The heart rate response to immersion of the face in water, as an isolated manoeuvre or in combination with apnoea, was studied in eight normal volunteers to establish the conditions under which it could be used as a standardized, simple, non-invasive and reproducible test of parasympathetic activity. 2. The following procedures were evaluated: (a) 10 s apnoea in air at different lung volumes; (b) facial immersion in water for 2 min at various temperatures (5, 15 and 25 degrees C), with respiration maintained through a closed circuit; (c) combination of immersion and apnoea at different lung volumes. Three volunteers were re-evaluated after pharmacological blockade with atropine sulphate (0.04 mg/kg body weight). 3. The results showed that: (a) apnoea in air triggered lung volume-dependent heart rate responses; (b) facial immersion in water induced transient bradycardia which was maximum between 20 and 30 s of immersion; (c) there was no appreciable difference in the bradycardia evoked by immersion at different temperatures; (d) the combination of immersion and apnoea caused heterogeneous heart rate responses with no potentiation of bradycardia in relation to each manoeuvre as performed separately; (e) atropine did not reduce the magnitude of bradycardia induced by immersion in two of the subjects studied. 4. The variability of responses observed in the present study was probably due to the multiple receptors and afferent pathways that are simultaneously excited during these manoeuvres. As a consequence, the autonomic efferent response will depend on the unpredictable net effect of interaction of these mechanisms. This is a limiting factor for the standardization of this test as a simple and reproducible method for the assessment of parasympathetic activity. 5. Furthermore, the results obtained under pharmacological blockade indicate that the vagal efferent mechanism is not the only factor responsible for the bradycardia caused by facial immersion without apnoea.
