A strong, well-conformed and developed musculoskeletal system is essential to provide structural support and limb soundness in exercising horses of all ages. These needs are greatest in the athletic horse to withstand the loading, strain and concussive forces imposed on bones and joint structures. Bone and joint injuries account for up to 70% of the downtime or lost training days in racing and equestrian event horses, with the type of musculo-skeletal injury changing during a horse’s athletic career (Bailey, 1998). The lower forelimb below the knee of horses is most likely to develop structural damage leading to lameness in all classes of athletic horses (Davies, 2003). Over the past decade, there have been numerous studies that have provided insight into the reactive properties of bone and limb structures as they adapt to the increase in body weight and exercise loading from birth and throughout a horse’s life (Lawrence, 2003b).
Musculo-skeletal unsoundness, particularly related to bone failure and joint injury in racing, equestrian and other athletic horses, can be linked to overloading of bone structures relative to the body weight of the horse, the age at which the young horse is first worked, the speed of exercise and degree by which the bone and joint structures are able to adapt over time to additional body weight and loading forces (Ireland, 1998; Davies, 2001). After each period of exercise, even in growing horses, the bones remodel or react to increase strength, circumference and mineral density (collectively called bone mass) while internal trabecular structures adapt to withstand the increased loading forces. This is a relatively slow process, which can take up to four months to complete in a progressive remodeling process in the young horse exercising during the growth phase or in athletic training before maturity (Lawrence, 2003b).
If the increase in loading force exceeds the rate at which the cross-sectional area and mineral density of cortical bone can adapt, then there is a risk of bone reaction. This results in bone surface (periosteal) inflammation; and in bone subjected to the repeated stress of high loading, there is the risk of bone shaft and joint microfracture and failure (Davies, 2001). One of the classic examples of the failure of bone modeling to increase bone mass and resilience at an optimum rate in response to exercise loading is dorsal metacarpal disease, commonly known as shin soreness or ‘bucked shins’ in young Thoroughbred racehorses. (Bailey, 1998; Lawrence, 2003b; Davies, 2003). A similar overloading-induced reaction and metacarpal fracture also affects the metacarpals of racing greyhounds, referred to as metacarpal periostitis, when dogs are exercised on a ‘too fast – too early’ program on a tight turn racetrack (Boemo, 1998; Ireland 1998).
The highest weight loading is imposed on the bone structure of the front limbs of racing Thoroughbreds when cornering at the gallop at speeds of up to 15 meters/second (Bailey, 1998). Studies have shown that loading forces on the front limbs of up to twice that of a horse’s bodyweight are imposed when galloping in a straight line (Lawrence, 2003b). For example, when a horse is galloped around a corner on a racetrack, an estimated combined centrifugal and momentum-related loading force of up to 5-10 times the animal’s body weight is placed on bone and joint structures in the lower limbs (Ireland, 1998). Up to 80% of lameness conditions occur in the front limbs of galloping racehorses, with up to 80% of these injuries and failures or ‘breakdowns’ focused on the bones, joints, ligaments and tendons below the knee (Bailey. 1998). Failure of the musculoskeletal system is most often associated with injury to the hard tissue or bone structures of the lower limb, with tendons and joints also being subjected to ‘wear and tear’ and overload in over-galloped young horses (Lawrence, 2003b).
Bone development in growing horses
Bone is a dynamic living tissue that is responsive to the loading forces imposed during exercise from birth, with most response occurring in the first six months of life. A number of studies have indicated that joint diseases or the failure of proper joint and associated bone development known as osteochondrosis, which refers to a primary lesion or defect in the growth and maturation of cartilage and subchondral bone, is most common as cartilage changes to bone as a foal grows (Jeffcott, 2001; Firth, 2003a; Lawrence, 2003a). The mineralization of the cartilaginous skeletal bone structures commences in the unborn foal during the last three months of gestation as it doubles in size prior to birth (Jeffcott, 2001).
At birth, the foal’s skeleton contains only 17% of the mature bone mineral content, increasing to 68.5% by six months of age, and 76% by yearling age in athletic breeds of horses (Lawrence, 2003a; Firth, 2003a). Studies have shown that cartilage defects occur within the cartilage of the joint surface or at the epiphyseal junction, or growth plate on the ends of the long bones, as the skeleton develops in the growing horse.
