The racing Thoroughbred is trapped between a rock and a hard place. The rock is speed, which evolved slowly by natural selection for 50 million years, then rapidly by human hand the last 500. The hard place is where we find our ward today, beset by vulnerable feet, a grain-bothered gut, hot behavior, bleeding lungs, a sloping vulva, gastric ulcers, tying-up, crooked legs, and developmental orthopedic disease. The rock and the hard place appear to be linked genetically and positively and, if so, selecting against any of these undesirable traits will also reduce the genetic potential for speed.
Heritability or the genetically determined fraction of racing performance has been estimated as 0.1 to 0.2 based on racing times, and 0.3 to 0.4 based on earnings or handicap ratings. That leaves at least 0.6 of the variation in racing performance to be accounted for by environmental factors and genetic-environmental interactions. Annual genetic improvement of British Thoroughbreds has been estimated as 0.94 pounds of weight assigned in a free handicap. Slow improvement in winning times of English classics has been attributed to over-estimation of speed heritability or to physiological limits.
Heritability is probably higher for sprinting and for staying than for middle-distance performance, according to recent studies in Japan and Australia. This fits with physiological limits of performance, which are different for speed or stamina. Genetic studies have focused on high rates of production and clearance of lactic acid that enable sprinting, and maximal oxygen uptake for staying.
My hypothesis is different—the limits of breeding for speed are most probably expressed as pathophysiological side effects. Patho-physiological implies some normal function deviates from and fails to return to its customary range; in effect, function becomes abnormal.
The argument is certain side effects are positively genetically correlated with speed, so selection against any such side effect in addition to selection for speed will reduce genetic improvement for speed. A positive genetic correlation will result in a negative phenotypic expression—a horse genetically endowed for speed will run faster up to the point when expression of a side effect will slow it down. An obvious example is the bleeder that runs fast until it bleeds.
If this hypothesis is correct, then certain limiting side effects of breeding for speed will prove manageable by environmental but not genetic methods. This practical difference may be best understood if examples of genetic management are illustrated first.
Severe combined immunodeficiency (SCID) of newborn Arabians has no apparent advantage. It is inherited by a recessive gene, which may remain latent for two or three generations. The silent carriers can be identified, however, by pedigree analysis. Then they are not used for breeding.
Hyperkalemic periodic paralysis (HYPP) in Quarter Horses is also easy to deal with genetically. The decision is complicated, however, because this “bad gene” also confers an advantage. Its phenotype has a well-defined and prominent musculature which is admired, especially in halter class. Nevertheless, this statuesque physique can be obtained without the embarrassment of an undesirable gene, which may therefore be eliminated from the breeding program.
Any genetic problems in the Thoroughbred that cannot be dealt with by genetic methods, because of their linkage with speed, must be managed by environmental methods: mechanical, nutritional, behavioral, physiological, surgical, medical, or pharmacological.
Eight examples are discussed here. The first two are evolutionary kinks, which concern features of the horse that evolved before its domestication. The remaining six were inadvertently created by the human hand.
Hoof and Shoe
The progressive loss of toes of equine forebears suggests a steady direction of evolution from five toes to one. The single toenail became thick, strong, and suited to a nomadic animal grazing on the unkept grasslands of steppes and savannas.
The horse’s environment was changed when the Romans built roads of stones—rough-surfaced polygonal blocks of lava set in concrete—about 200 BC, and their horses’ feet started to crack and chip. Roman horses soon were wearing the first horseshoes or, more exactly, Roman sandals. Leather soles turned up over the hoof walls and were held in place by straps. The next step was to place a metal plate shaped like the sole in the sandal. Curved metal plates with nail holes, the Celtic shoe, appeared about 800 years later.
Heavy shoes are suitable for the slow-moving feet of a draft horse. But a Thoroughbred galloping at 12 seconds a furlong (37.5 mph) has front feet that stop six times a second, twice per stride (front and back). The feet accelerate to 60 to 75 mph, and then decelerate to the next stop in about 0.15 second.
Does speed kill?
No. Force kills, and force is mass times acceleration. Acceleration from 0 to 60 mph followed by deceleration to 0 mph in 0.15 second corresponds to an algebraic mean of 800 mph/second. In the evolving horse, mass and force were minimized by a slender leg and small foot (achieved with only one toe), presumably by mutations that favored speed. Man has changed the environment and added a mass—the shoe.
