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	Figure 1. Japanese Ama divers operating from the shore and from a boat. A catch net is carried and a surface float is used for storing harvest. Goggles with side air bulbs for pressure equalization were used before the transition to diving masks. Reproduced, with permission, from Rahn and Yokoyama (321).
	Figure 2. A competitive freediver surfaces from a constant weight dive to 103 m. A straining maneuver called a hook breath is being used to promote increased blood flow to the brain to help prevent hypoxic blackout (author photo).
	Figure 3. Effect of immersion to the neck on internal body pressures in cmH2O. Pressures across the diaphragm in italics are taken from Ref. (2), while other numbers are estimates based on respective hydrostatic distributions. External water pressure acts at chest and abdomen centroids. Vertical ordinates Zp of pleural pressure Pp and Za of abdominal pressure Pa are measured from neck Z1 and diaphragm Z2 reference levels. Blood volume shown in gray shifts into the chest upon immersion, distending the heart H and pulmonary vasculature.
	Figure 4. Heart rate (HR), systolic (SBP), and diastolic (DBP) blood pressure responses to a breath‐hold on air of 320 s. A hypertensive response is seen during the latter phase. A secondary drop in heart rate is also seen, possibly brought on by hypoxia. Results suggest intense sympathetic and parasymapthetic coactivation. Modified with permission from Perini et al. (303).
	Figure 5. Apnea with face immersion at rest induces diving bradycardia. Exercise alone raises heart rate. Combining face‐immersed apnea with exercise results in attenuating influences and an intermediate heart rate response. Modified, with permission, from Wein et al. (399).
	Figure 6. Reduction in spleen volume is seen during five repeated apneas, associated with increasing apnea times. Greater response is seen in trained divers. Splenectomized persons had shorter apnea times. Recovery of spleen volume takes over 1 h. Reproduced, with permission, from Bakovic et al. (24).
	Figure 7. Apnea with face immersion delays the drop in arterial hemoglobin saturation compared with apnea in air, suggesting that the diving response has an oxygen conserving effect. Reproduced, with permission, from Andersson and Schagatay (17).
	Figure 8. Respiratory system compliance curve showing lung volume versus airway pressure (PAW) during a dive with depths shown. Lungs are packed above total lung capcity (TLC) to V1. Air compression to V2 below residual volume (RV) is partially compensated by blood volume VB shifting into the chest shown in gray. Results are from computer simulation.
	Figure 9. Airway pressure in cmH2O versus depth during a breath‐hold descent predicted by computer simulation. The model incorporates immersion, air compression, respiratory system compliance, and thoracic blood shift. Lung packing extends the pressure reversal depth ZR from 27 to 43 msw. Small ripples are from heart beat volume oscillations.
	Figure 10. Computer model estimates of percent alveolar closure and reopening during dives to various depths. First alveolus reaches closing volume CV around 18 m. Lungs reach the fully collapsed state around 235 m assuming an inital lung volume of 9.2 L. Dashed lines indicate ascent to first alveolar reopening. Modified, with permission, from Fitz‐Clarke (127).
	Figure 11. Glossopharyngeal breathing used by tetraplegics has been adopted by BH divers for hyperinflation or ‘lung packing’ above TLC. Reproduced, with permission, from Warren (398).
	Figure 12. Alveolar oxygen and carbon dioxide levels during a resting breath‐hold on air started at total lung capacity (TLC) or functional residual capacity (FRC). Reproduced, with permission, from Hong et al. (177).
	Figure 13. Apnea time on a breath of pure oxygen is limited by intolerable carbon dioxide accumulation. The right‐hand side of the curve tracks alveolar PACO2 rise with apnea time to the breakpoint. Preceding hyperventilation adds the time shown on the left‐hand side by having lower initial PACO2. Total apnea time is the sum of both sides. Reproduced, with permission, from Klocke and Rahn (204).
	Figure 14. Alveolar CO2 rises and O2 falls during a breath‐hold on air (dashed curve). Involuntary diaphragmatic contractions begin at the physiological breakpoint. Apnea becomes intolerable at the conventional breakpoint. Hypoxic blackout occurs if oxygen level falls below about 20 to 30 mmHg. Modified, with permission, from Agostoni (1).
	Figure 15. Computer‐simulated gas levels during a swimming breath‐hold dive to 6 msw indicated at the bottom. Initial arterial PaCO2 is 29 mmHg (left) after normal breathing and the breakpoint is reached after 1.5 min when PaCO2 reaches 60 mmHg (circle). Ascent avoids critical hypoxia, and the dive is safe. In contrast, predive hyperventilation (right) lowers initial PaCO2 to 22 mmHg and allows a longer dive without the urge to breathe. PaO2 drops below 30 mmHg on ascent and hypoxic blackout (BO) occurs near the surface.
	Figure 16. Brain lesions caused by decompression injury in an Ama diver. The large areas of infarction suggest the etiology might involve arterial embolism from nitrogen bubbles released during repetitive diving. Reproduced, with permission, from Kohshi (206).
	Figure 17. Deepest human breath‐hold dives in constant weight CW (fin swimming) and no‐limits NL (weight or sled assisted) categories since 1949. The dive to 253 msw resulted in loss of consciousness and serious neurological injury.
	Figure 18. Hypothetical depth limiting factors in breath‐hold diving. Statistics of risk are unavailable to calibrate curves due to the small number of very deep dives. Progressive lung collapse causes some curves to drop. Gas narcosis decreases cognitive function. DCS = decompression sickness, CW = constant weight, NL = no‐limits.

