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Hypoxic Blackout in Serial Freediving, Protective Mechanisms and Risk Factors

Authors: Frank Pernett
DOI / Source: https://www.diva-portal.org/smash/record.jsf?pid=diva2%3A1848785&dswid=3164
Date: 03 May 2024

Reading level: Advanced

Why This Matters for Freedivers

This thesis is basically a deep investigation into why “serial diving” (many breath-holds in a row) can quietly push divers toward blackout even when each individual dive feels manageable. The big takeaway is that short, pre-dive hyperventilation can stack the risk across a series by worsening oxygen debt and desaturation, and your natural protective mechanisms (diving response and spleen contraction) help—but they don’t fully cancel that added risk.

Synopsis

Freedivers often think about blackout risk as something that happens on a single “too hard” dive. This doctoral thesis argues that the real danger for many recreational divers is serial freediving—repeating dives with short rests—because oxygenation can steadily deteriorate across the series. The work focuses on two main questions: what protects us from hypoxia in freediving, and what pushes us toward hypoxic blackout when we do repeated dives.

Across four linked studies, Pernett examines the protective mechanisms (the diving response and spleen contraction) and the major risk factor that keeps showing up in real life: hyperventilation—sometimes even when divers think they are avoiding it. One key finding is that hypoxia alone can trigger a spleen contraction fast enough to matter during long breath-holds, increasing hemoglobin concentration and improving oxygen-carrying capacity. But when dives are repeated in a series, especially when they’re preceded by short hyperventilation, oxygen saturation can progressively drop lower and lower. Crucially, the body does not “upgrade” its defenses to match that extra risk: the diving response and spleen contraction do not become bigger just because the desaturation is becoming more severe across the series.

The thesis also aims to turn these findings into practical tools. It explores a method to detect hyperventilation using a force sensor on a chest belt (with the goal of identifying risky breathing patterns in real settings), and it proposes a “static apnea ramp test” designed to identify divers who desaturate faster and might therefore be at higher risk during real freediving sessions. The overall message is safety-focused and highly applicable: repeated dives plus hyperventilation can create a hidden slide toward blackout, and better detection and screening tools could help prevent accidents.

Abstract

Breath-hold diving or freediving exposes the body to stressors such as low oxygen and high carbon dioxide levels in the blood, increased hydrostatic pressure, and cold. The reduction in blood oxygen levels is considered a primary factor for loss of consciousness while diving. This is known as hypoxic blackout. My thesis aimed to enhance the understanding of the factors that lead to hypoxic blackout in serial freediving. This includes studying the physiological mechanisms that protect the body against hypoxia and exploring how hyperventilation affects those mechanisms, with a specific focus on repetitive dives. The protective mechanisms, splenic contraction (Studies I, II) and diving bradycardia (Studies II and IV), were tested in experimental conditions. The effect of hyperventilation on simulated serial dives (Study II) was investigated, and a strategy to identify actual hyperventilation during diving was developed and explored (Study III). A static apnea test allowing identification of individuals at particular risk for blackout was developed (Study IV).

The results showed that hypoxia-induced splenic contraction occurs rapidly enough to be protective in long-duration breath-holds (Study I). Serial simulated dives, preceded by short-term hyperventilation, lead to longer apnea duration and progressive oxygen desaturation (Study II). Despite the more severe desaturation resulting from hyperventilation, these consecutive apneas do not show an augmented diving response or splenic contraction. Hyperventilation was also observed when divers intended to avoid it (Studies II, III, and IV). Therefore, the possibility of estimating hyperventilation from the signal of a force sensor attached to a chest belt was explored (Study III). A stronger diving bradycardia and a bigger spleen were found to be protective against hypoxia and are related to slower oxygen desaturation (Study IV).

The main conclusion is that oxygenation is impaired by the accumulation of an oxygen debt when consecutive dives are preceded by hyperventilation. The protective mechanisms, such as splenic contraction and the diving response, are beneficial at the individual level but do not offset the increased risk across a series of dives. However, splenic contraction does offer protection even during the first dive of a series. A chest belt-mounted force sensor could be used to identify when freedivers are hyperventilating. Additionally, a novel static apnea ramp test is effective in identifying freedivers who are at a high risk of faster desaturation during freediving.

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