Training Regimens in Europe

Yearlings arrive in the yards for breaking from the sales in September and October and, unlike the situation in North America, often go straight to the trainer for breaking rather than to a specialist pretraining center.

After breaking, the yearlings usually start steady cantering exercise until Christmas. As the racing season approaches, horses showing precocity and ability to withstand faster exercise step up in pace throughout February and March. The first 2-year-old races occur in April, encouraging hard training of skeletally immature horses. However, until the racing calendar changes and while these races are open and available, trainers will train horses for them.

All-weather racing has altered the seasonal impact of flat racing in the United Kingdom forever, and some flat race horses now train throughout the year. However, most of the high-quality flat race horses do not compete on the all-weather circuit and are put into a slow-speed maintenance program from November until January, involving light cantering and trotting. Fillies may be turned out for a period.

All this is substantially different from the position in North America, where the horses often do not arrive at the racetrack until they are fully broken, in cantering exercise, and ready to do fast work. The breaking and pretraining often takes place in specialized pretraining centers, away from the city center tracks. This has important effects on the perception of racetrack veterinarians in North America concerning the incidence of developmental orthopedic disease linked to lameness. In North America, developmental orthopedic disease often causes lameness leading to diagnosis and removal from training before a horse reaches the racetrack; therefore horses with developmental orthopedic disease are not commonly seen by track veterinarians. An example is a subchondral bone cyst in the medial femoral condyle. Subchondral bone cysts are a regular occurrence in the annual intake of yearlings in the United Kingdom, diagnosed by the trainers’ veterinarians. Discussion with colleagues working at California racetracks reveals that they rarely see horses with subchondral bone cysts, presumably because of the effect of the earlier screening at the pretraining centers.

Once on the track in North America the racing is often less seasonal and less age specific, removing a lot of the pressure for success at 2 or 3 years of age within a short season. Whether a horse races on turf or dirt does not matter: historically, all training took place on dirt, and this should be borne in mind by veterinarians assessing horses for potential purchase to move from Europe to America. Asking potential purchasers whether the horse is intended for turf or dirt racing is largely irrelevant because the daily training almost certainly will be on dirt. The dirt surface is more testing in many ways than anything these horses have seen before, and horses able to train and perform well on grass sometimes fail to make the transition to dirt. In the past couple years, a few training tracks and racetracks in North America have moved to synthetic surfaces. It will be interesting to see whether this makes for an easier transition for horses moving from Europe to race in North America, and what impact it has on the types and frequency of training and racing injuries.

Clinical History

Taking a detailed history is a prerequisite for a medical examination in any species. In racehorse practice one often sees a succession of lame horses during any morning in several different yards, and the detailed information may be limited. The trainer may not be present to supply it. However, one should always try to ascertain the following information before examining a TB racehorse for lameness:

1 How old is the horse? This is probably the single biggest determinant for different types of lameness. The chronological age is important, but far more important is the skeletal naivete of the horse. An unbroken horse of 3 or 4 years of age behaves in essentially the same way as an unbroken yearling, regardless of the difference in age, and may suffer similar problems when confronted with an inappropriate training program.

2 What stage of training has the horse reached? Has a horse reached race-speed exercise yet; is it simply trotting; or has it entered normal conditioning cantering exercise? For a yearling that is lame while being broken or in early cantering exercise, one has to consider subchondral bone cysts and other osseous cystlike lesions, osteochondritis dissecans (OCD), and associated osteoarthritis (OA). Problems may be bilateral, resulting in a peculiar gait. Bilateral ilial wing stress-related bone injury or sacroiliac joint pain considerably affects the freedom of movement of the hindlimbs and may mimic the clinical signs of exertional rhabdomyolysis, but plasma creatinine kinase (CK) levels often will be normal or only slightly raised (500 to 1500 IU/L).

Stress-induced bone injuries are more likely to become apparent as work intensity increases. Stress-induced bone injuries include all of the long bone stress fractures of the humerus, tibia, the McIII, and the MtIII, and the ilial wing and shaft of the pelvis. Similarly, in a 2-year-old that has reached advanced training speed, the carpus and metacarpophalangeal joint are common sources of forelimb lameness, and lateral condylar stress injuries of the MtIII are common causes of hindlimb lameness. A 2-year-old in advanced training is less likely to have lameness associated with a subchondral bone cyst, osseous cystlike lesion, or OCD because these lesions usually cause lameness when the horse is younger and beginning its conditioning exercise. However, occasionally subchondral bone cysts and osseous cystlike lesions may arise or result in clinical signs for the first time at 3 years of age or even older.

