Int J Sports Med 2017; 38(2): 85-91
DOI: 10.1055/s-0042-107351
Physiology & Biochemistry
© Georg Thieme Verlag KG Stuttgart · New York

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

Lars Eichhorn
1   Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin, Universitätsklinikum Bonn, Bonn, Germany
,
Felix Erdfelder
1   Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin, Universitätsklinikum Bonn, Bonn, Germany
,
Florian Kessler
1   Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin, Universitätsklinikum Bonn, Bonn, Germany
,
Ramona C. Dolscheid-Pommerich
2   Institut für Klinische Chemie und Klinische Pharmakologie, Universitätsklinikum Bonn, Bonn, Germany
,
Berndt Zur
2   Institut für Klinische Chemie und Klinische Pharmakologie, Universitätsklinikum Bonn, Bonn, Germany
,
Uwe Hoffmann
3   Institut für Physiologie und Anatomie, Deutsche Sporthochschule Köln, Köln, Germany
,
R. Ellerkmann Ellerkmann
1   Klinik und Poliklinik für Anästhesiologie und Operative Intensivmedizin, Universitätsklinikum Bonn, Bonn, Germany
,
Rainer Meyer
4   Physiologisches Institut 2, Rheinische Friedrich-Wilhelms-Universität Bonn, Bonn, Germany
› Author Affiliations
Further Information

Publication History



accepted after revision 18 April 2016

Publication Date:
25 July 2016 (online)

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.

 
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