Physiology of freediving, also called breath-hold diving physiology, concerns the physiological responses, adaptations and pathological effects associated with freediving and prolonged voluntary apnea. Freediving combines several physiological stresses: interruption of pulmonary ventilation, immersion, exercise, and, during depth diving, large changes in ambient pressure. These produce progressive hypoxemia, hypercapnia and acid–base disturbance, while hydrostatic pressure alters lung volume, pulmonary blood volume and the partial pressures of respiratory gases. Humans respond to apnea and immersion with the diving response, which includes bradycardia, peripheral vasoconstriction and redistribution of blood flow towards organs with high oxygen requirements. During deep dives, compression of pulmonary gas is accompanied by an increase in central and pulmonary blood volume, commonly called the blood shift. These responses extend tolerance of apnea and pressure but do not prevent progressive depletion of oxygen stores or the development of pulmonary, cardiovascular and neurological limits. At physiological extremes, mechanisms that are normally protective can become inadequate or contribute to pathology. Important adverse phenomena include hypoxic loss of motor control, freediving blackout, pulmonary barotrauma of descent ("lung squeeze"), middle-ear and sinus barotrauma, cardiac rhythm disturbances, and, in sufficiently deep or repetitive diving, decompression sickness.
Terminology Terminology in freediving overlaps with, but does not always match, physiological and medical usage. A prolonged voluntary apnea is commonly divided into an easy-going phase and a struggle phase. The transition, or physiological breakpoint, is marked by the onset of involuntary breathing movements (IBMs), commonly called contractions by freedivers. Hypoxic neurological impairment without complete loss of consciousness is termed loss of motor control (LMC); the associated tremulous or jerking movements are commonly called a "samba". Terminology for hypoxic blackout is inconsistent. The term shallow-water blackout has been applied both to hypoxic blackout during shallow or approximately constant-pressure breath holding, particularly following hyperventilation, and to blackout during the final part of ascent from a deep breath-hold dive. In the latter, falling ambient pressure causes a rapid decline in alveolar and arterial oxygen partial pressure. This mechanism is more unambiguously termed ascent blackout; deep-water blackout has also been used for it, although the term can be misleading because loss of consciousness commonly occurs near the surface. Glossopharyngeal insufflation is commonly called lung packing or packing. Redistribution of blood into the thoracic and pulmonary circulation during immersion and lung compression is commonly termed the blood shift. Pulmonary injury associated with extreme compression during descent is commonly called lung squeeze.
Physiology of prolonged apnea
Easy-going phase and physiological breakpoint
Maximal voluntary apnea is commonly divided physiologically into an easy-going phase followed by a struggle phase. During the easy-going phase, ventilation is voluntarily suppressed and overt involuntary respiratory muscle activity is absent or limited, although PaCO2 is progressively rising and PaO2 is falling. The duration of this phase depends on factors including initial blood gases, lung volume, metabolic rate and individual chemosensitivity to oxygen and carbon dioxide. The transition between the phases is termed the physiological breakpoint and is associated with the appearance of involuntary breathing movements (IBMs), commonly called contractions by freedivers. These movements are generated as chemical and neural respiratory drive becomes sufficiently strong to produce involuntary activity of the diaphragm and other respiratory muscles despite continued voluntary closure of the airway. The onset of IBMs does not appear to be determined by a single oxygen or carbon dioxide value. In an experiment that varied inspired oxygen and carbon dioxide and obtained arterial samples at IBM onset, Breskovic et al. identified a possible PaCO2 threshold of approximately 6.5 ± 0.5 kPa (48.8 ± 3.8 mmHg). No equivalent single PaO2 threshold was found, and the results indicated an interaction between oxygen and carbon dioxide in determining the breakpoint. The value is therefore an experimental estimate rather than a universal threshold for the first "contraction".
Struggle phase and involuntary breathing movements During the struggle phase, repeated IBMs generate fluctuations in intrathoracic and abdominal pressure. The movements may influence venous return, stroke volume and cerebral circulation while the diver becomes progressively more hypoxemic and hypercapnic. They also impose repeated mechanical work on the diaphragm and other respiratory muscles, and respiratory-muscle fatigue after prolonged or repeated maximal apnea has been proposed as an additional performance limitation. A 2026 multimodal case study of a world-champion freediver illustrates the magnitude of this response. During a maximal dry static apnea lasting 6 min 7 s, the first 2 min 20 s comprised the easy-going phase and the remaining 3 min 47 s the struggle phase; electromyography recorded 48 involuntary breathing movements. End-tidal carbon dioxide rose from 21 mmHg after preparatory breathing to 65 mmHg at termination, while oxygen saturation fell from 97% to 73%. Muscle oxygenation declined substantially, whereas cerebral oxygenation was relatively preserved until late in the breath hold. Because end-tidal gases were measured before and after the apnea rather than at the first IBM, the terminal PETCO2 of 65 mmHg should not be interpreted as the threshold for contraction onset.
Human diving response
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