The immature bone is composed mainly of cortical or external wall or compact bone, and cancellous or porous, trabecular reinforcing bone within the bone’s internal structure (Lawrence, 2003a). Mineralization of cortical bone with deposition of calcium, phosphorus and magnesium, the principal bone minerals, continues as the body weight and exercise loading increases throughout the first year of life. Subchondral bone and structural shaft bone must continually adapt, strengthen by additional mineralization and repair themselves when subjected to loading, compression and concussion during exercise as the skeletal system develops in the young horse. After each period of exercise, the bones react to remodel or adapt their internal structure and strength by increasing the cortical cross-section, circumference and mineral density (Lawrence, 2003b; Davies, 2001).
The area of cortical or shaft bone increases from around 30% at birth to 60% at six months to 80% of the skeletal bone structure in the mature horse (Firth, 2003b). Davies (2001) describes the remodeling and changes in cortical shape of bone in horses as they progress through a training program. A technique of Radiograph Index to measure the cortical thickness of the front cannon bones has been developed and is used to assess the state of remodeling relative to the stage of training in young Thoroughbred horses, and may be used to predict the extent of bone reaction and shin soreness (Davies, 2003).
Bone adaptation to exercise
One of the earliest studies in America on Thoroughbred and Quarterhorse weanlings concluded that bone strengthens by increasing its mineral density, principally by depositing calcium within bones (Raub et al., 1989). These researchers found that over an 111-day period the cannon bones of weanlings exercised by trotting, initially over 400 meters and increasing to over 4 km per day, accumulated 25% more bone calcium than weanlings that had been stalled overnight and turned out into pens during the day.
Numerous other studies, cited by Jeffcott (2001), Firth (2003a) and Lawrence (2003b) in a review of osteochondrosis and response to exercise in horses, have reported similar adaptive responses in foals and weanlings up to five months of age, with a lower bone density in the cortical shaft and subchondral bone mass in non-exercised compared to exercised young horses. After six months of identical exercise, the young horses in the original non-exercised group remodeled the bone, in this case the stifle joint, to establish an equal mineral density and cross-sectional area (Lawrence, 2003b).
The mineralisation of the skeletal and the structural subchondral base of joint cartilage, as well as the calcification of long bones and formation and internal organization of the tendon structure, is largely completed by six months of age. It has been established that the amount and type of exercise has a direct influence on joint cartilage, subchondral bone, bone cortical mass and maturation in young horses as they develop.
It is important that young growing horses have access to free paddock exercise to encourage the formation of sound cartilage and subchondral bone, while over-exercise and excessive weight loading in heavy weight young horses can result in damage to the developing joint cartilage and subchondral bone in joints (Firth, 2003a).
Jeffcott (2001) and Firth (2003a) concluded that the effects of high energy:nutrient ratios, confinement to small yards and over-exercise or lack of adequate exercise, high weight loading and inadequate trace minerals and calcium balance, all adversely influence the cartilage development, bone mineralisation and maturation of the skeleton in the formative years of a horse’s life.
INCREASED BONE TURNOVER
One of the other major problems in bone repair is triggered by the stress of everyday training. The bones must continually adapt and remodel themselves to maintain strength in response to training. The stress of continuous high loading results in the bone itself becoming less dense during this modeling process, triggered in response to ongoing high load exercise. During each hard workout, the high stress loading on the bones can cause microfractures or other microscopic changes within the cortical bone, ultimately causing a repair response within the bone (Davies, 2001).
BONE STRESS CONDITIONS
Studies of shin soreness in Thoroughbred racehorses have shown that after a hard gallop over 200-300 meters (1 – 1½ furlongs), the cannon bone in a young horse becomes reactive and attempts to strengthen itself by depositing calcium within its front cortical wall for the next 10-12 days (Nunamaker et al., 1990; Davies, 2001). When too many ‘breeze-up’ or ‘allout’ gallops are given successively at 2-3 day intervals in an accelerated ‘get fit’ or ‘too fast – too early’ training program, the bone itself cannot respond rapidly enough, and can become inflamed, as occurs in shin soreness (Davies, 2001).
