Mid Sweden University

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 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.

Breath-hold diving or freediving exposes the body to stressors such as low oxygen and high carbon dioxide levels in the blood, increased hydrostatic pressure, and cold. The reduction in blood oxygen levels is considered a primary factor for loss of consciousness while diving. This is known as hypoxic blackout. My thesis aimed to enhance the understanding of the factors that lead to hypoxic blackout in serial freediving. This includes studying the physiological mechanisms that protect the body against hypoxia and exploring how hyperventilation affects those mechanisms, with a specific focus on repetitive dives. 

The protective mechanisms, splenic contraction (Studies I, II) and diving bradycardia (Studies II and IV), were tested in experimental conditions. The effect of hyperventilation on simulated serial dives (Study II) was investigated, and a strategy to identify actual hyperventilation during diving was developed and explored (Study III). A static apnea test allowing identification of individuals at particular risk for blackout was developed (Study IV).

The results showed that hypoxia-induced splenic contraction occurs rapidly enough to be protective in long-duration breath-holds (Study I). Serial simulated dives, preceded by short-term hyperventilation, lead to longer apnea duration and progressive oxygen desaturation (Study II). Despite the more severe desaturation resulting from hyperventilation, these consecutive apneas do not show an augmented diving response or splenic contraction. Hyperventilation was also observed when divers intended to avoid it (Studies II, III, and IV). Therefore, the possibility of estimating hyperventilation from the signal of a force sensor attached to a chest belt was explored (Study III). A stronger diving bradycardia and a bigger spleen were found to be protective against hypoxia and are related to slower oxygen desaturation (Study IV). 

The main conclusion is that oxygenation is impaired by the accumulation of an oxygen debt when consecutive dives are preceded by hyperventilation. The protective mechanisms, such as splenic contraction and the diving response, are beneficial at the individual level but do not offset the increased risk across a series of dives. However, splenic contraction does offer protection even during the first dive of a series. A chest belt-mounted force sensor could be used to identify when freedivers are hyperventilating. Additionally, a novel static apnea ramp test is effective in identifying freedivers who are at a high risk of faster desaturation during freediving.

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.

While MRI and CT are the gold standards for assessments of splenic size in clinical settings, ultrasonography is particularly suited due to its portability, cost efficiency and easy utilization. However, ultrasonography is associated with subjective assessment, potentially resulting in increased variation. We used a test–retest design aiming to determine the reliability of splenic measurements assessed by ultrasonography during apnea. In addition, we compared reliability between different equations for volume calculations: Koga, Prolate ellipsoid and Pilström. Twelve healthy participants (6 women) performed two tests separated by 15 min, comprising a maximal voluntary apnea in a seated position. Splenic dimensions were measured via ultrasonography for 5 min before and immediately following apnea. Resting splenic volume displayed high test–retest reliability between tests (Pilström: 157 ± 39 mL vs 156 ± 34 mL, p = .651, ICC = .970, p < .001, CV = 2.98 ± 0.1%; Prolate ellipsoid: 154 ± 37 mL vs 144 ± 43 mL, p = .122, ICC = .942, p < .001, CV = 5.47 ± 0.3%; Koga: 142 ± 37 mL vs 140 ± 59 mL, p = .845, ICC = .859, p < .001, CV = 9.72 ± 1.4%). Apnea-induced volumes displayed similar reliability (127 ± 29 mL vs 129 ± 28 mL, p = .359, ICC = .967, p < .001, CV = 3.14 ± 3.1%). Reliability was also high between equations (Pilström vs Prolate ellipsoid: ICC = .818, p < .001, CV = 7.33 ± 0.3%, bias =  − 3.1 mL, LoA =  − 46.9 to 40.7 mL; Pilström vs Koga: ICC = .618, p < .01, CV = 11.83 ± 1.1%, bias =  − 14.8 mL, LoA =  − 76.9 to 47.3 mL). We conclude that splenic ultrasonographic measurements have practical applications during laboratory and field-based research as a reliable method detecting splenic volume change consistently between repeated tests. The Pilström equation displayed similar reliability compared to the prolate ellipsoid formula and slightly higher compared to the Koga formula and may be particularly useful to account for individual differences in splenic dimensions.

Breath-hold diving (freediving) is an underwater sport that is associated with elevated hydrostatic pressure, which has a compressive effect on the lungs that can lead to the development of pulmonary edema. Pulmonary edema reduces oxygen uptake and thereby the recovery from the hypoxia developed during freediving, and increases the risk of hypoxic syncope. We aimed to examine the efficacy of SpO2, via pulse-oximetry, as a tool to detect pulmonary edema by comparing it to lung ultrasound B-line measurements after deep diving. SpO2 and B-lines were collected in 40 freedivers participating in an international deep freediving competition. SpO2 was measured within 17 ± 6 min and lung B-lines using ultrasound within 44 ± 15 min after surfacing. A specific symptoms questionnaire was used during SpO2 measurements. We found a negative correlation between B-line score and minimum SpO2 (rs = −0.491; p = 0.002) and mean SpO2 (rs = −0.335; p = 0.046). B-line scores were positively correlated with depth (rs = 0.408; p = 0.013), confirming that extra-vascular lung water is increased with deeper dives. Compared to dives that were asymptomatic, symptomatic dives had a 27% greater B-line score, and both a lower mean and minimum SpO2 (all p &lt; 0.05). Indeed, a minimum SpO2 ≤ 95% after a deep dive has a positive predictive value of 29% and a negative predictive value of 100% regarding symptoms. We concluded that elevated B-line scores are associated with reduced SpO2 after dives, suggesting that SpO2 via pulse oximetry could be a useful screening tool to detect increased extra-vascular lung water. The practical application is not to diagnose pulmonary edema based on SpO2 – as pulse oximetry is inexact – rather, to utilize it as a tool to determine which divers require further evaluation before returning to deep freediving.