Physiology of Static Breath Holding in Elite Apneists
Authors: Anthony R. Bain, Ivan Drvis, Zeljko Dujic, David B. MacLeod, Philip N. Ainslie
DOI / Source: https://doi.org/10.1113/ep086269
Date: 02 March 2018
Reading level: Intermediate
Why This Matters for Freedivers
This review explains what actually keeps you alive in a max static: not “being tough,” but the body’s oxygen-saving reflexes plus the brain’s ability to protect its oxygen supply when saturation drops frighteningly low. It also flags a serious point for competitive-style training: repeated extreme hypoxia/hypercapnia may have long-term brain risks, so “pushing to the edge” should be a rare tool, not a daily habit.
Synopsis
Static apnea looks simple from the outside: you lie still and hold your breath. But inside your body it turns into a controlled emergency, and elite apneists are basically experts at managing that emergency for minutes longer than most people think is possible.
This review walks through what happens during a maximal dry static in trained divers, and it breaks the experience into two very real phases. First is the “easy” phase, where you’re relatively calm and still suppressing the urge to breathe. Then comes the “struggle” phase, where involuntary breathing movements (diaphragm contractions) ramp up and the main challenge becomes mental control: keeping the glottis closed, staying relaxed, and not wasting oxygen while your body screams for air.
The paper makes a key point about the true limit in elite statics: once you can mentally tolerate the struggle phase, the breath-hold ends mainly because oxygen drops to a level where consciousness is threatened. Elite divers have been measured at shockingly low oxygen saturations near the end, meaning the body has to work hard to keep oxygen flowing to the brain.
That’s where the diving response takes over as the star of the show: - Bradycardia (heart rate slowing) reduces oxygen use by the heart. - Peripheral vasoconstriction tightens blood vessels in limbs/skin to “spend” less oxygen there and protect blood flow to brain and heart. - Blood pressure rises during long statics, especially late, partly because of strong sympathetic activation and the mechanical effects of the struggle phase. - Spleen contraction can release extra red blood cells, slightly boosting oxygen-carrying capacity.
Then the review zooms in on the brain, because that’s the real “boss fight” in a max static. To defend oxygen delivery, cerebral blood flow can rise massively (often close to doubling), driven mainly by CO₂ buildup (hypercapnia) and high blood pressure. Even though oxygen saturation drops, the increased blood flow can help keep overall cerebral oxygen delivery from collapsing. Interestingly, near the very end of prolonged statics, the review discusses evidence that the brain may also reduce its oxygen use (a drop in cerebral oxidative metabolism), likely triggered by extreme CO₂ rather than low oxygen alone—basically a last-ditch efficiency mode to delay blackout.
Finally, the review steps back and asks the bigger question: what does long-term training do? It outlines likely adaptations (better relaxation, larger lung volumes, stronger diving response, improved “tolerance” to CO₂ discomfort), but it also highlights emerging concerns: markers suggesting temporary blood–brain barrier opening after extreme breath-holds, and research hints that repeated severe hypoxia (and repetitive deep apnea patterns) might relate to cognitive changes in some athletes. The practical message is balanced: understanding these mechanisms can make training safer and smarter—but chasing extremes for ego has a cost.
Abstract
Competitive static breath holding has grown rapidly in the past few decades, and ultra-elite apneists can suppress breathing urges until oxygen levels near the limits of consciousness. In these extreme breath holds, oxygen conservation is critical and relies on responses associated with the diving reflex, including peripheral vasoconstriction and bradycardia. To protect brain oxygen delivery during prolonged apnea, cerebral blood flow can increase dramatically from resting values. Recent studies also suggest that near the end of prolonged dry static breath holds, cerebral oxidative metabolism can decrease, likely due to extreme hypercapnia rather than hypoxaemia alone. This review summarizes recent findings on cardiovascular, metabolic, and especially cerebrovascular function during maximal static breath holds in elite apneists, discusses potential adaptations and maladaptations with training, and highlights the need to better understand possible long-term health impacts of extreme breath holding.