Once horses reach maturity at four years of age, the bone remodeling process is less active. Studies have shown that in the young horse, an injury to a bone can affect the response within 2-5 days, but in an older horse this may take up to 10-12 days, depending on the type and extent of the exercise overloading (Firth, 2003b).
ABNORMAL BONE TURNOVER
In response to high loading forces, the bone needs to remodel to either repair itself, or to strengthen the target site where the overload has occurred. In the athletic horse, there are a number of sites that are more likely to fracture when working because of abnormal bone turnover during exercise. Studies using radio-isotope labeling of bone calcium and other minerals, as well as traditional radiographs of the bones, can help monitor the structure and density of the bone. Recent developments, such as scintigraphy of the bone, can map the responsive nature of bone and identify the sites where active remodeling and calcium deposition is occurring as new bone is formed. These studies have shown that certain bones in the horse’s skeleton undergo a high rate of repair and remodeling during training. If this rate of remodeling is unable to be maintained to strengthen and rebuild bone in response to exercise, the bone itself is more likely to fracture and fail when loaded. These include the edges of the pedal bone in the hooves, the sesamoid bones behind the fetlocks and the knee and hock bones in racing and hard working horses (Firth, 2003b).
ADAPTATION TO FAST EXERCISE
Studies have investigated the effects of exercise on the bone density and strength in growing and adult horses at both training and racing intensities of exercise. It has been revealed that when a horse is worked below its maximum speed during long periods, in both young and adult horses, there is no dramatic alteration in the density or mass of bone in the front cannon bones (Lawrence, 2003b). However, once horses start galloping at a much faster speed in fast work, there is an increase of bone density relative to the speed of exercise, and a reduction in the porous structure of the bone as more calcium is loaded into the bone to strengthen it in response to exercise (Davies, 2001).
DORSAL METACARPAL DISEASE (SHIN SORENESS OR BUCKED SHINS)
Dorsal metacarpal disease, or ‘bucked shins’ in the severe case, is a common example of bone overload and associated bone reaction. Thoroughbred trainers in the United States, Australia and New Zealand often have young horses that develop dorsal metacarpal disease. It is a widespread belief held by many trainers in Australia that young Thoroughbreds in early race training need to develop shin soreness to ‘toughen’ their cannon bones (Bailey, 1998). This condition, however, is a symptom of excessive bone loading resulting from a program of too fast-too early pace work or breeze-ups.
Although much research has been carried out investigating the classic changes that occur (Nunamaker et al., 1990; Davies, 2001), many researchers fail to understand the relationship between speed and radius of a circular training track. Ireland (1998) highlights the relationship between body weight, speed and radius of the corner on a race track that influences the rate of injuries and incidence of metacarpal periostitis in young greyhounds analogous to shin soreness in horses.
Ireland (1998) provides evidence of a direct relationship of these factors to the degree of centrifugal force loading that occurs when a horse or greyhound sprints around a bend on a racetrack. When the track surface has an adequate crossfall to the inside rail or is banked in proportion to the speed of movement and radius of the track corner, the horse is able to lean over to be perpendicular to the track slope and the centrifugal force is negated, reducing its high loading forces on the limbs (Ireland, 1998).
Galloping in a straight line will not induce periosteal reaction to the same degree as occurs when the cannon bones are loading as a horse is galloped around a compacted, inadequately banked bend on the racetrack. In Australia and the southern hemisphere, dry compacted track surfaces that increase limb concussion combined with over-galloping young horses on circle tracks are the major contributing causes of forelimb metacarpal periostitis and shin soreness (Bailey, 1998). Shin soreness in young horses can vary in severity, but it describes the inflammation and pain that develops over the front surface of the foreleg cannon bones in young racehorses galloping at racing speed. A much better understanding of bone remodeling processes has led to revised training and management guidelines to reduce the risk of it developing in young racehorses.
Surveys indicate that the risk of metacarpal remodeling in horses (and greyhounds) is influenced by the track surface (moisture content and compaction) and design (banking and length of straight gallop), radius and crossfall of bends and end circles, seasonal conditions and the speed and distance of fast exercise in the training program (Ireland, 1998; Bailey, 1998; Table 1).
