Mid Sweden University

Blackout (BO) in breath-hold diving is attributed to cerebral hypoxia, yet direct observations are rare. We continuously recorded arterial oxygen saturation (SpO₂) and heart rate (HR) in 11 trained freedivers (5 females) performing two dynamic apneas (75 m, 100 m) using a waterproof forehead oximeter. One diver experienced BO at the end of a 100 m dive (SpO₂ 51 %), recovering within 5 s. Group SpO₂ fell from 98 ± 1 % to 77 ± 9 % (75 m) and 68 ± 9 % (100 m; range 51–83 %), while mean HR declined from 83 ± 12 to 43 ± 8 and 40 ± 4bpm, respectively. No arrhythmias were detected. Within-diver SpO₂ nadirs were consistent between distances (r = 0.93), whereas HR nadirs were not (r = 0.40). This case confirms BO can occur at SpO₂ values around 50 %, even in the absence of arrhythmia. The BO diver consistently showed the lowest SpO₂, indicating profound hypoxemia as the most likely contributing factor. Findings support individualized risk screening based on early desaturation patterns in submaximal dives. 

Purpose: This study investigated whether trained freedivers can sustain a 1:1 apnea-to-recovery ratio without progressive arterial or cerebral oxygen desaturation. Methods: 21 trained freedivers (6 females) performed 7 static apneas of fixed 2-min duration, each followed by 2-min of rest, in a supine laboratory setting. Arterial oxygen saturation (SpO₂) and heart rate (HR) were measured continuously. Near-infrared spectroscopy (NIRS) assessed cerebral and peripheral muscle oxygenation. A chest force sensor recorded involuntary breathing movements (IBM). End-tidal CO₂ (EtCO₂) was measured pre- and post apnea. Results: SpO₂ declined most during the first apnea (94 ± 3 %) but stabilized thereafter (p < 0.005). Lowest HR increased from 61 ± 15 to 65 ±13 bpm across the series (p = 0.02), and the intial apnea tachycardia declined by 10 bpm (p = 0.012). Cerebral oxygenation increased above baseline only during the first apnea (1.0 ± 2.3 %); in subsequent apneas it remained stable, although slightly below baseline. Muscle oxygenation declined during all apneas but was more pronounced in the first (-6.7 ± 3.1 %). IBM onset was progressively delayed; 63 % of participants showed no IBM during the final apnea. EtCO₂ increased after each apnea by ≈ 1.0kPa (p < 0.001) but did not change progressively across the series. Conclusion: A 1:1 apnea-to-recovery ratio was physiologically sustainable in trained freedivers at rest, without inducing progressive oxygen desaturation. The initial apnea elicited the strongest oxygen-conserving responses, which progressively attenuated across the series, suggesting that physiological regulation during repeated submaximal apneas is adaptable to meet situation-specific demands. The progressive IBM delay despite stable CO2 levels suggests additional mechanisms beyond chemoreflex-driven stimulation of breathing may contribute to ventilatory drive. 

Breath-hold diving performances are typically better in men than in women. However, it is still being determined if there are differences in the physiological responses to breath-holding between the sexes. We conducted a study comparing the maximum breath-hold duration, heart rate (HR) reduction, peripheral oxygen saturation (SpO2), and spleen volume and contraction in 37 men and 44 women, all of whom had no prior breath-holding experience. They performed two dry apneas separated by 2 min; the first was limited to 60 s, followed by a maximal effort apnea. HR and SpO2 were measured continuously. Spleen diameters were measured via ultrasonography before and immediately following each apnea. The maximal apneic duration was longer in men (78 +/- 19 s) compared with women (61 +/- 18 s, p < 0.001), while the HR reduction was similar (women: 16% +/- 19% versus men: 16% +/- 17%, p = 0.973). The absolute splenic contraction was greater in men (59 +/- 56 mL) compared with women (35 +/- 28 mL, p < 0.001) in the first apnea, while the relative contraction was similar (women: 21% +/- 17% versus men: 23% +/- 13%, p = 0.528). In addition, the lowest SpO2 during the maximal apnea was similar between sexes (women: 93.3% +/- 4.4%; men: 91.9% +/- 4.3%, p = 0.161). We conclude that men have larger spleen size and contraction, lung size, and maximal apneic duration than women. The cardiovascular diving response is similar between sexes for those inexperienced with apneic diving. The longer breath-hold duration in men may be partly due to greater oxygen storage capacity, which results from larger vital capacity and greater spleen size and contraction.

