Abstract
Three harbor seals were immersed in five different water temperatures ranging from 7 to 37 °C. Unlike the response in men, the bradycardia observed during immersion was not influenced by water temperature. When the faces of four seals were rendered insensible by neurotomy and local anesthetic, the bradycardia during immersion followed the same time course as that observed during periods of forced apnea while the seals were in air. In two seals with insensible faces, which were forcefully respired during immersion, the heart rate did not drop from the rate observed before immersion. The data presented are consistent with the hypothesis that the two principal sensory contributions to the bradycardia of immersion are: (1) a cessation of the movements of the lungs and rib cage; (2) a change in neural activity in receptors located in the face.

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