The Human Diving Response, Its Function, and Its Control
Authors: G. E. Foster, A. W. Sheel
DOI / Source: https://doi.org/10.1111/j.1600-0838.2005.00440.x
Date: 29 October 2004
Reading level: Beginner
Why This Matters for Freedivers
The diving response is the core “built-in survival mode” that makes freediving possible: it slows the heart, squeezes blood away from the limbs, and helps preserve oxygen for the brain and heart. Understanding what triggers it (and what weakens it) helps you train smarter, stay calmer, and reduce risk—especially the risk that comes from pushing hypoxia too far or using habits that blunt your natural warning signals.
Synopsis
This review explains the human diving response in a simple way: when you stop breathing (apnea), your body automatically shifts into an oxygen-saving mode. The main features are: - Bradycardia: heart rate drops through increased vagal (parasympathetic) activity. - Peripheral vasoconstriction: blood vessels in limbs and some organs constrict, sending more blood toward vital organs. - Sympathetic activation: the body increases “fight-or-flight” signals to maintain blood pressure and control circulation. It also describes a newer (at the time) addition: splenic contraction, which can release extra red blood cells and slightly increase oxygen-carrying capacity during repeated apneas.
A big question the authors address is: what is this response for? Their conclusion is that its main job is oxygen conservation—slowing how fast oxygen stores are used, and protecting oxygen-sensitive tissues like the brain and heart. The review summarizes evidence showing that a stronger diving response (especially with face immersion) can slow the rate of oxygen desaturation during breath-holds, and that apnea triggers oxygen-conserving effects that are not explained by “asphyxia stress” alone.
The most useful part for training is the control model: the diving response is not one switch, but a network of inputs that converge in the brainstem. Key drivers include: - Apnea itself (the “master switch”). - Facial cold receptors (water on the forehead/eyes/nose makes the response stronger; other skin cooling doesn’t do the same). - Chemoreceptors (low O₂ and high CO₂ amplify some parts of the response, especially vasoconstriction). - Baroreceptors (blood pressure feedback). - Pulmonary stretch receptors and lung volume (how full your lungs are changes the response; smaller lung volumes generally allow a stronger bradycardia because stretch-receptor input is reduced).
The review also highlights a key safety-relevant point: trained breath-hold athletes often show blunted ventilatory responses to hypoxia/hypercapnia (the “urge to breathe” signal can be weaker). That can improve performance, but it may also reduce warning signs—meaning a diver can feel “fine” while oxygen is already dangerously low. The authors suggest more research is needed to understand how these adaptations relate to safety.
Abstract
The purpose of this review is to outline the physiological responses associated with the diving response, its functional significance, and its cardiorespiratory control. This review is separated into four major sections. Section one outlines the diving response and its physiology. Section two provides support for the hypothesis that the primary role of the diving response is the conservation of oxygen. The third section describes how the diving response is controlled and provides a model that illustrates the cardiorespiratory interaction. Finally, the fourth section illustrates potential adaptations that result after regular exposure to an asphyxic environment. The cardiovascular and endocrine responses associated with the diving response and apnea are bradycardia, vasoconstriction, and an increase in secretion of suprarenal catecholamines. These responses require the integration of both the cardiovascular system and the respiratory system. The primary role of the diving response is likely to conserve oxygen for sensitive brain and heart tissue and to lengthen the time before the onset of serious hypoxic damage. We suggest that future research should be focused towards understanding the role of altered ventilatory responses in human breath-hold athletes as well as in patients suffering from sleep-disordered breathing.