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  • Author or Editor: Harold F. Hintz x
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Objective—To determine whether equine motor neuron disease (EMND) could be induced in adult horses fed a diet low in vitamin E and high in copper and iron.

Animals—59 healthy adult horses.

Procedure—Horses in the experimental group (n = 8) were confined to a dirt lot and fed a concentrate low in vitamin E and high in iron and copper in addition to free-choice grass hay that had been stored for 1 year. Control horses (n = 51) were fed a concentrate containing National Research Council–recommended amounts of copper, iron, and vitamin E. The hay fed to control horses was the same as that fed to experimental horses, but it had not been subjected to prolonged storage. Control horses had seasonal access to pasture, whereas experimental horses had no access to pasture. Horses that developed clinical signs of EMND were euthanatized along with an age-matched control horse to determine differences in hepatic concentrations of vitamin E, vitamin A, copper, iron, and selenium.

Results—4 experimental horses developed clinical signs of EMND. Plasma concentrations of vitamin E decreased in all 8 experimental horses. There were no significant changes in plasma concentrations of vitamin A, selenium, and copper or serum concentrations of ferritin. There were no significant differences in those analytes between experimental horses with EMND and experimental horses that did not develop EMND. No control horses developed EMND.

Conclusions and Clinical Relevance—Results suggest that lack of access to pasture, dietary deficiency of vitamin E, or excessive dietary copper are likely risk factors for EMND.

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in American Journal of Veterinary Research


To determine whether feeding a low-carbohydrate, high-fat diet would decrease severity of exercise-induced muscle injury in horses with exertional rhabdomyolysis.


19 horses with a history of exertional rhabdomyolysis.


Case series.


Specimens of the semitendinosus or semimembranosus muscle were obtained for histologic examination, and serum creatine kinase (CK) and aspartate transaminase (AST) activities 4 hours after exercise were determined. Horses were then fed a low-carbohydrate, high-fat diet, and serum CK and AST activities 4 hours after exercise were reevaluated at approximately monthly intervals for 3 to 6 months.


Serum CK and AST activities 4 hours after exercise were high before any change in diet. All 19 horses had evidence of chronic myopathic change and abnormal glycogen accumulation in muscle biopsy specimens; 11 horses also had evidence of complex polysaccharide accumulation. Adaptation to diet change required approximately 3 to 6 months. Sixteen horses did not have any episodes of exertional rhabdomyolysis after 3 to 6 months of diet change, and 3 horses had mild episodes of exertional rhabdomyolysis following either a reduction in dietary fat intake or restriction in exercise. Postexercise serum CK and AST activities 3 to 6 months after the change in diet were significantly less than initial values.

Clinical Implications

Results indicated that exertional rhabdomyolysis may be a result of abnormal carbohydrate metabolism in some horses. Feeding a diet with low carbohydrate and high fat content may reduce severity of exercise-induced injury in some horses with exertional rhabdomyolysis. (J Am Vet Med Assoc 1998;212:1588–1593).

Free access
in Journal of the American Veterinary Medical Association