Blood flow in the carotid artery during breath-holding in relation to diving bradycardia

The present study investigated the mechanism of diving bradycardia. A group of 14 healthy untrained male subjects were examined during breath-holding either out of the water (30-33°C), in head-out immersion, or in whole-body submersion (27-29°C) in a diving pool. Blood velocity, blood volume flow in the carotid artery, diastolic blood pressure and electrocardiogram were measured and recorded during the experiments. The peak blood velocity increased by 13.6% (P <0.01) and R-wave amplitude increased by 57.1% (P <0.005) when the subjects entered water from air. End-diastolic blood velocity (v(ed)) in the carotid artery increased significantly during breath-holding, e.g. v(ed) increased from 0.20 (SD 0.02) m.s^-1 at rest to 0.33 (SD 0.04) m.s^-1 (P <0.001) at 50.0 s in breath-hold submersion to a 2.0-m depth. Blood volume flow in the carotid artery increased by 26.6% (P <0.05) at 30 s and 36.6% (P <0.001) at 40 s in breath-hold submersion to a 2.0-m depth. Diastolic blood pressure increased by 15.4% (P <0.01) at 60 s during breath-holding in head-out immersion. Blood volume flow, v(ed) and diastolic blood pressure increased significantly more and faster during breath-holding in submersion than out of the water. There was a good negative correlation with the heart rate: the root mean square correlation coefficient r was 0.73 (P <0.001). It was concluded that an increased accumulation of blood in the aorta and arteries at end-diastole and decreased venous return, caused by an increase in systemic peripheral resistance during breath-holding, underlies diving bradycardia.