For speed, the lightest possible shoe is needed to minimize its added force, which will tend to provoke over-swings and altered impacts on the ground. Standard extra light shoes weigh 200 to 250 grams, which accelerating (or decelerating) at 800 mph/second gives forces of 160 to 200 kg/mph/sec, respectively (4,300 to 5,400 kg.m-1.s-1). If these calculations are nearly right, the feet of a galloping horse take an almost unimaginable hammering from shoes. Fortunately, progress is being made with resilient adhesives and lighter materials.
Remembering the Romans, we should strive to improve track surfaces. Ideal track conditions need to be determined for training and month-by-month development of strong tendons, ligaments, and bones.
Gut and Grain
Equine forebears grazed on steppes and savannas. To digest fibrous fodder, they evolved an exaggerated large bowel that acted as a fermentation vat. Here a diverse population of bacteria, protozoa, and fungi break down cellulose and other plant materials that escape hydrolysis in the small intestine. Fermentative digestion is allied to the habit of almost continuous consumption of a large mass of forage, which was abundant in the environment. Apparently directional evolution of this nutritional strategy gave a survival advantage to the horse over its competitors that had simple digestive tracts more suited to less abundant food.
The human environment was abruptly changed when cereals were domesticated about 20,000 years ago around the Euphrates, Tigris, and, a little later, the Nile. A trickle of grain began to sustain the war-horses of the Romans, Mongols, and Muslims. It became a flood about 300 years ago, when farmers started seriously to select and breed animals and plants for high production. The soil was tilled and fertilized scientifically, that is, chemically. Many horses pulled ploughs on the land and wagons in the street. A few pampered horses were bred and reared for sport and racing. The required food energy exceeded the limits of forage consumption, and this difficulty was overcome by feeding more concentrated energy in the form of oats and other grains.
Heavy grain feeding increased a horse’s energy intake and efficiency, and reduced its bowel ballast and water needs—all features favoring speed. It encountered upper limits, however, because the horse’s ability to secrete enzymes that break down starch and complex sugars in its small intestine had subsided during the course of its evolution. Now the environment was changed, and the microbes in the fermentation vat ran riot on the new diet.
Rapid fermentation in the large bowel has been associated with digestive disturbances, such as osmotic diarrhea, colitis, colic, and laminitis. Grain meals also cause a feeding-fasting cycle of metabolites and hormones that apparently initiates metabolic disorders, such as certain forms of laminitis, rhabdomyolysis (tying-up), and developmental orthopedic disease.
These equine grain-associated disorders (EGAD) may be regarded as side effects of feeding for speed. In a broader view, feeding for speed became a health risk only when a man-made environmental change turned against 50,000 years of evolutionary progress. The laboratory at Virginia Tech has been developing fat-and-fiber feeds for the last decade that promote performance and avoid EGAD.
Does heart or the will to win overlap an over-aggressive temperament? Has the evolutionary development of a survival strategy of rapid retreat over 50,000 years been refined or altered by human selection for a combatively competitive horse?
About 1,400 years ago, the prophet Mohammed, when spreading his religion by conquest, demanded fanatic fervor in his soldiers and steeds. He deprived his battle horses of water for seven days, then allowed them access to the watering place. As they ran to drink, he sounded his battle horn. Immediately a few mares rallied to the call for battle, despite their maddening thirst. These few became the founders of his elite herd, the forebears of our Arabians. So the story goes (see Dossenbach’s The Noble Horse); we may accept at least that Mohammed selected his war-horses for their focus and impetus. A high temperament became concentrated in the Arabian breed.
An influx of Eastern sires to England started about 600 years ago and brought a lean physique and stamina along with an apparently heritable undaunted racing temperament—hot blood. In the mid-16th century, a respected breeder, Thomas Blunderville, chronicled the mingling of Arabians with “rough-bred” mares from Ireland and northern England. Virginia’s 20th century chronicler of the Thoroughbred, Alexander Mackay-Smith, gives more credit to the Irish for the development of speed in their stubby racing cobs. The thick muscles of the cobbies contributed the power needed for sprinting. Is it reasonable to presume that racing cobbies were also selected for a competitive temperament?
The combination of two racing temperaments tended to excess and became exaggerated in Eclipse (born 1764). The champion was unbeaten in 18 races on the turf, but his unruly manners nearly cost him his race against the castration knife. Thank goodness—he won that 19th race against the knife and so dominated as a sire that his blood continues in every Thoroughbred today.