Background and aim: Hyperventilation before breath-hold diving (freediving) is widely accepted as a risk factor for hypoxic syncope or blackout (BO), but there is no practical way to address it before dives. This study explores the feasibility of using a force sensor to predict end-tidal carbon dioxide (PETCO2) to assess hyperventilation in freedivers.

Methods and results: Twenty-one freedivers volunteered to participate during two national competitions. The divers were instructed to breathe normally and perform three dry apneas of 1, 2, and 3-min duration at 2-min intervals in a sitting position. Before and after the apneas, PETCO2 was recorded. The signal from the force sensor, attached to a chest belt, was used to record the frequency and amplitude of the chest movements, and the product of these values in the 60 s before the apnea was used to predict PETCO2. The mean PETCO2 was below 35 mmHg before all apneas. The mean amplitude of the signal from the force sensor increased from apnea 1 to apnea 3 (p < 0.001), while the respiratory rate was similar (NS). The product of the respiratory rate and amplitude from the force sensor explained 34% of the variability of the PETCO2 in the third apnea.

Conclusion: This study shows that a force sensor can estimate hyperventilation before static apnea, providing a basis for further research. More studies are needed to confirm its effectiveness in preventing issues. Freedivers may hyperventilate without noticing it, and such a system could improve awareness of this condition. Additional underwater tests are essential to determine whether this system can enhance safety in freediving.

The human spleen contracts in response to stress-induced catecholamine secretion, resulting in a temporary rise in haemoglobin concentration ([Hb]). Recent findings highlighted enhanced splenic response to exercise at high altitude in Sherpa, possibly due to a blunted splenic response to hypoxia. To explore the potential blunted splenic contraction in Sherpas at high altitude, we examined changes in spleen volume during hyperoxic breathing, comparing acclimatized Sherpa with acclimatized individuals of lowland ancestry. Our study included 14 non-Sherpa (7 female) residing at altitude for a mean continuous duration of 3 months and 46 Sherpa (24 female) with an average of 4 years altitude exposure. Participants underwent a hyperoxic breathing test at altitude (4300 m; barrometric pressure = ∼430 torr; (Formula presented.) = ∼90 torr). Throughout the test, we measured spleen volume using ultrasonography and monitored oxygen saturation ((Formula presented.)). During rest, Sherpa exhibited larger spleens (226 ± 70 mL) compared to non-Sherpa (165 ± 34 mL; P < 0.001; effect size (ES) = 0.95, 95% CI: 0.3–1.6). In response to hyperoxia, non-Sherpa demonstrated 22 ± 12% increase in spleen size (35 ± 17 mL, 95% CI: 20.7–48.9; P < 0.001; ES = 1.8, 95% CI: 0.93–2.66), while spleen size remained unchanged in Sherpa (−2 ± 13 mL, 95% CI: −2.4 to 7.3; P = 0.640; ES = 0.18, 95% CI: −0.10 to 0.47). Our findings suggest that Sherpa and non-Sherpas of lowland ancestry exhibit distinct variations in spleen volume during hyperoxia at high altitude, potentially indicating two distinct splenic functions. In Sherpa, this phenomenon may signify a diminished splenic response to altitude-related hypoxia at rest, potentially contributing to enhanced splenic contractions during physical stress. Conversely, non-Sherpa experienced a transient increase in spleen size during hyperoxia, indicating an active tonic contraction, which may influence early altitude acclimatization in lowlanders by raising [Hb]. 