The leading foreleg has a 20% higher risk of developing shin soreness, although both front cannons are affected in 70% of young horses (Bailey, 1998). Colts and fillies are affected equally. The direction of cornering also influences the severity of shin soreness on the inside limb next to the running rail, with the leading inside foreleg cannon bone developing a more severe periosteal inflammatory response and remodeling reaction. The cannon bones must change their cross-sectional shape to provide reinforcement along the stress pathways imposed by high speed exercise (Davies, 2001). It is a slow natural process that must happen to enable the bones to withstand high-speed strain forces without developing stress related microfractures that radiate into the anterior cortex of the cannon bones.
Dorsal metacarpal disease has been shown to be initiated by increased strain forces from concussion, increased weight forces and centrifugal turning forces in horses exercising at racing speeds on tracks with unbanked, small radius bends (Ireland, 1998). The cannon bones change in shape and diameter as the horse adapts to training (Ireland, 1998; Davies, 2001). Very high bone strain, compression and cyclic loading forces in the front third metacarpal (shin) bones have been recorded in early training (Davies, 2001).
When a young horse is worked below maximum speed for extended periods, there is no dramatic alteration in the density or mass in the front cannon bones (Davies, 2001). Generally the risk of shin soreness can be reduced by adopting a revised training program allowing the cannon bones to be challenged with controlled strain loads by galloping over short distances at an earlier stage of training (Nunamaker et al., 1990; Boston and Nunamaker, 2000). This incremental loading pattern allows the bone to undergo the required remodeling changes with more time to adapt to fast work at racing speeds. If a horse is pushed too fast too early, the stress loading on the immature bone stimulates emergency modeling with deposition of weaker fibrous elastic bone to reinforce the bone so that it can withstand the forces of galloping (Davies, 2001).
Table 1. Incidence and reasons for occurrence of dorsal metacarpal disease in the UK, US and Australia1.
1Bailey, 1998Centrifugal force (Cf) or loading on the cannon bone is related to the following equation (Ireland, 1998):Radius of the track end circle
||9 – 17
||Soft training surfaces, on peat moor areas, straight line gallops, long pre-race preparations
(12-14 wks) – low risk of bone strain and adequate time to adapt.
||65 – 70
||Dirt tracks, some banking on tight end circles, 10-12 weeks race preparation – increased bone
stress and less time to adapt.
||60 – 80
||In Australia, most horses are trained on circle racetracks. Dry hard track surfaces, small radius
bend(s) in tracks, no banking, 8-10 weeks race preparation – high risk of bone strain and
overload, little time to adapt to racing speed with a ‘too fast-too early’ program.
This equation illustrates that heavy, faster 2-year olds galloping at racing speeds on unbanked, compacted small tight circle tracks have a higher risk of bone overloading and bone reaction.
When a horse is turned out and rested in the paddock after going acutely shin sore, with shortened stride, swollen, painful ‘bucked shins’ on the anterior surface of the forelimb cannon bones, the weak fibrous bone is resorbed, returning the bone to its immature cross section and lower load bearing capacity over a period of 4-8 weeks (Boston and Nunamaker, 2000).
Ideally, the front cannon bones should be encouraged to adapt slowly from the start of training, allowing accumulation of extra high density mineralised cortical bone to strengthen the anterior surface of the cannon bones to enable them to withstand concussion and increased weight bearing loads. Rapid reinforcement with fibrous bone involves the reabsorption of calcium from the sides to strengthen the front surface, reducing the bone’s side rigidity or ‘stiffness’ against bending under high strain loads. This can result in painful stress fractures developing on the anterior surface of the front cannon bones as they distort under extreme loading forces of high speed galloping and symptoms of ‘bucked shins’ and risk of metacarpal fracture and failure during racing (Nunamaker et al., 1990).Practical management for prevention
Based on my 30 years of experience as an equine veterinarian and my professional role as a consultant to many racehorse trainers in Australia, I have developed a management program which can be implemented by race trainers to significantly reduce the risk of bucked shins, or assist the rehabilitation of horses that have developed severe periosteal inflammation and cortical microfractures. This program is based on the research outlined in this review and is intended as a practical guide.GENERAL INFORMATION
Most Thoroughbred racehorses train at speeds much slower than those at which they need to race to be competitive, where they can reach peak speeds of up to 50 km/hr (15 meters/second). Therefore, a horse may be modeling its cannons to withstand the loading imposed by slower conditioning, which is much lower than the strains imposed at racing speed. Thus, when the horse actually undergoes prolonged fast work, such as a barrier trial or its first race, the risk of sudden and intense bone overload and damage is increased, especially if it is galloped at speed around a tight circle track after being trained on a relatively straight track. The cannon bone has to model from a circular, even-walled cross-section in the immature horse to a cross-section with a thickened inside edge, with up to twice the average wall (cortical bone) thickness of the cannon bone shaft.