Competitive temperament appears linked to winning and probably with speed. It can be molded by several environmental means: housing and habitat; handling, training, and regulating physical activity; diet and feeding management; and drugs.
The Darley Arabian arrived in England in 1704. His most accomplished son was Flying Childers, who combined an unrivaled burst of speed with a tendency to bleed. Subsequent bleeders of renown were Herod in the 18th century and Diomed in the 19th. In the 20th century, an apparent increase in the frequency of bleeders may be attributable to one pervasive sire line.
Bleeding, or exercise-induced pulmonary hemorrhage (EIPH), is caused by huge pressures in pulmonary arterioles that are attained only in full flight. These pressures burst arterioles and release blood into air spaces. They correlate with mechanical effort and speed. It follows pathophysiologically that bleeding may be another side effect of breeding for speed.
Bleeding may be abated by lowering body weight, hence mechanical effort, and by lowering blood volume, hence blood pressure. Both body weight and blood volume can be decreased by a drug that stimulates urine production—furosemide. Is this drug used primarily to ameliorate an inherited weakness? If so, it benefits the individual horse but may weaken the breed.
Another major sire line has a high frequency of legs that are imperfectly conformed, especially in the front. Worse, if a yearling in this line has straight legs, the cognoscente are unwilling to forgive this lack of a famous fault.
The economic interests of owners of this sire line are not likely to benefit from a thorough genetic investigation. The dollar value of the line would probably diminish. Also, the chances of finding a genetic remedy for these crooked legs, which are so closely associated with speed, are limited. Clearly, it is not the mechanics of the crooked legs that favor speed or durability. So these crooked legs are probably associated with something else in these horses that enables them to run so fast.
Is this covert trait for speed a larger heart, a greater blood supply to muscles, thicker and faster motor neurons, more fast-twitch muscle fibers, a cooler brain, or competitive temperament? We do not know. So the paradoxical association of crooked legs with race-winning speed in this sire line is a daunting prospect for the separation of the desired and the undesired traits by genetic means.
Environmental management of angular limb deformities has included corrective shoeing, stall confinement, splints, and casts. Surgical procedures employ staples, plates, screws, wires, and periosteal stripping. Effectiveness is in question. In one study, the percentages of 2-year-olds that started in a race were 39% and 46% in the stripped group and control siblings, respectively. The corresponding breed mean is 16% starters, much lower than in the higher performing families prone to angular limb deformities.
Consequently, these deformities may be regarded as side effects of selection for speed.
The developmental orthopedic disease (DOD) complex is partially inherited and partially responsive to weight for age, obesity (body condition score), and diet. The interaction of a twist in evolution and the diet was mentioned above in regard to the avoidance of a risk factor—large grain meals.
Much of the DOD complex originates as dyschondroplasia, a disorder of proliferation of cartilage cells in certain joints and growth plates of long bones. A later stage, osteochondrosis, is more often seen clinically. Its heritability was 17% to 23% in one sample of Swedish Standardbreds, 23% to 52% in another. A clinical follow-up study in Italy indicated that racing careers at two and especially three years of age were better for horses previously treated for osteochondrosis than for unaffected horses from the same farms and stables. The investigator concluded that selection for speed was incidentally selecting for a side effect, a predisposition to osteochondrosis. My thinking is that selection for precocious growth is associated on the one hand with precocious speed, and on the other with a predisposition for osteochondrosis.
Maturation of chondrocytes is influenced directly by many factors, perhaps the most important being growth hormone and its main mediator, insulin-like growth factor-1 (IGF-1). Our current studies at Virginia Tech are revealing that feeding a fat-and-fiber pasture supplement minimizes fluctuations in these hormones. These studies suggest that imperfect maturation of cartilage into bone results from interactions between feeding and breeding for speed.
Like DOD, the syndrome of equine rhabdomyolysis (ER) has a complex etiology or multiple etiologies (sets of causes), which include genetic and environmental factors. Most of the pathological changes converge on muscle cell membranes, and the eventual disturbances of membrane functions give rise to the common, shared clinical signs, which are treated symptomatically.
A mode of inheritance, autosomal dominance with variable expression, has been found in a form of recurrent ER (RER) in Thoroughbreds traced back for 70 years. The RER trait has also been associated with faster contraction and relaxation in muscle biopsy samples, and faster twitch muscles may be conducive to speed.
Another mode of inheritance, autosomal recessive, has been found in another form of ER, polysaccharide storage myopathy (PSSM), which affects mainly cold- and warm-blood horses, Quarter Horses and, rarely, a Thoroughbred. It involves increased muscle glucose uptake and glycogen synthesis.
