Abstract
Multi-unit recordings of muscle-nerve sympathetic activity (m.s.a) or skin-nerve sympathetic activity (s.s.a) were made in the left peroneal nerve of sixteen healthy volunteers during simulated diving by immersion of the face in a tub of water. The procedure was varied by the use of different water temperatures, by diving with snorkel breathing, by apnoea without diving, and by apnoea with a stream of air against the face instead of immersion in water. Diving for 12 s elicited a pronounced activation of m.s.a., the mean increase from control periods being 360%. The response was stronger with lower water temperatures. Immersion of the whole face evoked a stronger increase in m.s.a. than immersion of mouth and nose only. Diving without apnoea elicited a significant but weaker increase in m.s.a., whereas apnoea only for 12 s did not influence the sympathetic outflow. Cool air against the face during apnoea for 12 s was associated with a significant increase in m.s.a. The increase in m.s.a. usually occurred before the bradycardia. On emersion, m.s.a. ceased abruptly, whereas the bradycardia persisted for a few seconds. Mental arithmetic during diving did not change the m.s.a. response but reduced the bradycardia. M.s.a. increased despite increasing blood pressure levels. On emersion, m.s.a. did not reappear until the pre-diving blood pressure level was attained. S.s.a was inhibited on diving, with concomitant vasodilatation in the skin as recorded in the big toe. It is concluded that the response of m.s.a. to diving is initiated by a central 'pattern recognition' of an input from facial receptors, that this input and the effects of apnoea, acting by mutual reinforcement, maintain the strong sympathetic outflow, and that the mechanism releasing m.s.a. on diving overrides the normal blood pressure regulatory function of m.s.a. Diving exerts differentiated influence on different parts of the sympathetic nervous system, as illustrated by the inhibition of s.s.a.