BLOOD-FLOW IN THE CAROTID-ARTERY DURING BREATH-HOLDING IN RELATION TODIVING BRADYCARDIA

The present study investigated the mechanism of diving bradycardia. A group of 14 healthy untrained male subjects were examined during breat h-holding either out of the water (30-33 degrees C), in head-out immer sion, or in whole-body submersion (27-29 degrees C) in a diving pool. Blood velocity, blood volume flow in the carotid artery, diastolic blo od pressure and electrocardiogram were measured and recorded during th e experiments. The peak blood velocity increased by 13.6% (P < 0.01) a nd R-wave amplitude increased by 57.1% (P < 0.005) when the subjects e ntered water from air. End-diastolic blood velocity (v(ed)) in the car otid 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. Bl ood 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(e d) and diastolic blood pressure increased significantly more and faste r 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-d iastole and decreased venous return, caused by an increase in systemic peripheral resistance during breath-holding, underlies diving bradyca rdia.