Abstract
Prolonged breath-hold causes complex compensatory mechanisms such as increase in blood
pressure, redistribution of blood flow, and bradycardia. We tested whether apnea induces
an elevation of catecholamine-concentrations in well-trained apneic divers.
11 apneic divers performed maximal dry apnea in a horizontal position. Parameters
measured during apnea included blood pressure, ECG, and central, in addition to peripheral
hemoglobin oxygenation. Peripheral arterial hemoglobin oxygenation was detected by
pulse oximetry, whereas peripheral (abdominal) and central (cerebral) tissue oxygenation
was measured by Near Infrared Spectroscopy (NIRS). Exhaled O2 and CO2, plasma norepinephrine and epinephrine concentrations were measured before and after
apnea.
Averaged apnea time was 247±76 s. Systolic blood pressure increased from 135±13 to
185±25 mmHg. End-expiratory CO2 increased from 29±4 mmHg to 49±6 mmHg. Norepinephrine increased from 623±307 to 1 826±984 pg
ml−1 and epinephrine from 78±22 to 143±65 pg ml−1 during apnea. Heart rate reduction was inversely correlated with increased norepinephrine
(correlation coefficient −0.844, p=0.001). Central (cerebral) O2 desaturation was time-delayed compared to peripheral O2 desaturation as measured by NIRSabdominal and SpO2.
Increased norepinephrine caused by apnea may contribute to blood shift from peripheral
tissues to the CNS and thus help to preserve cerebral tissue O2 saturation longer than that of peripheral tissue.
Key words
apnea - blood pressure - catecholamine - hypoxia - NIRS - SpO
2