A technique of radiographic index (RI) with radiographs taken to measure the thickness of the bone wall (cortical bone) on the front and inside edge of the front cannon bones at weekly intervals can help monitor the adequacy of the remodeling process in response to bone loading during training. If the RI exceeds the established value at a set stage of training, it is an indication that excessive bone remodeling and inflammatory reaction has occurred. In this case, the speed and distance of fast work should be reduced to allow the remodeling process to catch up to the degree of strain loading. If the RI is below the established limits at a particular stage of training, it is possible that horses that are over-galloped have a high risk of developing shin soreness.
Many trainers believe in long, slow work to ‘build bone’. While this program works to build and condition the muscles, joints and limbs, the bone that the horse is building is more suited to long, slow work rather than to racing. If the shins become severely inflamed with deposition of a bone splint or a ‘bucked shin’ swelling, the bone laid down is a weaker form of fibroelastic bone as a temporary reinforcement to prevent bone failure. This type of bone has little residual strength; and if the horse is rested from training, this temporary reinforcement ‘splint’ is resorbed. The bone profile or cross-section returns to its original weaker structure that is unable to withstand the increased loading imposed by galloping too fast-too early when training resumes. Harness horses do not develop sore shins because they race at slower speeds on banked tracks and have two legs on the track surface at any one time to share the additional loading.
Training programs should be designed to allow the cannon bones to experience and adapt to the loading and deformation strain imposed by higher speed galloping. The leading forelimb is subjected to the greatest amount of strain, particularly when cornering, so it is recommended that the initial high speed work should be carried out down the straight to model the shins, reducing to a slower pace around the turns.Short gallops in early training
Commence a program of short, straight-line gallops over 200 meters twice weekly (at least 4-5 days apart) from the third week of training to progressively load the cannon bones. Short gallops in a straight line do not cause undue stress on bones or muscles after 2-3 weeks of initial conditioning exercise. As the horse develops in fitness, increase the speed and distance traveled to 300-400 metres at each fast workout. Bone modeling is a slow process as is bone fracture healing, so a stepwise increase in loading over 8-10 weeks will allow time and stimulate modeling in response to the loading forces imposed. A measurement of Radiographic Index to evaluate the remodeling response of the bone can be carried out at weekly intervals to monitor the bone thickness in response to fast work.Avoid tight circle tracks
Do not gallop young horses around tight, compacted curves or end circles on the track too early in their training preparation. Gallop only up straights initially, then work progressively faster into corners and around end circles to allow adaptation to the centrifugal sideways strain forces, starting after 6-8 weeks of training. Avoid sudden introduction to fast work and limit speed of galloping around unbanked, relatively tight bends initially, especially on dry, compacted tracks.Adequate calcium and vitamin D
Ensure high grain diets are supplemented with calcium, phosphorus, magnesium, vitamin A and vitamin D to provide adequate minerals for bone development and modeling in response to loading as the shin bones model as they thicken and adapt in cross sectional shape to withstand the increased stress loads.Train on the same track
It is best to train on the same track, so that the bends and surfaces are consistent, avoiding compacted areas on the rails when galloping on fast work mornings. The majority of racetracks have training tracks built inside the main grass, turf surface or sand track. These have smaller end circles and can impose additional loading, especially on odd shaped, rather than oval track designs, constructed to provide the length of straight required within the available land area.Avoid heavy work riders
