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Muscles and Poor Performance
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Muscular disorders make up an important subset of diseases that cause poor performance. Commonest are the exertional myopathies which are often subclinical, and easily overlooked. A variety of acquired factors underlying the development of exertional rhabdomyolysis are proposed. Unfortunately, for some causes, the evidence remains speculative. Current and historical acquired causes include overexertion or exhaustion, oxidative injury, eccentric contraction, hormonal influences and electrolyte abnormalities.
We currently recognise two common forms of exerciserelated myopathy in horses with underlying genetic causes. These include a condition examined extensively in a small group of Thoroughbreds in the USA that has been termed ‘recurrent exertional rhabdomyolysis’ (RER) and another condition, termed ‘polysaccharide storage myopathy’ (PSSM or EPSM). They have clinical similarities and are managed similarly, though they also have key differences and breed susceptibilities. The word ‘recurrent’ in Thoroughbreds with exerciserelated myopathy has been used variably to describe certain Thoroughbreds with documented abnormalities in muscle calcium regulation, a wider group of Thoroughbreds with an apparent inherited form and all Thoroughbreds with the syndrome.
Estimates of the prevalence of exercise-associated rhabdomyolysis in Thoroughbreds suggests that 5-7% are affected. Pedigree analysis in the USA supports autosomal dominant inheritance. The abnormality in muscle calcium regulation identified in some Thoroughbreds shares certain experimental similarities with malignant hyperthermia (MH). In particular, muscle from affected horses and other species with MH is hypersensitive to agents (such as caffeine and halothane) that stimulate release of calcium from the muscle calcium store (sarcoplasmic reticulum) through a calcium release channel known as the ryanodine receptor (RYR1). However, though MH has been reported in some horses following halothane anaesthesia, and indeed, though an RYR1 receptor mutation has been identified in MHsusceptible Quarter horses, Thoroughbreds with abnormal calcium regulation do not share the same mutation and there is evidence suggesting that the RYR1 receptor is not mutated in Thoroughbred RER. Despite this, the basic research similarities between RER and MH do still suggest the possibility of involvement of another protein or proteins that regulate intracellular calcium concentration in muscle. Indeed mutations in other proteins are known to cause or are implicated in human MH. Novel research methods may prove useful in the future investigation of the disease.
Polysaccharide storage myopathy can be definitively diagnosed by muscle biopsy. Pathognomonic changes include diastase-resistant inclusions detected by Periodic Acid Schiff staining. This disease was first reported in detail in Quarter Horses with exertional rhabdomyolysis in the USA and has since been reported in a variety of other breeds worldwide. Although there are sometimes clinical differences in the presentations of this disease (rhabdomyolysis in athletic animals and weakness or muscle atrophy in the draught horses) these animals share the same underlying genetic cause. The disease is inherited as an autosomal dominant inheritance of a glycogen synthase 1 mutation. [...]
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