AbstractAn animal model of defective muscle glycolysis can be produced by intra‐aortic injection of iodoacetate which blocks the glycolytic enzyme glyceraldehyde‐3‐phosphate dehydrogenase. The animals show exercise‐induced, electrically silent muscle cramps and postexercise rhabdomyolysis. Exercised, cramped soleus and extensor digitorum longus muscles from these animals show marked depletion of the high energy compounds adenosine triphosphate (ATP) and creatine phosphate and accumulation of fructose‐1, 6‐diphosphate. This finding supports the hypothesis that exercise‐induced muscle contracture and cell damage in disorders of muscle glycolysis/glycogenolysis are the result of depletion of high energy molecules in the