Autonomic pathways responsible for bradycardia on facial immersion

Abstract
The autonomic pathways mediating the bradycardia response to facial immersion (FI) are not fully elaborated in man. By parasympathetic and sympathetic blockade, the heart rate response to FI was studied in 9 highly trained young swimmers, at rest and during dynamic cycle exercise. With no blockade, heart rate at rest declined with FI 36 .+-. 18%. Under .beta.-blockade with propranolol or .alpha.-blockade with phentolamine FI produced a similar decrement. Atropine reduced the response. During exercise FI produced 48 .+-. 9% decline without blockade. The response was similar with .beta.-blockade, but was completely abolished with atropine. Systolic blood pressure responses to FI measured by cuff in 3 subjects were small and bore no relation to the heart rate response. The results are compatible with parasympathetic efferent mediation of the heart rate response to FI. They are compatible with a role for sympathetic mediation, except as a complex interaction between parasympathetic and sympathetic influences. Hypertension and other sympathetic responses to FI do not play a role in production of bradycardia, but are apparently incidental effects. The heart rate decrement produced by FI increases with greater steady-state heart rate.

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