Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

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 O-2 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) O-2 desaturation was time-delayed compared to peripheral O-2 desaturation as measured by NIRSabdominal and SpO(2). Increased norepinephrine caused by apnea may contribute to blood shift from peripheral tissues to the CNS and thus help to preserve cerebral tissue O-2 saturation longer than that of peripheral tissue.