: the swing phase, the grounding or impact, the support period and the thrust.
While the horse uses muscles throughout its body to move, the legs perform the functions of absorbing impact, bearing weight, and providing thrust. Good movement is sound, symmetrical, straight, free and coordinated, all of which depend on many factors, including conformation, soundness, care and training of the horse, and terrain and footing.
The proportions and length of the bones and muscles in the legs can significantly impact the way an individual horse moves. The angles of certain bones, especially in the hind leg, shoulders, and pasterns, also affect movement.
The forelegs carry the majority of the weight, usually around 60 percent, with exact percentages depending on speed and gait. Movement adds concussive force to weight, increasing the likelihood that a poorly built leg will buckle under the strain.
In the sport of dressage, horses are encouraged to shift their weight more to their hindquarters, which enables lightness of the forehand and increased collection. While the forelimbs carry the weight the hind limbs provide propulsion, due to the angle between the stifle and hock.
This angle allows the hind legs to flex as weight is applied during the stride, then release as a spring to create forward or upward movement. The range of motion and propulsion power in horses varies significantly, based on the placement of muscle attachment to bone.
The legs of a horse used for cutting, in which quick starts, stops and turns are required, will be shorter and more thickly built than those of a Thoroughbred racehorse, where forward speed is most important. However, despite the differences in bone structure needed for various uses, correct conformation of the leg remains relatively similar.
The ideal horse has legs which are straight, correctly set and symmetrical. Correct angles of major bones, clean, well-developed joints and tendons, and well-shaped, properly-proportioned hooves are also necessary for ideal conformation.
Individual horses may have structural defects, some of which lead to poor movement or lameness. Poor conformation and structural defects do not always cause lameness, however, as was shown by the champion racehorseSeabiscuit, who was considered undersized and knobby-kneed for a Thoroughbred.
Common defects of the hind limbs include the same base-wide and base-narrow stances and problems with the feet as the fore limbs, as well as multiple issues with the angle formed by the hock joint being too angled (sickle-hocked), too straight (straight behind) or having an inward deviation (cow-hocked). Feral horses are seldom found with serious conformation problems in the leg, as foals with these defects are generally easy prey for predators.
Foals raised by humans have a better chance for survival, as there are therapeutic treatments that can improve even major conformation problems. However, some of these conformation problems can be transmitted to offspring, and so these horses are a poor choice for breeding stock.
A polo pony with its legs wrapped for protectionLameness in horses is movement at an abnormal gait due to pain in any part of the body. It is frequently caused by pain to the shoulders, hips, legs or feet.
Lameness can also be caused by abnormalities in the digestive, circulatory and nervous systems. While horses with poor conformation and congenital conditions are more likely to develop lameness, trauma, infection and acquired abnormalities are also causes.
The majority of lameness is found in the forelimbs, with at least 95 percent of these cases stemming from problems in the structures from the knee down. Lameness in the hind limbs is caused by problems in the hock and/or stifle 80 percent of the time.
There are numerous issues that can occur with horses legs that may not necessarily cause lameness. Stocking up is an issue that occurs in horses that are held in stalls for multiple days after periods of activity.
Fluid collects in the lower legs, producing swelling and often stiffness. Although it does not usually cause lameness or other problems, prolonged periods of stocking up can lead to other skin issues.
A shoe boil is an injury that occurs when there is trauma to the burial sac of the elbow, causing inflammation and swelling. Multiple occurrences can cause a cosmetic sore and scar tissue, called a capped elbow, or infections.
Wind puffs, or swelling to the back of the fetlock caused by inflammation of the sheaths of the deep digital flexor tendon, appear most often in the rear legs. While horses periodically lie down for brief periods of time, a horse cannot remain lying in the equivalent of a human's bed rest because of the risk of developing sores, internal damage, and congestion.
“Functional Anatomy of the Equine Interphalangeal Joints” (PDF). ^ Lawson, San E. M.; Château, Henry; Purcell, Philippe; Dennis, Jean-Marie; Crevier-Denoix, Nathalie (May 2007).
“Effect of toe and heel elevation on calculated tendon strains in the horse and the influence of the proximal interphalangeal joint”. ^ Ferraro, Gregory L.; Stover, Susan M.; Whit comb, Mary Beth.