3 Has the horse raced yet? If a horse has raced successfully at 2 years of age, the horse is unlikely to have hidden osseous cystlike lesions or OCD. Also, the skeleton has probably been conditioned adequately, and the incidence of stress fractures can be expected to be lower. However, in countries where racing is seasonal, 3-year-olds can “detrain” through the closed season if they are not maintained in cantering exercise. Stress fractures then may occur in the following season if speed training starts too quickly. A Californian study showed an associative link between the occurrence of stress fracture of the humerus and previous long-term removal from training.²

If a horse did not race at 2 years of age, then all the differential diagnostic criteria used in the recently broken 2-year-old should be applied to the 3-year-old.

4 Has the horse had any previous orthopedic problems? Often in practice one knows each horse individually, and one is able to recall the problems that affected the horse in its early years. The history of a horse with previous problems may guide the use of diagnostic analgesia in an unorthodox, but timesaving, manner to establish whether the current lameness is a recurrence of a previous problem.

5 What is the pattern of the lameness? One should ascertain whether the lameness is constant from day to day and for how many days the horse has shown a gait abnormality. The veterinarian should ask whether the lameness gets better or worse within an exercise period. In some conditions, such as proximal suspensory desmitis (PSD), the lameness tends to get worse as the horse exercises, only to resolve with 24 to 48 hours of rest. Horses with lameness from other causes, such as OA, often warm out of clinical signs considerably from the start of exercise.

In horses with acute-onset, severe lameness, questions of clinical history become less important because the horse is often not bearing weight, and a suspicion of skeletal failure is raised. Knowing whether this horse has been a good mover before onset of severe lameness is often helpful because some injuries (McIII/MtIII bone condylar fractures, PSB fractures) often are associated with poor gait before the actual fracture takes place. The same is true of horses with slab fractures of the third carpal bone, which often are preceded by a long period of subchondral bone sclerosis associated with bilateral third carpal bone pain (Figure 107-2). One of the most useful questions to ask about a horse with severe lameness is what stage of training the horse has reached because only advanced training to fast canter or gallop speeds usually results in bone failure. However, bacterial infection subcutaneously or within the hoof also can produce severe lameness.

6 Has the horse had a prolonged layoff for any reason? Horses brought back from a long period of box rest after illness or injury, without adequate previous bone conditioning, can get bizarre injuries from unusually low-speed exercise. These include complete, displaced scapular and humeral fractures, bilateral fractures of the PSBs and tibias, or displaced fractures of the proximal phalanx or condyles of the McIII. This is a reminder of the vital need for time to allow adequate skeletal conditioning necessary to avoid injury.

Fig. 107-2 Flexed dorsal 60° proximal-dorsodistal oblique radiographic images of the left third carpal bone (C3) of three Thoroughbreds (TBs). Lateral is to the right. A, Normal. However, this complete lack of increased radiopacity is rare in a TB in advanced training, most of which show some degree of radiopacity of the radial fossa of C3. B, Dense increased radiopacity of the radial fossa of C3. Normal trabecular pattern is lost, and the bone has a “ground glass” appearance. There is increased osteolysis at the site of a normal nutrient foramen (arrow in the center of increased radiopacity). This stiffening of the bone predisposes it to injury or fracture. C, A nondisplaced sagittal fracture of C3 that propagates through the center of an area of severe increased radiopacity representing mineralization of bone (arrows).

Clinical Examination

The veterinarian always should get the horse out and see it walk and trot to determine which limb is lame. Riders are notoriously unreliable at detecting the correct lame limb. The veterinarian should determine whether the lameness is unilateral or bilateral by the way the horse moves. Many racehorses are slightly lame in all limbs and have a typical crouching, shuffling trot or may try repeatedly to break into a canter because trotting is so uncomfortable. New lameness may be superimposed on a chronic level of unsoundness.

Increasing experience usually leads one away from the belief that any one injury is linked to a particular gait. Lameness typical of a shoulder or a stifle tends to become a more remote belief because so-called typical lamenesses so often are linked eventually to the most unexpected site. However, a few types of lameness do remain that seem to be linked to one particular pathological syndrome. Young TBs often show bilateral forelimb lameness related to carpal pain. These horses often trot with the limbs abducted from the midline and not fully flexed during forward motion. This gives a rolling, stiff-legged forelimb gait. The horse’s attempt to get the contralateral limb down quickly to get off the sore limb as soon as possible shortens the forward phase of the stride, leading to a choppy, stilted action. However, horses affected with bilateral front fetlock pain or PSD trot in a very similar way if the pain level is the same in both limbs, and it may simply be that because carpal lameness is a common manifestation of this gait, we have come to link the two more firmly than we should.

Pain associated with the metatarsophalangeal joint is often bilateral and leads to a fairly characteristic gait typified by low limb flight, often with dragging of the toe during protraction, and an exaggerated rocking pelvic excursion dorsoventrally on both sides (sometimes termed the Marilyn Monroe trot) because the horse dips off each painful limb. Horses with a humeral stress fracture often abduct the limb, with shortened cranial protraction at the walk. One Newmarket trainer described this gait recently as “trotting like a pig in a tight skirt,” which, although not a likely scenario, is in fact just how they look..

