Isolated muscle segments from the parasitic roundworm Ascaris suum were shown to contract when perfused with acetylcholine (ACh). The muscle responded to ACh concentrations of 1 microM and was maximally contracted at 50 microM ACh. In fed muscle segments perfused with saturating levels of ACh the glycogen synthase Ka values for glucose 6-phosphate increased from 0.5 to 0.95 mM. In starved segments stimulated by ACh, the muscle utilized glycogen at a rate that was 1.41 micrograms.min-1.g tissue-1 greater than the saline-perfused controls. The cyclic AMP (cAMP) levels remained relatively constant at 0.34 +/- 0.08 nmol/g muscle during perfusion with ACh. Contraction in the muscle could be inhibited in a dose-dependent manner by gamma-aminobutyric acid (GABA). The presence of GABA in starved muscle prevented the decrease in Ka values and phosphorylase activity ratios brought about by glucose. Perfusion of GABA did not change cAMP levels in the muscle. Starved muscle perfused with GABA utilized glycogen at a rate that was 0.41 microgram.min-1.g-1 greater than saline-perfused controls. The results indicated that muscle contraction could be elicited by ACh, and that the energy for this process was derived from endogenous glycogen stores, which were depleted during contraction. Muscle contraction was also correlated with inactivation of glycogen synthase and activation of phosphorylase. These processes appeared to function via a cAMP-independent mechanisms.