Once the young horse is controllable, change to a fast work rider (50-60 kg) to reduce excessive loading as the horse is worked faster at the start of regular fast work. Each extra kg of rider weight is magnified 5-10 times by centrifugal forces when galloping around bends.Minimise concussion
Cushion depth and type of surface is important to reduce concussion, vibration and ‘jarring’ on the front cannon bones. Properly maintained synthetic, woodchip and grass tracks are less concussive on the legs than dry finely packed sand surfaces. Avoid hard compacted cinder or dirt tracks with tight bends and little banking. Work out from the compacted areas away from the rails and choose dampened, more cushioned areas, if possible, for galloping.Cold therapy after galloping
Apply cold therapy, such as cold water hosing for 10-15 minutes, or preferably by ice boots or an ice block under a pressure bandage for 5-10 minutes, after each gallop in the later stages of training. Ice packs can be wrapped on both front cannons during the walk to cool-out, or during the trip home from the track to help reduce minor inflammation and soreness as training progresses. A magnetic bandage with 1500 gauss field strength wrapped on both forelimb cannon bones may be helpful to increase the rate of deposition of calcium and bone minerals and hasten the modeling and strength of bone laid down as it adapts to higher loading during fast work. The bandage can be wrapped in the afternoon and overnight when the horse is resting in its stable or yard.Check shins regularly for heat or soreness
Watch for abnormalities in gait and shortening of stride. If early soreness is detected, cut back on the speed of fast work for 2-3 weeks to allow the shins adequate time to model and thicken the bone along the stress pathways. Apply cold packs after training, or if discomfort is more severe, apply a warming liniment overnight or alternatively (not at the same time) a clay poultice overnight until symptoms subside. In severe cases, it is best to rest the horse for 3-4 weeks until the soreness settles down, and then recommence on a revised program as outlined above. When horses are rested, the cannon bone actually becomes even less rigid as modeling of new bone occurs along the stress lines.Re-program training after down time
For each week that a young horse is rested because of other problems (e.g. respiratory disease, joint problems, severe tying-up), back step its training program by two weeks to avoid shin soreness as the cannon bones may start to resorb calcium and weaken during the lighter work period.Compounding feeds to promote skeletal development
The requirement for a balanced and well formulated diet is paramount to ensure optimum growth and skeletal development, as well as remodeling in response to exercise, in young horses in their formative years. It is important that feeds are formulated to provide adequate digestible nutrients to meet these requirements. There is a wealth of information and nutrient recommendations from equine nutritional research over the past two decades. Most companies that produce blended feeds, or large horse breeding farms and training stables are provided with up-to-date advice by equine specialists.RATION FORMULATION FOR GROWTH AND DEVELOPMENT PHASES
It is important that rations are formulated to meet the various phases of reproduction in mares. It is particularly important in the last trimester that pregnant mares be provided with an adequate amount and balance of macrominerals, trace minerals and vitamins to ensure the formation of cartilage and bone framework prior to birth in the unborn foal. It is important that trace minerals such as iron, copper, zinc, manganese and vitamins including vitamins A, D and E are supplemented or incorporated into feed mixes to allow adequate foetal liver storage prior to birth. After birth, during the more rapid phase of growth, a low glycaemic diet should be provided, containing adequate energy and quality protein as well as minerals, trace minerals and vitamins to meet the growth and mineral needs of the developing musculoskeletal structure. It is beyond the scope of this paper to provide specific guidelines. However, there are a number of aspects of feed formulation that should be kept in mind when blending feeds, premixes and supplement concentrates for use in growing and exercising horses. These issues are rarely addressed by formulators or advisory consultants.These include: Limit the concentration of alkaline mineral sources.
