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We investigated the effects of chemical hypoxia on the central pattern generator controlling swimming in stage 42 Xenopus laevis larvae. We recorded motoneuron activity from ventral roots of immobilized tadpoles and evoked swim episodes by brief electrical stimulation of the tail skin. In the presence of the metabolic inhibitor, sodium azide (5 mM, NaN3), swim episode duration and cycle frequency decreased until swim motor patterns could not be evoked. On recovery, cycle frequency returned to preazide levels; however, episode duration remained short for at least an hour. In addition, recovery induced spontaneous, short bouts of swimming similar to the slow rhythm that is evoked by N-methyl-D-aspartic acid. We conclude that abiotic features of the environment can have long-term modulatory effects on circuit function in the CNS.