Teaching Material

J. R. Fitz-Clarke. Breath-Hold Diving. Compr Physiol. 8: 2018, 585-630.

Didactic Synopsis

Major Teaching Points:

1. Immersion in water shifts blood from the lower body into the heart and chest vasculature.
2. A diving response triggered by apnea and face immersion causes bradycardia and vasoconstriction.
3. Spleen contraction releases red blood cells into the circulation, prolonging apnea time.
4. Depth can compress lungs below residual volume, causing negative airway pressure.
5. Some divers experience alveolar capillary barotrauma and pulmonary edema called ‘lung squeeze’.
6. Competitive divers use predive hyperinflation called “lung packing” to increase lung volume.
7. Apnea times are limited by carbon dioxide accumulation and urge to breathe.
8. Elite apneists can breath-hold on air for over 10 min, limited by lung oxygen storage.
9. Breath-hold divers can blackout from hypoxia due to drop in oxygen partial pressure during ascent.
10. Neurological decompression sickness can occur following deep and repetitive breath-hold dives.

Didactic Legends

The figures—in a freely downloadable PowerPoint format—can be found on the Images tab along with the formal legends published in the article. The following legends to the same figures are written to be useful for teaching.

Figure 1. Japanese Ama divers operating from the shore and from a boat. A catch net is carried and a surface float is used for storing harvest. Goggles with side air bulbs for pressure equalization were used before the transition to diving masks. Reproduced, with permission, from Rahn and Yokoyama (321).

Figure 2. A competitive freediver surfaces from a constant weight dive to 103 m. A straining maneuver called a hook breath is being used to promote increased blood flow to the brain to help prevent hypoxic blackout (author photo). Teaching Point: Forcefully raising static chest pressure is an attempt to squeeze more blood from the aorta into the cerebral vasculature when the diver is on the verge of hypoxic blackout.