The human spleen acts as a reservoir for red blood cells, which is mobilized into the systemic circulation during various conditions such as hypoxia and physical exertion. Cross-country (XC) skiers, renowned for their exceptional aerobic capacity, are regularly exposed to high-intensity exercise and local oxygen deficits. We investigated a putative dose-dependent relationship between splenic contraction and concomitant hemoglobin concentration ([Hb]) elevation across four exercise intensities in well-trained XC skiers. Fourteen male XC skiers voluntarily participated in a 2-day protocol, encompassing a serial apnea test and a VO2max test (day 1), followed by three submaximal exercise intensities on a roller skiing treadmill corresponding to 55, 70, and 85% of VO2max (day 2). Spleen volume was measured via ultrasonic imaging, and venous blood samples were used to determine [Hb] levels. Baseline spleen volume was similar (266(35) mL) for all conditions (NS). Notably, all conditions induced significant splenic contractions and transient [Hb] elevations. The VO2max test exhibited the most pronounced splenic contraction (35.8%, p < 0.001) and a [Hb] increase of 8.1%, while the 85% exercise intensity led to 27.1% contraction and the greatest [Hb] increase (8.3%, < 0.001) compared to baseline. The apnea test induced relatively smaller responses (splenic contraction: 20.4%, [Hb] = 3.3%, p < 0.001), akin to the response observed at the 70% exercise intensity (splenic contraction = 23%, [Hb] = 6.4%, p < 0,001) and 55% (splenic contraction = 20.0%, [Hb] = 4.8%, p < 0.001). This study shows a discernible dose-dependent relationship between splenic contraction and [Hb] increase with levels of exercise, effectively distinguishing between submaximal and maximal exercise intensity.

Swimming and diving are popular recreational activities, representing an effective option in maintaining and improving cardiovascular fitness in healthy people. To date, only little is known about the cardiovascular adaption to submersion in children. This study was conducted to improve an understanding thereof. We used a stepwise apnea protocol with apnea at rest, apnea with facial immersion, and at last apnea during whole body submersion. Continuous measurement of heart rate, oxygen saturation, and peripheral resistance index was done. Physiologic data and analysis of influencing factors on heart rate, oxygen saturation, and peripheral vascular tone response are reported. The current study presents the first data of physiologic diving response in children. Data showed that facial or whole body submersion leads to a major drop in heart rate, and increase of peripheral resistance, while the oxygen saturation seems to be unaffected by static apnea in most children, with apnea times of up to 75 s without change in oxygen saturation. 

Syncope or "blackout" (BO) in breath-hold diving (freediving) is generally considered to be caused by hypoxia. However, it has been suggested that cardiac arrhythmias affecting the pumping effectivity could contribute to BO. BO is fairly common in competitive freediving, where athletes aim for maximal performance. We recorded heart rate (HR) during a static apnea (STA) competition, to reveal if arrhythmias occur. Four male freedivers with STA personal best (PB) of 349 ± 43 s, volunteered during national championships, where they performed STA floating face down in a shallow indoor pool. A non-coded Polar T31 chest strap recorded R-R intervals and a water- and pressure-proof pulse oximeter arterial oxygen saturation. Three divers produced STA near their PB without problems, whereas one diver ended with BO at 5 min 17s, which was 12 s beyond his PB. He was immediately brought up by safety divers and resumed breathing within 10 s. All divers attained similar lowest diving HR (47 ± 4 beats/min), but HR recordings displayed a different pattern for the diver ending with BO. After a short tachycardia, the three successful divers developed bradycardia, which became more pronounced during the second half of the apnea. The fourth diver developed pronounced bradycardia earlier, and at 2.5 min into the apnea, HR started alternating between approximately 50 and 140 beats/min, until the diver lost consciousness. At resumed breathing, HR returned to baseline. Nadir oxygen saturation was similar for all divers. We speculate that arrhythmia could have contributed to BO, by lowering stroke volume leading to a systolic blood pressure drop, affecting brain perfusion.NEW & NOTEWORTHY Heart rate during prolonged breath-holding until the point of loss of consciousness has not previously been published. The recordings show that blackout was preceded by a period of persistent alterations in R-R intervals, whereby an ectopic beat followed every normal heartbeat. Explanations for this deviating heart rate pattern could be either premature atrial contractions or premature ventricular contractions following every atrial beat, i.e., bigeminy, which could have compromised cardiac pumping function and caused/contributed to blackout.

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.