An Insulin-Based Model to Explain Changes and Interactions in Human Breath-Holding
Authors: Rosita Dangmann
DOI / Source: https://doi.org/10.1016/j.mehy.2015.02.010
Date: 19 February 2015
Reading level: Advanced
Why This Matters for Freedivers
This paper is a hypothesis piece (not a direct experiment), but it’s interesting because it proposes a different “main driver” for the breath-hold breakpoint: not just oxygen and CO₂, but insulin and glucose handling under hypoxia. If parts of this are true, it could help explain why diaphragm/respiratory-muscle training and certain recovery strategies change how a breath-hold feels near the end, and why some divers experience neurological issues (LMC/blackout/seizure-like symptoms) when they push past warning signals. Treat it as a thought-provoking model, not settled fact.
Synopsis
Most freedivers are taught a simple story: you hold your breath, oxygen falls, CO₂ rises, discomfort increases, and eventually you hit a “breakpoint” where you must breathe. But for decades, researchers have struggled to show that any single oxygen or CO₂ number reliably predicts that breakpoint in humans. This paper argues we might be missing a major regulator: insulin.
The author’s core idea is metabolic. When oxygen is low, the body relies more on anaerobic metabolism, which produces far less energy per glucose molecule than aerobic metabolism. That means under hypoxia the body may need more glucose availability to keep the brain and muscles functioning. Insulin, which helps move glucose into cells and influences the body’s redox state, is therefore placed at the center of the model.
The proposed chain goes like this: breath-holding creates hypoxic stress and increases reactive oxygen species (ROS), which interacts with hypoxia signaling pathways such as HIF-1α. HIF-1α is linked to changes in insulin secretion and glucose regulation. Rising insulin (in this hypothesis) could stimulate parts of the respiratory control system—especially carotid bodies—increasing respiratory drive and contributing to the “urge to breathe.” Meanwhile, the paper discusses how the diaphragm and vagus nerve might modulate insulin secretion: inspiration-related lung stretch receptor signals (via vagal pathways) may suppress insulin secretion, and diaphragm fatigue toward the end of a breath-hold could change this balance, possibly contributing to late-stage contractions and the breakpoint.
Finally, the paper connects insulin and glucose swings to potential neurological effects. It highlights the hippocampus’ vulnerability in hypoxia and discusses mechanisms by which insulin-related signaling could influence excitability and seizure risk—offering one possible pathway for severe symptoms if a diver pushes beyond the breakpoint.
Abstract
This article proposes that insulin may be a key regulator in hypoxic conditions during voluntary breath-holding, potentially influencing the breath-hold breakpoint more than oxygen or carbon dioxide alone. The hypothesis links hypoxia-related oxidative stress (ROS), hypoxia signaling (including HIF-1α), and insulin regulation, arguing that low-oxygen states increase glucose demand and therefore place insulin at the center of metabolic control.
The paper further suggests that insulin may affect breathing control through actions on the carotid bodies and diaphragm, and that vagal mechanisms related to inspiratory lung stretch may suppress insulin secretion during a held breath. It also discusses how insulin-, glucose-, and stress-hormone–related changes in the brain—particularly in the hippocampus—could contribute to neurological events (such as seizure-like symptoms, LMC, or blackout) when divers push beyond the breakpoint.