Plasma Adenosine Release Is Associated with Bradycardia and Transient Loss of Consciousness During Experimental Breath-Hold Diving
Authors: Fabrice Joulia, Mathieu Coulange, Frédéric Lemaître, Guillaume Costalat, Frédéric Franceschi, Vlad Gariboldi, Laetitia Nee, Julien Fromonot, Laurie Bruzzese, Gilles Gravier, Nathalie Kipson, Yves Jammes, Alain Boussuges, Michele Brignole, Jean Claude Deharo, Régis Guieu
DOI / Source: https://doi.org/10.1016/j.ijcard.2013.08.053
Date: 27 August 2013
Reading level: Advanced
Why This Matters for Freedivers
This paper helps explain why some divers are more blackout-prone than others, even when performing similar dives. It shows that the molecule adenosine — a natural signal released during low oxygen — can slow the heart so much that it contributes to loss of consciousness. Understanding this chemistry reinforces why deep relaxation is not always safe: too much slowing of the heart or vasodilation, especially after long statics or deep dives, can push a diver over the edge.
Synopsis
This study investigated whether adenosine, a chemical released by the body during hypoxia, plays a role in the bradycardia and transient loss of consciousness (T-LOC) sometimes observed in breath-hold diving. Adenosine is known to act on several receptor types in the cardiovascular system. The A₁ receptor slows the heart rate, while the A₂A receptor dilates blood vessels — both of which can drop blood pressure and reduce brain perfusion.
The researchers recruited 20 elite freedivers (19 men, 1 woman, average age 37) who participated in the 2012 World Championships. Eleven of them had experienced blackouts (T-LOC) in the previous two years, and nine had not. Ten healthy non-divers served as controls.
Each diver performed a series of short warm-up breath-holds to activate the diving response, followed by a single submaximal static apnea while lying down. Heart rate, blood pressure, and oxygen saturation were recorded continuously. Blood samples were taken before the dive (T₀), at the end of the breath-hold (T₁), and after ten minutes of recovery (T₂). The samples were analyzed for adenosine plasma concentration (APC).
Results (Table 1, page 3; Figure 1, page 4):
- At baseline, divers had higher APC than non-divers, especially those with a history of blackouts (median 0.9 µM vs 0.67 µM in controls).
- During apnea, APC rose sharply, reaching a median of 2.4 µM overall — but the increase was far greater in blackout-prone divers (3.4 µM) than in others (1.7 µM).
- Heart rate fell significantly (from ~71 bpm to ~58 bpm), and the lowest heart rates were seen in the high-adenosine group.
- Oxygen saturation dropped from near 99% to around 82%.
- There was a strong negative correlation between APC and both heart rate (r = −0.49, p = 0.02) and oxygen saturation (r = −0.86, p = 0.001).
- Blood pressure increased modestly during apnea and returned to baseline within ten minutes.
No subjects blacked out during the experiment, but the clear biochemical and cardiovascular differences between groups support the hypothesis that excess adenosine contributes to apnea-related loss of consciousness by intensifying bradycardia and possibly causing transient atrioventricular (AV) block.
The authors propose that measuring resting adenosine levels and heart rate could help identify divers at higher risk of blackout. More broadly, it reinforces the idea that blackouts are not just a matter of oxygen depletion — they also depend on how individual cardiovascular systems react to hypoxia.
Abstract
During breath-hold diving, transient loss of consciousness (T-LOC) can occur due to extreme bradycardia and hypotension. This study assessed plasma adenosine concentration (APC) in 20 elite freedivers and compared those with a prior history of T-LOC to those without. Blood samples taken before, during, and after a maximal static apnea revealed that APC increased markedly at the end of the breath-hold, particularly in divers with prior T-LOC (3.4 µM vs 1.7 µM, p < 0.01). APC was inversely correlated with heart rate (r = −0.49) and oxygen saturation (r = −0.86). These findings suggest that adenosine release during hypoxia contributes to the pronounced bradycardia and transient loss of consciousness observed in some breath-hold divers, likely via A₁ receptor–mediated cardiac effects. Basal heart rate and APC may help screen individuals at risk.