Heritability remains undetermined for any form of equine ER. A set of blood proteins has been found to identify Swedish Standardbreds at risk of ER, with no reference to pathologic type. These studies used hundreds of horses but, unfortunately, no assessment of racing performance in ER and non-ER groups was reported. They sought but failed to find the modes of inheritance of RER and PSSM, which were previously described in American horses, in Swedish Standardbreds.
Given that ER has been present for many generations, it is presumably not being selected against despite its eventual phenotypic disadvantage. Instead, ER is probably being retained because of its likely but as yet unquantified genotypic association with speed.
Conformation and Infertility
The postulated association of selection for speed and the side effect of female infertility relates to conformation, replacing a right-angle triangle with an oval-shaped hindquarter. Prior to about 1950, the hindquarters of most Thoroughbred fillies had a flat rump and a perpendicular drop from the base of the tail. Feces propelled out of an extended anus usually fell clear of a vertical vulva. Only a few fillies had the rounded rump and the bulging gluteals more typical of colts. This conformation included a sloping vulva, more prone to soiling and associated chronic infection. These few fillies were candidates for the Caslick procedure in which the lips of the vulva are stitched together save for a small opening to allow urination.
In general, colts were faster than fillies, and one of the reasons was thought to be the more powerful shape of their hindquarters. To obtain faster fillies, females were selected for male-like conformation. Today, nearly all Thoroughbred broodmares are Caslicked. And every equine reproductive clinic sees chronic uterine infections in formerly top racing mares.
When the desired conformation for speed conflicts with the conformation more suitable for reproduction, which will be favored by Thoroughbred breeders? In 1990, I attended a meeting in which a panel of three veterinarians and three farm managers in Kentucky agreed with each other that they had bred the sloping vulva into their Thoroughbred population in 35 years. This claim fits my observational period and, if generally valid, it illustrates the power of genetics to create a side effect of breeding for speed.
A species’ genome is its complete genetic material described at the molecular level. It can be pictured as a map that allows identification of particular sites associated with genetic defects and specific functions in the animal. Contributions from 22 laboratories are being coordinated in the Horse Genome Project. This research offers enormous promise for improving the genetic management and welfare of the horse.
Current practical outcomes of genome research concern simply inherited conditions. Guided by disease-causing genes in other species, sites on the equine genome have been associated with SCID, HYPP, and the lethal white syndrome of Paint horses. Genetic tests for these simply inherited diseases are now available.
In contrast, most important components in conformation, performance, and complex side effects of breeding for speed are probably dependent on many sites on the genome map. The association of increasing numbers of sites with speed and side effects will require correspondingly more complicated mathematical models. Hopefully this research will identify genetic markers in foals, hence halving generation length and potentially doubling the rate of genetic manipulation. Another great expectation is that the increasing power of genomics will eventually enable the dissociation of breeding for speed from its current side effects.
Until the promise of genomics is fulfilled, the side effects of selection for speed in the racing Thoroughbred must be managed by environmental measures. These include better habitats, tracks, shoes, tack, diets, physical and mental conditioning, medicines, and surgeries.
A genetic option would be to split the Thoroughbred breed into two divisions—racing and sporting. The sporting Thoroughbred would be used for combined training, jumping, foxhunting, polo, dressage, hacking, and companionship. Its selection would back off from speed in favor of durability, because the sport horse is educated and developed for several years, and it must remain usable for sufficient years to justify its schooling.
In contrast, the racing Thoroughbred would continue on its merry way to ultimate speed, when it will have only enough soundness for one race, perhaps viewed on a large screen run by a computer simulation following numerous sub-maximal tests in the casino’s exercise physiology laboratory.
This dismal prospect of an increasingly fragile racing Thoroughbred is a challenge to owner/breeders. They are left to grapple with the ethical issues, the economic realities, and the inevitable conundrum—that environmental management of the side effects of breeding for speed aims to help the individual horse while weakening the breed.
About the Author
The late David S. Kronfeld, PhD, DSc, MVSc, MRCVS, Dipl. ACVN, Dipl. ACVIM, was the Paul Mellon Distinguished Professor of Agriculture and professor of Veterinary Medicine at the Virginia Polytechnic Institute and State University, in Blacksburg, Va. He was also previously the Elizabeth Clark Professor of Nutrition and Chief of Medicine at New Bolton Center at the University of Pennsylvania.
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