Figure 3. Effect of immersion to the neck on internal body pressures in cmH₂O. Pressures across the diaphragm in italics are taken from Ref. (2), while other numbers are estimates based on respective hydrostatic distributions. External water pressure acts at chest and abdomen centroids. Vertical ordinates Zp of pleural pressure Pp and Za of abdominal pressure Pa are measured from neck Z₁ and diaphragm Z₂ reference levels. Blood volume shown in grey shifts into the chest upon immersion, distending the heart H and pulmonary vasculature. Teaching point: Pressure of static fluids in the body always increases in downward direction due to gravity causing a vertical increase in hydrostatic pressure. Knowledge of vertical distances, fluid densities, and wall boundary compliances that introduce discontinuities allows estimation of the overall pressure distribution inside the body.

Figure 4. Heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure responses to a breath-hold on air of 320 s. A hypertensive response is seen during the latter phase. A secondary drop in heart rate is also seen, possibly brought on by hypoxia. Results suggest intense sympathetic and parasympathetic coactivation. Modified with permission from Perini et al. (303). Teaching Point: Heart rate and vascular resistance efferents are normally regulated by the autonomic nervous system in response to baroreceptor and chemoreceptor afferents. Breath-holding modifies these interactions through the diving response.

Figure 5. Apnea with face immersion at rest induces diving bradycardia. Exercise alone raises heart rate. Combining face-immersed apnea with exercise results in attenuating influences and an intermediate heart rate response. Modified with permission from Wein et al. (399). Teaching Point: Diving induces bradycardia. Exercise induces tachycardia. When both stimuli occur together, the autonomic nervous system produces an intermediate response between these conflicting demands.

Figure 6. Reduction in spleen volume is seen during five repeated apneas, associated with increasing apnea times. Greater response is seen in trained divers. Splenectomized persons had shorter apnea times. Recovery of spleen volume takes over one hour. Reproduced with permission from Bakovic et al. (24). Teaching point: Apnea is a stimulus for spleen contraction, which releases stored red blood cells into the general circulation. The additional oxygen carried by the increase in hemoglobin is associated with longer tolerable apnea times. Subjects lacking a spleen do not exhibit this augmentation.

Figure 7. Apnea with face immersion delays the drop in arterial hemoglobin saturation compared with apnea in air, suggesting that the diving response has an oxygen conserving effect. Reproduced with permission from Andersson and Schagatay (17). Teaching Point: One can infer that face immersion with apnea results in a lower rate of tissue oxygen uptake from blood, and hence a slower drop in arterial hemoglobin oxygen saturation.

Figure 8. Respiratory system compliance curve showing lung volume versus airway pressure (P_AW) during a dive with depths shown. Lungs are packed above total lung capacity (TLC) to V₁. Air compression to V₂ below residual volume (RV) is partially compensated by blood volume (V_B) shifting into the chest shown in grey. Results are from computer simulation. Teaching Point: A standard respiratory system compliance curve relates airway pressure to lung volume. It incorporates lung and chest wall compliances. Immersion and lung gas compression at depth due to Boyle's law together cause airway pressure to drop below the external water pressure beyond a critical depth due to chest wall recoil, causing a relative negative pressure in the chest relative to ambient pressure.

Figure 9. Airway pressure in cm H₂O versus depth during a breath-hold descent predicted by computer simulation. The model incorporates immersion, air compression, respiratory system compliance, and thoracic blood shift. Lung packing extends the pressure reversal depth Z_R from 27 to 43 msw. Small ripples are from heart beat volume oscillations. Teaching point: Theoretical calculations allow estimation of airway pressure versus depth. Lung packing shifts the curve toward a more positive pressure.

Figure 10. Computer model estimates of percent alveolar closure and reopening during dives to various depths. First alveolus reaches closing volume CV around 18 m. Lungs reach the fully collapsed state around 235 m assuming an initial lung volume of 9.2 L. Dashed lines indicate ascent to first alveolar reopening. Modified with permission from Fitz-Clarke (127). Teaching point: Alveolar sacs collapse causing atelectasis when the lung is forced to low volume at depth. Expanding air on ascent reopens these alveoli at a rate depending on the statistical distribution of alveolar opening pressures.

