These muscle ATPace enzymessenzymes (myoATPace; named here to distinguish from other ATPace's) speeds up this reaction, as all good enzymes do, but a dead body does not lose its myoATPace on death, so why doesn't the muscle contract at random intervals during this environment prime for spontaneous ATP disassociation? Perhaps this is controlled by the lack of neural impulse, the lack of sarcoplasmic reticulum activation, the lack of calcium release, and the lack of a binding site from the rotation of tropomyosin.