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Extreme Hypoxia Causing Brady-Arrythmias During Apnea in Elite Breath-Hold Divers

Authors: Thomas Kjeld, Anders Brenøe Isbrand, Katrine Linnet, Bo Zerahn, Jens Højberg, Egon Godthaab Hansen, Lars Christian Gormsen, Jacob Bejder, Thomas Krag, John Vissing, Hans Erik Bøtker, Henrik Christian Arendrup
DOI / Source: https://doi.org/10.3389/fphys.2021.712573
Date: 03 December 2021

Reading level: Intermediate

Why This Matters for Freedivers

This study shows that during very long maximal breath-holds, elite freedivers can develop real rhythm disturbances (not just “a low heart rate”), likely driven by extreme hypoxia. It supports a practical safety message: pushing maximum apneas carries a cardiac conduction risk you can’t “mind over matter” away, and it reinforces why max attempts should be rare, well-supervised, and followed by proper recovery.

Synopsis

Most freedivers know the diving reflex slows the heart rate. What’s less appreciated is that if oxygen drops far enough, the heart’s electrical system can start misfiring—producing rhythm patterns that would look alarming in a hospital patient. This paper set out to document exactly what happens to oxygen saturation, blood pressure, blood glucose, and heart rhythm during truly maximal static apneas in elite breath-hold divers.

Nine elite divers performed a maximum static apnea in a pool (head immersed, head-down) after three warm-up apneas to “switch on” the diving response. The setup was unusually rigorous: they had an arterial catheter for continuous blood pressure monitoring and blood sampling, ECG monitoring, and a saturation sensor placed on the neck to reduce water/vasoconstriction artifacts. On a separate day, six of the divers repeated a maximal dry apnea with full 12-lead ECG monitoring.

The headline result is how extreme the physiology gets. During the maximum pool apnea (around 6 minutes on average), oxygen saturation fell from near 100% to about the high-50% range—levels most people would consider severe. Blood pressure climbed dramatically into exercise-like territory and then plateaued after about 3–4 minutes, suggesting the diving reflex and vasoconstriction were “maxed out.” Heart rate dropped into the 40s and then stabilized. And crucially, several divers developed conduction abnormalities during the most hypoxic phase—patterns like junctional rhythm and atrioventricular dissociation/blocks—seen both in pool and in dry apneas (confirmed on 12-lead ECG). Everyone stayed conscious in this controlled setting, but the rhythms themselves underline that maximal apnea is not a harmless party trick.

An interesting side note: blood glucose did not drop; it stayed stable or rose slightly. The authors argue this supports the idea that the brady-arrhythmias were driven primarily by hypoxia rather than hypoglycemia, and they connect it to earlier work suggesting unusual lactate handling in elite divers.

Abstract

Introduction: The heart’s electrical conduction system is sensitive to low oxygen, which can lead to slow-heart rhythms and conduction disturbances. Elite breath-hold divers can reach very low oxygen levels during maximal apnea, so the study tested whether hypoxia is associated with brady-arrhythmias during maximum breath-holds.

Methods: Nine elite breath-hold divers performed a head-immersed maximal static pool apnea after three warm-up apneas. Heart rhythm was monitored by ECG, oxygen saturation was measured with a neck sensor, and mean arterial pressure plus blood glucose were sampled via a radial arterial catheter. On a separate day, a subset repeated a maximal dry apnea with 12-lead ECG monitoring.

Results: During maximal pool apneas, oxygen saturation fell to very low levels, mean arterial pressure rose substantially and then plateaued after several minutes, and heart rate decreased and stabilized at a low level. Brady-arrhythmias were observed, including junctional rhythm and atrioventricular dissociation/blocks. In the dry apneas, similar rhythm disturbances were confirmed with 12-lead ECG. Blood glucose remained stable or increased slightly.

Conclusion: In elite divers performing maximal apneas, the diving reflex reaches a stable maximum after a few minutes, and severe hypoxia appears to be the key driver of observed brady-arrhythmias rather than low blood glucose.

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