Having ascertained which limb is the lamest, the limb should be examined in detail using basic examination protocols (see Chapters 4 through 8 and 10). The following specific points apply to the TB racehorse.

1 Many racehorses show a pain response to squeezing of the foot with hoof testers, which is not related to a current lameness. The TB has a thin-soled foot, which often is shod incorrectly, causing soft-tissue bruising on the palmar aspect of the foot. If the horse responds to hoof testers in the lame limb, I normally test the contralateral foot to see whether the response is different. If the response to hoof testers is the same in both limbs, the foot may not be the primary source of pain causing lameness.

2 Suspensory branches are best appraised by centering each branch between opposing thumbs and following the branch from the most proximal portion that is palpable distally to the PSB. Subtle thickening in the suspensory branch not palpable with fingertips may be detected as the thumbs separate running toward the PSB.

3 The metacarpophalangeal joint should be checked for distention of the palmar pouch of the joint capsule. Thumb pressure is applied to the dorsoproximal aspect of the proximal phalanx and the dorsodistal aspect of the McIII, common sites for fragmentation and impingement lesions producing soreness. The limb then should be flexed partially and the response to flexion of the metacarpophalangeal joint monitored. Many young horses show a mild pain response to flexion, and the contralateral limb should be compared to gauge whether a difference exists. However, in a 2-year-old a bilateral pain response may reflect true problems in both limbs. In a normal horse the metacarpophalangeal joint should not be painful to flex.

4 The proximal aspect of the suspensory ligament (SL) should be examined with the limb raised by squeezing the ligament between the thumb or fingertips and the palmar surface of the McIII, first medially and then laterally. Normal untrained horses show no pain response. However, many young racehorses show a variable degree of discomfort on SL palpation. Differentiating pathological and normal response to palpation associated with increased training can be difficult.

5 The dorsal surface of the McIII should be squeezed using the fingertips with the limb raised and the pain response noted as an indication of sore shins. The surface of the shin should be palpated for periosteal thickening or even focal callus formation associated with a stress fracture.

Running a finger distally on the shin with a horse bearing weight often causes a horse to buckle the limb even if it has been months or even years after shin soreness has subsided and is not a reliable diagnostic test.

6 To detect distention of the antebrachiocarpal or middle carpal joint capsules, pushing on the dorsal surface of the joint with the finger and thumb of one hand while observing the palmar pouches of the joints is useful. Mild effusion then may be detected.

7 Many young racehorses resent extension of the shoulder joint in the absence of a lesion.

8 Many racehorses mildly object to forced tarsal flexion equally in both hindlimbs unrelated to a lesion. A profound response to flexion of the tarsus of the lame limb, which is not matched in the contralateral limb, usually signifies a tarsal bone fracture or a stress fracture of the distal aspect of the tibia. If pain is noted on flexion, thumb pressure should be applied to the proximodorsal aspect of the MtIII and the dorsolateral surface of the tarsal bones to determine a pain response. Pain response is often marked if there is a slab fracture of the third tarsal bone.

9 The tibia is a common site for stress fractures and is examined by curling the fingers around the caudal surface of the tibia from the medial aspect and squeezing on a common predilection site for stress fracture, the caudal surface of the distal third of the tibia. Torsion of the tibia also is attempted by flexing the limb, applying lateral traction to the os calcis with one hand while maintaining firm contact on the stifle with one’s shoulder, and medially twisting the distal aspect of the MtIII with the other hand (Figure 107-3). A horse with an incomplete linear stress fracture will show a profound pain response to torsion and may try to kick. It may also not want to take weight on the limb for a few seconds after its release, which is a sign characteristic of marked cortical involvement. The other limb should be examined, bearing in mind that these fractures can be bilateral, although pain and degree of lameness are often asymmetrical.

10 The pelvis is another frequent site of stress fractures and is examined by monitoring the position of the bony landmarks—the tubera sacrale, tubera coxae, third trochanter of the femurs, and tubera ischia—looking for displacement (see Chapter 49). Response to deep palpation of the muscles that lie between these sites is also noted. The most common clinical sign in horses with a nondisplaced pelvic fracture is guarding of the musculature as a response to deep palpation. Guarding gives a hard, boardlike texture to the muscle and often is accompanied by fasciculation of the gluteal mass and an avoidance response. Similar clinical signs can be seen in horses suffering from exertional rhabdomyolysis, and this may be a difficult differential diagnosis to establish. Muscle enzyme concentrations may be elevated (CK, 500 to 1500 IU/L) in horses with a pelvic fracture. The tail should be raised and lowered, and tail tone should be monitored. A flaccid tail often indicates a sacral or coccygeal fracture.