North American Trainer - Triple Crown 2010 - Issue 16

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A horse with raised muscle enzymes, whether it is a single isolated incident or a regular occurrence, is always a cause for concern for trainers. When present at a high level in blood, the muscle enzymes aspartate aminotransferase (AST) and creatine phosphokinase (CPK) usually indicate muscle damage. This may simply indicate overexertion during training but can also signify a more serious issue in the form of exertional rhabdomyolysis (ER) or ‘tying up.’ These horses, which are quite often fillies, can be notoriously difficult to train with many lost training days resulting in a decreased opportunity to race. By Dr Catherine Dunnett BSc, PhD, R.Nutr.

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HERE has been a slow but steady increase in our knowledge of this disease or syndrome, which in more recent years has been helped by the application of genetic-based tests for some forms. An increase in our understanding of the metabolic basis for the syndrome is imperative and will help us to better manage these horses in terms of nutrition and training. Characteristics of ERS ER is a metabolic disorder involving the musculature which is characterized by some of the following clinical signs: sweating; a raised respiratory rate; stiffness of gait and/or a reluctance or inability to move; and hard and painful muscle groups usually but not limited to the quarters. In severe cases the urine may be discolored or reddened due to the excretion of myoglobin (the oxygen-carrying pigment in muscle). It is this myoglobinurea which is of greatest clinical risk, as it can precipitate kidney damage and even death. One of the most commonly noted signs of ER is muscle damage, as evidenced by the ‘leakage’ of the two muscle enzymes AST and CPK into blood. Classification ER is not a single disease, but a syndrome consisting of different sub-types with some common clinical signs. ER can be described as sporadic, where episodes are isolated or infrequent; or chronic, where horses have repeated episodes nearly always accompanied by raised muscle enzyme concentration in blood. Sporadic rhabdomyolysis – this is the term used to describe occurrences of muscle damage in horses where there is no prolonged previous history of ER. These cases can often be explained by muscle strain due to overexertion or overtraining and sub-optimal dietary intake of electrolytes, vitamin E and or selenium are sometimes apparent. In addition, it is not unusual for individual horses to

Breeders' Cup Ladies Classic winner Life is Sweet was retired in March due to a mild bout of tying up af ter a workout. Earlier in the year, she had been scratched from her intended 2010 debut for the same reason

exhibit sporadic ER where a viral challenge such as influenza or herpes virus is present. Chronic rhabdomyolysis is characterized by a genetic metabolic defect that leads to two quite different forms of ER, namely polysaccharide storage myopathy (PSSM), which is primarily found in Quarter Horses, Warmbloods and draft breeds; and, in Thoroughbreds in race training, the more prevalent chronic form of ER is recurrent exertional rhabdomyolysis (RER). When presented with a Thoroughbred in training with raised muscle enzymes in blood, we are likely to be dealing with either sporadic ER or recurrent ER and it is upon these two sub-types that this article will now focus. The prevalence of ER in horses in training in a study from the United Kingdom has been reported to be about 7%, with 80% of trainers stating that they had at least one horse within the barn with ER. Within this group of horses, the chance of more than one episode of ER occurring was a high 74% and the average

number of training days lost was six days. Progress has been made in recent years in understanding the genetic basis and metabolic defect involved in chronic ER. Studies in the US have suggested that this form is triggered by abnormal calcium regulation within muscle cells. Calcium is intimately involved in muscle contraction, and every time a muscle contracts, calcium is released from the sarcoplasmic reticulum, a storage site within the muscle. The calcium is then slowly taken back up and re-stored within the sarcoplasmic reticulum in the muscle in order for the muscle to relax. In horses with the chronic form of ER, it is believed that calcium is released too readily from the sarcoplasmic reticulum, leading to excessive muscle contraction. It should be made clear, however, that this mechanism is completely unconnected to dietary calcium intake, which will not modify this process. Although this mechanism is not completely proven it is supported by the relative success of dantrolene sodium to help control this

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