Effects of hyperventilation on oxygenation, apnea breaking points, diving response, and spleen contraction during serial static apneas

Abstract

Purpose: Hyperventilation is considered a major risk factor for hypoxic blackout during breath-hold diving, as it delays the apnea breaking point. However, little is known about how it affects oxygenation, the diving response, and spleen contraction during serial breath-holding.

Methods: 18 volunteers with little or no experience in freediving performed two series of 5 apneas with cold facial immersion to maximal duration at 2-min intervals. In one series, apnea was preceded by normal breathing and in the other by 15 s of hyperventilation. End-tidal oxygen and end-tidal carbon dioxide were measured before and after every apnea, and peripheral oxygen saturation, heart rate, breathing movements, and skin blood flow were measured continuously. Spleen dimensions were measured every 15 s.

Results: Apnea duration was longer after hyperventilation (133 vs 111 s). Hyperventilation reduced pre-apnea end-tidal CO₂ (17.4 vs 29.0 mmHg) and post-apnea end-tidal CO₂ (38.5 vs 40.3 mmHg), and delayed onset of involuntary breathing movements (112 vs 89 s). End-tidal O₂ after apnea was lower in the hyperventilation trial (83.4 vs 89.4 mmHg) and so was the peripheral oxygen saturation nadir after apnea (90.6 vs 93.6%). During hyperventilation, the nadir peripheral oxygen saturation was lower in the last apnea than in the first (94.0% vs 86.7%). There were no differences in diving response or spleen volume reduction between conditions or across series.

Conclusions: Serial apneas revealed a previously undescribed aspect of hyperventilation; a progressively increased desaturation across the series, not observed after normal breathing and could heighten the risk of a blackout.

Keywords: Blackout; Breath-hold diving; Hypocapnia; Hypoxia.

Fig. 1

Apnea protocol used for normal breathing (NB) and hyperventilation (HV) series, which were done in weighted order. The green circle indicates 15 s of hyperventilation

Fig. 2

Recordings from the chest bellows show breathing movements in the same participant before the fifth apnea during hyperventilation (top panel) and normal ventilation (bottom panel). The grey areas indicate apneas. AU, arbitrary units

Fig. 3

Mean apnea duration for apnea 1–5 (A1–A5), with SD bars, for the two conditions: normal breathing (NB) and hyperventilation (HV). *p < 0.05, **p < 0.01 and ***p < 0.001 compared with A1 in the same condition (n = 18)

Fig. 4

End-tidal carbon dioxide pressures (PE_TCO₂) at a the start of each apnea 1–5 and b at the end of apnea 1–5 in the two breathing conditions. End-tidal oxygen pressures (PE_TO₂) at c the start of each apnea 1–5 and d at the end of apnea 1–5 in the two conditions. *p < 0.05, **p < 0.01, and ***p < 0.001 between conditions; ^†p < 0.05, ^††p < 0.01, and ^†††p < 0.001 compared with A1 in the same condition (n = 13)

Fig. 5

Duration of the easy (a) and struggle (b) phases for apneas 1–5 (A1–A5) after normal breathing (NB) and hyperventilation (HV) for the seven subjects with involuntary breathing movements (IBM) in all apneas. ***p < 0.001, **p < 0.01, and *p < 0.05 between conditions

Fig. 6

O₂–CO₂ diagram showing individual alveolar values during NB (a) and HV (b). Circles represent values at the start of apnea. Triangles represent values at the end of apnea. Filled symbols indicate NB (a) and empty symbols indicate HV (b). Colors show apnea series. Horizontal dashed lines show the range of normal P_ACO₂. Black continuous lines represent the conventional apnea breaking point (Agostoni 1963) (n = 13)

Fig. 7

S_pO₂ recording in one participant during series of five dives after normal breathing (NB) and hyperventilation (HV)

Fig. 8

Mean baseline pre-apnea SpO₂ from A1–A5 (a) and at post-apnea nadir (b). *p < 0.05, **p < 0.01, ***p < 0.001 compared with A1 in the same condition; ^†p < 0.05, ^††p < 0.01, ^†††p < 0.001 compared with HV (n = 18)

Fig. 9

Mean (SE) SpO₂ in NB (a) and HV (b) series during A1–A5. The grey boxes indicate apnea time. Negative time values before apnea time indicate breathing just before apneas. Positive values after apnea time indicate recovery time directly after apneas and partly overlap with pre-apnea values of the subsequent apnea. The gap in the middle of apnea time has variable duration, as apnea duration was different between participants. *p < 0.05, **p < 0.01, ***p < 0.001 indicates significance compared with A1 in the same condition; ^†††p < 0.001 indicates significance compared with HV (n = 18)

Fig. 10

Heart rate average for baseline (a), HR_peak (b), and during apnea (c). ***p < 0.001 between normal (NB) and hyperventilation (HV) conditions; ^†††p < 0.001, ^††p < 0.01, and ^†p < 0.05 compared with A1 in the same condition

Fig. 11

Mean (SE) heart rate during apnea 1–5 at Normal (a) and HV (b). The grey boxes indicate apnea time. Negative time values before apnea time indicate breathing. Positive values after apnea time indicate recovery time and overlap with the previous values of the subsequent apnea. The gap in the middle of apnea time has variable duration, as apnea time was different between participants (n = 18)

Fig. 12

SkBF reduction in percentage from baseline in both conditions from apnea 1 to apnea 5 (a) and recordings from one participant in the fifth apnea comparing both conditions (b). PU, perfusion units. (n = 18)

Fig. 13

Mean spleen volume during the NB and HV apnea series. The grey boxes indicate apneas. Negative values before A1 indicate baseline measurements 5 min before starting. Positive values after every apnea indicate recovery time in minutes. The brackets indicate that an average period was compared. ***p < 0.001 compared with baseline; ^###p < 0.001 compared with apnea values