Bones of contention - how to maintain a strong skeleton
/By Catherine Dunnett
The expression ‘no foot no horse’ should perhaps be extended to cover all the bones of the skeleton, for as far as racehorses are concerned, without strength and durability in this area a trainer’s job is fraught with difficulties. The number of training days lost to lameness in a season is testament to this. A racehorse’s diet should help to maintain the skeletal system during rigorous training. This task is no doubt easier when the skeletal foundations have been firmly laid in utero and during the rapid growing phase.
The formation of cartilage and its subsequent conversion to bone ‘proper’ is one of the key processes to highlight. Long bones develop in the foetus from early bone templates that are composed entirely of cartilage. Conversion of cartilage to bone occurs initially within a central area of ossification (bone formation) within the long bones, known as the diaphysis and then also at each end of the bone (epiphysis).
There are various abnormalities that can occur during the development of bones and joints that may involve problems during the localised conversion of cartilage to bone, or with bone lengthening, or changes within the bone after it has formed, once a horse has commenced training.
Nutrition is only one of many factors involved in DOD Osteochondrosis (OCD) involves disruption to the normal conversion of cartilage to bone within the areas of ossification. For many years, researchers viewed nutrition as the key to OCD, however, it is now recognised that genetic predisposition, body size and mechanical stress, as well as trauma are all additional factors that must be considered. Whilst diets that simply oversupply energy have been demonstrated to increase the incidence of OCD, the previously hypothesised causal link with excessive protein intake has not been proven.
This suggests that the source of the energy in feed is an important issue. Recent research supports this, as it has been reported that diets with a high glycemic nature, i.e. those with a high starch and sugar content (typical of the more traditional stud and youngstock rations), appear to be more likely to trigger OCD.
However, one would suspect that this would be more apparent in genetically susceptible animals.
Many mineral imbalances in the diet have also been implicated as causative factors in OCD, but few have any strong evidence to support their role. For example, OCD lesions have been reproduced experimentally in foals maintained on a very high phosphorus intake. This type of diet could arise inadvertently by feeding straight cereals such as oats, without a suitable balancer or complementary feed such as alfalfa to redress the low calcium to phosphorus ratio in the grain. Less extreme versions of this diet could occur through excessive top dressing of ‘balanced’ coarse mix or cubes with additional cereals such as oats or barley, as is common practice in many yards.
A low copper intake, especially during the last trimester of pregnancy, has also been implicated in OCD. Copper has received particular focus due to its functional role in the activity of a key enzyme involved in formation of the collagen cross-links. However, other trace minerals including manganese and zinc may be equally important during this key stage in a foal’s development in utero, as they are necessary co-factors for important enzymes involved in regulating cartilage metabolism.
Blood tests that challenge the premise that horses are unaffected by molybdenum levels in grazing
In grazing youngsters, a secondary copper deficiency can be caused by excessive molybdenum levels in pasture. In cattle, bacteria in the rumen form complexes between molybdenum and sulphur. These thiomolybdate complexes will bind copper within the gut and when absorbed will then search out further copper to bind, either circulating in the blood or in association with copper dependent enzymes. This can severely impair the activity of some key enzymes involved in growth processes and cartilage turnover.
However, as a horses gut is somewhat different from a cow’s, in that the hindgut (the equivalent of the rumen) is positioned after the small intestine and not before, there is theoretically less opportunity for these thiomolybdates to be absorbed and ‘cause trouble’. At least this is what has been largely accepted from previous studies in horses that focussed on plasma copper levels and copper absorption.
However, new blood tests that can be used to measure the activities of key copper dependent enzymes, such as superoxide dismutase (SOD), in conjunction with traditional measurements of plasma copper status and the presence of thiomolybdate complexes suggest that this may not always be the case. Dr Stewart Telfer of Telsol Ltd, routinely carries out such tests in cattle and has to date analysed about 100 samples in horses suspected of having an issue with molybdenum interactions. He says, “From our work, it is clear that horses do suffer from molybdenum (thiomolybdate) toxicity. The interactions between copper, iron, molybdenum and sulphur will take place in the horse’s gut and in certain situations, not always linked to a high molybdenum intake, will result in the horse suffering from molybdenum (thiomolybdate) toxicity. Dr Telfer however, acknowledges that only relatively small numbers of samples in horses have been tested and the laboratory does not currently have a definitive reference range for horses.