Figure 11. Glossopharyngeal breathing used by tetraplegics has been adopted by BH divers for hyperinflation or “lung packing” above TLC. Reproduced with permission from Warren (398). Teaching point: Muscles around the mouth and upper airway can be used to force air into the lungs.

Figure 12. Alveolar oxygen and carbon dioxide levels during a resting breath-hold on air started at total lung capacity (TLC) or functional residual capacity (FRC). Reproduced, with permission, from Hong et al. (177). Teaching point: Larger lung volume provides greater oxygen storage and a larger capacitance into which metabolically produced carbon dioxide can be sequestered. Hence, gas levels change more slowly during apnea started at higher initial lung volume.

Figure 13. Apnea time on a breath of pure oxygen is limited by intolerable carbon dioxide accumulation. The right-hand side of the curve tracks alveolar P_ACO₂ rise with apnea time to the breakpoint. Preceding hyperventilation adds the time shown on the left-hand side by having lower initial P_ACO₂. Total apnea time is the sum of both sides. Reproduced with permission from Klocke and Rahn (204). Teaching Point: This curve shows how breath-hold time with pure oxygen is limited by subject tolerance of high-accumulated carbon dioxide. Hyperventilation shifts initial CO₂ level below the horizontal line, allowing a 10-min apnea time to be extended to 20 min. Hypoxia is impossible during an oxygen breath-hold because the lungs always contain a high fraction of oxygen. Carbon dioxide accumulation causing intolerable urge to breathe or delirium from narcosis are the end-points.

Figure 14. Alveolar CO₂ rises and O₂ falls during a breath-hold on air (dashed curve). Involuntary diaphragmatic contractions begin at the physiological breakpoint. Apnea becomes intolerable at the conventional breakpoint. Hypoxic blackout occurs if oxygen level falls below about 20-30 mmHg. Modified with permission from Agostoni (1). Teaching point: Carbon dioxide is stored in the body during apnea like fluid filling a tank. There is a gas component in the lungs and a dissolved component in blood and tissues. Width of the hypothetical tank at any depth represents whole-body solubility at that PaCO₂. The rise in alveolar CO₂ is plotted against the drop in alveolar O2. The boundary curves represent the possible end-points described earlier.

Figure 15. Computer simulated gas levels during a swimming breath-hold dive to 6 msw indicated at the bottom. Initial arterial PaCO₂ is 29 mmHg (left) after normal breathing and the breakpoint is reached after 1.5 min when PaCO₂ reaches 60 mmHg (circle). Ascent avoids critical hypoxia, and the dive is safe. In contrast, pre-dive hyperventilation (right) lowers initial PaCO₂ to 22 mmHg and allows a longer dive without the urge to breathe. PaO₂ drops below 30 mmHg on ascent and hypoxic blackout (BO) occurs near the surface. Teaching point: These plots illustrate why hyperventilation before a BH dive is potentially dangerous. Lowering arterial CO₂ shifts the curves allowing BH time to be extended to the point of critical hypoxia, such that the diver can blackout underwater.

Figure 16. Brain lesions caused by decompression injury in an Ama diver. The large areas of infarction suggest the etiology might involve arterial embolism from nitrogen bubbles released during repetitive diving. Reproduced, with permission, from Kohshi (206). Teaching point: It is not known where nitrogen bubbles initially form that cause DCS; whether it is directly at the site of injury, or if bubbles are transported through the circulation from elsewhere.

Figure 17. Deepest human breath-hold dives in constant weight CW (fin swimming) and no-limits NL (weight or sled assisted) categories since 1949. The dive to 253 msw resulted in loss of consciousness and serious neurological injury, and hence is not considered a record.

Figure 18. Hypothetical depth limiting factors in breath-hold diving. Statistics of risk are unavailable to calibrate curves due to the small number of very deep dives. Progressive lung collapse causes some curves to drop. Gas narcosis decreases cognitive function. DCS = decompression sickness, CW = constant weight, NL = no-limits.