Autonomic mechanisms of bradycardia during nitrox exposure at 3 atmospheres absolute in humans.
BACKGROUND: This experiment was designed to examine the involvement of the autonomic nervous systems and intrinsic component in the occurrence of hyperbaric bradycardia. METHODS: Eight male divers were exposed to a N2-O2 (Nitrox) environment at 3 atmospheres absolute (ATA) for 7 d. The heart rate (HR), plasma norepinephrine (NE), and a spectral power of the variability of cardiac interval were measured during a 4-d predive control period, a 7-d saturation period at 3 ATA, and a 4-d postdive period. In each dive period, atropine and propranolol were administered intravenously for cholinergic blockade and beta-adrenergic blockade, respectively. RESULTS: Basal HR decreased by -10% (p < 0.05) during the saturation period compared with that of the predive control. The HR after an administration of atropine was attenuated by 5.5 +/- 2.4% (p < 0.05) during hyperbaric exposure. The HR after a simultaneous administration of atropine and propranolol, the intrinsic HR, was similar throughout the dive periods. Plasma NE decreased at 3 ATA (p < 0.05). The basal level of high-frequency power of cardiac interval variability, an index of cardiac parasympathetic modulation, remained unchanged throughout the dive period, whereas this power was eliminated by atropine administration. CONCLUSIONS: These results suggest that reduced sympathetic activity plays a primary role in the reduction of HR in the present hyperbaric environment.