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Richter's hypothesized mechanism of sudden swimming deaths—parasympathetic overstimulation mediated by helplessness—is examined in domestic rats. EKG recordings of sudden swimming deaths (SSD) indicated a consistent pattern of cardiac function including severe bradycardias and arrhythmias followed by atrioventricular block leading ultimately to asystole. Rats which survived the swimming stress showed a transient bradycardia followed by a return to baseline HR levels. Swimming behavior and cardiac function were shown to be closely related. Anoxia is suggested as the mechanism of death and data indicating the involvement of the diving reflex in rats are presented. Helplessness induced by pretreatment with inescapable shock did not affect SSD. These data are consistent with a parasympathetic overstimulation hypothesis but disconfirm mediation by helplessness. The implications of these results for the generality of learned helplessness and for the study of psychosocial factors in SSD are discussed.

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