Autonomic pathways responsible for bradycardia on facial immersion.
The autonomic pathways mediating the bradycardia response to facial immersion (FI) have not been fully elaborated in man. By means of parasympathetic and sympathetic blockade we studied the heart rate response to FI in nine 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 three 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 incompatible 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.
D000293:Adolescent; D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure; D001919:Bradycardia / Q000209:etiology*; D002648:Child; D004525:Efferent Pathways / Q000503:physiopathology; D005145:Face; D005260:Female; D006339:Heart Rate; D006801:Humans; D007101:Immersion / Q000009:adverse effects / Q000503:physiopathology*; D008297:Male; D010275:Parasympathetic Nervous System / Q000503:physiopathology; D005082:Physical Exertion; D013178:Sports Medicine; D013550:Swimming