Calcium and phosphorus may be mobilized from bone to compensate for ‘acidic diets’
When yearlings first move into training yards, they usually experience a significant change in their diet that has consequences for bone metabolism during this period in their lives when some continued growth occurs and the skeletal system is put under considerable strain. In general terms, a ‘stud diet’ has what’s called a high dietary anion to cation ratio (DCAB). This is largely due to the high inclusion of ingredients like soya and forages. A ‘full race training diet’ on the other hand tends to have a much lower DCAB (is more acidic) due to the reduction in forage intake and higher inclusion of cereals such as oats. The significance of a low DCAB is that it reduces the efficiency of calcium absorption and retention within the body and may contribute to the reduction in bone density seen in horses in early training. This surely is an argument for limiting the intake of cereals and maximising forage intake during the early stages of training when a high cereal intake is largely unnecessary.
Calcium is the most abundant mineral in the horse's body, with the majority being present in the skeletal system. Phosphorus is also found in large amounts in bone in close association with calcium. A racehorse’s diet should provide an adequate intake of both minerals but also needs to provide a balanced calcium to phosphorus ratio of near to 2:1. Although exercise demands a slight increase in calcium intake above the requirements for maintenance, this is usually satisfied by the generalised increase in feed intake. However, the efficiency with which individual horses absorb calcium varies and should certainly be investigated when a calcium-related issue arises. This can be achieved by examining an individual horse’s calcium and phosphorus status, by looking at the diet and also within the body using a creatinine clearance test.
Topdressing – a national pastime
When using straight feeds, or when topdressing ‘straights’ onto a ‘balanced’ racing mix or cubes, be aware that certain types of feed are much higher in calcium relative to phosphorus and vice versa (see table). Alfalfa, with its high calcium to phosphorus ratio, makes an ideal partner for cereals, which are low in calcium relative to phosphorus.
Conversely, the traditional combination of oats and bran is not ideal, as it combines two feeds, which are low in calcium. Remember that you can use a supplement or feed balancer to carefully correct any deficiencies or imbalances when feeding straights. Equally excessive addition of oats to a balanced mix or cube can decrease the calcium to phosphorus ratio sufficiently to cause problems. Most commercial mixes or cubes have sufficiently high calcium to phosphorus ratios to practically be able to withstand the addition of 1-2kg of oats daily, however any increase beyond this is unwise without further corrective measures.
Feeds High in Calcium & Low in Phosphorus
Alfalfa, Sugar Beet, Seaweed
Feeds Low in Calcium & High Phosphorus
Oats, Barley, Maize, Wheat Bran
Horses have a complex regulatory system, involving certain hormones, for ensuring that the proportion of calcium in the body, relative to that of phosphorus, remains stable and that the level of active or ‘ionised’ calcium in the blood remains within tight limits. If for one reason or another the level of calcium relative to phosphorus in the blood drops, a number of safety systems will be triggered to redress the balance. Bone acts as a reservoir of both calcium and phosphorus, which can be drawn on when necessary. The body's balance of calcium and phosphorus is continually 'corrected' by either conservation or loss of calcium or phosphorus in the urine, via the kidneys or through the skeletal system. Sustained calcium and phosphorus imbalance can, however, contribute to developmental orthopaedic diseases (DOD) in young horses, or lameness and sometimes bone fractures in mature horses.
Research shows silicon is a trace mineral worth a second look. Moving on to a less well-recognised trace mineral as far as bone is concerned, there has been some interesting research carried out into the effects of supplemental silicon in the racehorse’s diet. Silicon is a natural constituent of plants and provides structure and rigidity to some of their cell walls. It therefore forms a natural part of the horse’s diet, however, the availability in horse feed is apparently limited. Silicon plays a role in the development of new bone and is also important for the calcification process. It is therefore a relevant micronutrient for horses in training, as bone is dynamic and is constantly undergoing change, in response to forces placed upon it during the training process.
Research carried out by Dr Brian Nielsen at Michigan State University in the early nineties reported a dramatic decrease in injury rates in quarter horses fed a bioavaiable form of silicon as sodium zeolite A. This program of research has also established that the silicon is available to foals via the milk of supplemented mares. However, thus far the group have not uncovered the mechanism by which the beneficial effects of silicon are brought about. However, the form in which sodium zeolite A is fed (a chalk like powder) and the level of intake used in these studies (about 200g per day for a 500kg horse) makes it impractical to use as a feed supplement unless it can be incorporated within a feed pellet.
In conclusion, attention to those factors within the diet that support bone turnover is likely to contribute to a reduction in injuries observed, however, the implementation of appropriate training techniques and use of suitable training surfaces also has a huge impact on the durability of horses in training in comparative terms.