Limit calcium carbonate, magnesium oxide and potassium chloride in the fines of a textured feed, premix or supplement which also contains trace minerals and vitamins. In textured feeds, calcium carbonate is commonly included in the fines at a rate of 1-3% by weight to provide calcium. In premixes and supplement concentrates, it is often used as the carrier at 50-80% of the total batch weight. The alkalinity of these carriers in the fines or bases can reduce the bioavailability and accelerate the degradation rate of vitamins surrounded by an alkaline environment, particularly in a moist feed blend or premix. The majority of essential vitamins, including retinol, cholecalciferol and tocopherols, thiamin, riboflavin and cyanocobalamin are more stable when the pH is maintained between 5-6 in the fines and premix carrier. Compounding a range of vitamins into a pelleted form for blending with alkaline carriers would significantly reduce the destructive interactions during storage. Overages of vitamins should be included to counteract the destructive interactions when these alkaline carriers are used. (Kohnke, 2002). The addition of calcium hydrogen phosphate, also known as dicalcium phosphate (DCP), an acidic mineral source (23-25% elemental calcium, 18% elemental phosphorus) as a dual calcium and phosphorus source, blended in a 60% dicalcium phosphate to 40% calcium carbonate ratio, relative to the mineral balance required, will maintain a more neutral pH environment to improve vitamin stability. Calcium carbonate (limestone carrier) has a pH of 8.41 (alkaline) when measured using 10 g in 20 ml distilled water while dicalcium phosphate has a pH of 6.68 (slightly acidic). A blend of 60% limestone with 40% dicalcium phosphate (12 g + 8 g in 15 mls distilled water) has a pH of 6.83. The use of buffered propionic acid mould inhibitors, such as Mold-Zap™
(Alltech Inc.) at standard addition rates, also helps to buffer the alkalinity of carriers to help improve vitamin stability (Kohnke, 2002; 2003, unpublished).
In addition, calcium is absorbed more effectively from the small intestine in an acidified environment. Mineral oxides, particularly iron oxide as well as copper oxide and zinc oxide, should be limited in premix blends Oxides generally reduce vitamin stability. Magnesium oxide appears to be less destructive to vitamins when used as a source of magnesium and, although it has an alkaline pH, it can be buffered to around neutral by dicalcium phosphate (Kohnke, 2002; 2003).Selenium and chromium from yeast: Sel-Plex® and BioChrome®
These minerals, critical to antioxidant protection (Se) and energy utilisation (Cr) are more easily metabolised and retained than inorganic forms (Dunnett, 2003).Mineral proteinates:
trace minerals Bioplexes supply key trace minerals in forms similar to those in plants: chelated to amino acids and peptides. In addition to being more available to the animal, these ‘organic’ mineral forms do not trigger oxidation and destruction of the fat-soluble vitamins in premixes. A study to compare the digestibility of inorganic and Bioplexed™
forms of copper and zinc, two very important trace-minerals required for cartilage formation in growing horses, indicated there was a significant advantage from the inclusion of Bioplex™
forms in the diets. These included higher copper digestibility, daily retention, retention as a percent of intake, and significantly higher apparent daily zinc retention, compared to those supplemented with inorganic forms of copper sulfate and zinc oxide (Baker, 2002).
Copper, zinc and manganese, along with selenium and vitamin E, are important factors in natural antioxidant defence. It is important to include adequate levels of antioxidant nutrients to limit the rate of lipid peroxidation and rancidity, particularly in feeds fortified with omega-3 (n-3) and omega-6 (n-6) fatty acids from vegetable oils. Omega-3 fatty acids are particularly prone to oxidation during storage, and additional levels of antioxidants help protect omega-3 fatty within muscle cell membranes once the feed or premix is consumed (Dunnet, 2003).
Careful formulation to reduce incompatibilities, chemical reactions, binding and known nutrient interactions will not only improve bioavailability of minerals and trace minerals, but minimise the need for excessive overages of vitamins and extend the shelf-life of premixes and supplements.Conclusion
The soundness of the skeletal structure in growing and exercising horses is largely dependent on providing an adequate diet with a balanced intake of bone and joint structural nutrients during the formative years of a horse’s life. Controlled exercise will assist in the skeletal development and allow remodeling in response to loading in both growing and exercising horses.
Care when formulating feeds, premixes and supplements to ensure optimum bioavailability and stability of skeletal nutrients is essential to maintain long term athletic soundness in all classes of horses.
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Author: JOHN R. KOHNKE
John Kohnke Consultancy Pty Ltd, Rouse Hill, New South Wales, Australia