Release of erythropoietin and neuron-specific enolase after breath-hold in competing free divers
Authors: T. Kjeld, T. Jattu, H.B. Nielsen, J.P. Goetze, N.H. Secher, N.V. Olsen
DOI / Source: https://doi.org/10.1111/sms.12309
Date: 26 August 2014
Reading level: Intermediate
Why This Matters for Freedivers
Freediving “feels fine” until it doesn’t—yet inside the body, a hard static plus a hard underwater swim can be a serious oxygen stress test. This paper suggests that after a competition-style session, markers linked to kidney hypoxia and neuronal stress can rise, even when heart markers stay normal. It’s a useful reminder that pushing hypoxia repeatedly may have hidden costs, especially if you’re stacking max efforts, having LMC/blackouts, or training too close to your limits.
Synopsis
Freediving competitions often combine two things that are individually challenging and, together, can be extreme: a maximal static breath-hold and a maximal underwater swim. We already know these efforts can drive oxygen levels down and trigger loss of motor control (LMC) or blackout in some divers. The big question this study asks is: after this kind of session, which parts of the body look most “stressed” when you check the blood.
Seventeen competitive freedivers took part during the Danish freediving championships. Most performed one maximal static in a warm shallow pool, and later (after several hours) attempted a maximal underwater swim in a standard pool. Blood samples were taken before the first apnea and again about three hours after the session, and the heart was also checked with echocardiography after the underwater swim.
The researchers looked at a set of blood markers that can hint at which tissues might have been affected by low oxygen: - Erythropoietin (EPO) as a signal linked to overall hypoxic stress and especially kidney oxygen sensing. - Neuron-specific enolase (NSE) and S100B as markers often discussed in the context of neuronal stress or injury. - Troponin T and pro-atrial natriuretic peptide (proANP) as markers related to heart strain or injury. - C-reactive protein (CRP) as a general inflammation marker.
What they found is striking in its pattern. After the combined session, EPO increased modestly and NSE increased clearly, suggesting that the hypoxic load was enough to trigger signals associated with renal hypoxia and neural tissue stress. At the same time, S100B did not rise—which the authors point out may be partly because sampling was done hours later (some markers can spike earlier and return toward baseline). Importantly, the “heart side” of the story was reassuring: troponin and proANP did not change significantly, and the echocardiography evaluation showed normal heart function.
The session itself was not gentle. Many divers experienced LMC or blackout in either the static or the dynamic attempt, which fits real-world competitive outcomes. Interestingly, the changes in the blood markers didn’t neatly track with who blacked out or how long the apneas were—so the stress response may depend on more than just time, such as individual sensitivity, dive preparation, packing/hyperventilation patterns, or how hard the underwater phase was.
The overall takeaway is that a competition-style “max static + max dynamic” can leave a biochemical footprint that points more toward kidney and brain stress than heart damage. It doesn’t prove long-term harm, but it supports the idea that repeatedly chasing extreme hypoxia could have consequences you don’t feel in the moment—especially if you normalize frequent LMC/blackouts as “just part of training.”
Abstract
Background: Free diving is associated with extreme hypoxia. This study evaluated the combined effect of maximal static breath hold and underwater swimming on plasma biomarkers of tissue hypoxemia: erythropoietin, neuron-specific enolase and S100B, C-reactive protein, pro-atrial natriuretic peptide and troponin T.
Methods: Venous blood samples were obtained from seventeen competing free divers before and 3 hours after sessions of static apnoea and underwater swimming. The heart was evaluated by echocardiography.
Results: Static apnoea for 293 ± 78 s (mean ± SD) and subsequent 88 ± 21 m underwater swimming increased plasma erythropoietin from 10.6 ± 3.4 to 12.4 ± 4.1 mIU/l (P = 0.013) and neuron-specific enolase from 14.5 ± 5.3 to 24.6 ± 6.4 ng/ml (P = 0.017); C-reactive protein decreased from 0.84 ± 1.0 to 0.71 ± 0.67 mmol/l (P = 0.013). In contrast, plasma concentrations of S100B (P = 0.394), pro-atrial natriuretic peptide (P = 0.549) and troponin T (P = 0.125) remained unchanged and, as assessed by echocardiography, the heart was not affected.
Conclusion: In competitive free divers, bouts of static and dynamic apnoea increase plasma erythropoietin and neuron specific enolase, suggesting that renal and neural tissue, rather than the heart is affected by the hypoxia developed during apnoea and underwater swimming.