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. 

Freeride skiing and snowboarding-collectively termed competitive freeriding-have evolved from niche extreme sports into formally recognized disciplines under the International Ski & Snowboard Federation (FIS). Unlike traditional alpine or freestyle events, competitive freeriding emphasizes creative line selection, technical execution, fluidity, style, and aerial maneuvers on natural, ungroomed mountain terrain. Athletes descend complex slopes based solely on visual inspection, without practice runs, facing unique physical and psychological challenges. This perspective article outlines the competition format and judging system, identifies key physiological and biomechanical demands, and reviews essential equipment and safety considerations. Despite growing popularity and institutional recognition, scientific research remains limited-primarily focused on avalanche risk and injury incidence-while other dimensions, such as psychological resilience, creative expression, and environmental connectedness, remain underexplored. Physiologically, competitive freeriders require high levels of eccentric and explosive strength, core stability, reactive control, and anaerobic endurance to navigate variable terrain and absorb impact during aerial maneuvers. Lower-extremity injuries-particularly anterior cruciate ligament (ACL) ruptures-are a major concern. Technological advances in drone-based filming, athlete monitoring, and protective equipment are reshaping freeride competition and broadcasting. As the sport moves toward potential Olympic inclusion, the central challenge lies in embracing innovation without compromising the core values of freedom, improvisation, and connection to the mountain environment.

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. 

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.

Freediving, underwater diving while breath-holding, imposes unique physiological challenges to the human body. This includes immersion, changes in hydrostatic pressure, hypercapnia, and hypoxia. Severe hypoxia can cause loss of consciousness, known as hypoxic blackout, and without immediate assistance drowning may occur. 

The aim of this thesis was to identify factors increasing the risk of hypoxic blackout, to determine if physiological responses mitigated these risks and to explore potential interventions that could promote safe freediving. This was done by utilizing a prototype water- and pressure-proof pulse oximeter (SUB) to measure heart rate (HR) and arterial oxygen saturation (SpO2) under various real-world freediving conditions, and through laboratory investigation of the effects of apnea- recovery pacing on repeated apneas, focusing on arterial, cerebral, and muscle oxygenation. 

Study 1 demonstrated the SUB's ability to record HR and SpO2 during deep sea dives up to 82 meters, marking an important advancement in underwater monitoring technology. Study 2 showed that deeper dives resulted in greater oxygen desaturation, potentially increasing the risk of hypoxic blackout, not only due to pressure effects on gas exchange, but also from increased physical exertion. In addition, some individuals experienced hypoxia upon reaching maximum depth, when hyperoxia is expected, suggesting that gas exchange may be compromised, which could increase the risk of blackout during ascent. In Study 3, a persistent cardiac arrhythmia preceded a blackout, suggesting that arrhythmias may be a contributing factor to increased risk of blackout. Study 4 showed that brain oxygen homeostasis was maintained across a series of submaximal apneas with equal dive-to-rest ratio, without progressive oxygen desaturation occurring, suggesting that pacing strategies can be effectively used to maintain safety in repeated freediving and should be individually tailored. Collectively, these studies confirm that well- trained freedivers exhibit a remarkable tolerance to hypoxia. However, the risk of hypoxic blackout is highly individual, suggesting that establishing a definitive blackout threshold based on SpO2 may be challenging. It is therefore concluded that there is a need for enhanced safety protocols in freediving, including personalized physiological monitoring, which could be enabled by innovative wearable technologies like the SUB to mitigate the risk of blackout in 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.

INTRODUCTION: Recreational freedivers typically perform repeated dives to moderate depths with short recovery intervals. According to freediving standards, these recovery intervals should be twice the dive duration; however, this has yet to be supported by scientific evidence. METHODS: Six recreational freedivers performed three freedives to 11 metres of freshwater (mfw), separated by 2 min 30 s recovery intervals, while an underwater pulse oximeter measured peripheral oxygen saturation (SpO2) and heart rate (HR). RESULTS: Median dive durations were 54.0 s, 103.0 s and 75.5 s (all dives median 81.5 s). Median baseline HR was 76.0 beats per minute (bpm), which decreased during dives to 48.0 bpm in dive one, 40.5 bpm in dive two and 48.5 bpm in dive three (all P < 0.05 from baseline). Median pre-dive baseline SpO2 was 99.5%. SpO2 remained similar to baseline for the first half of the dives, after which the rate of desaturation increased during the second half of the dives with each subsequent dive. Lowest median SpO2 after dive one was 97.0%, after dive two 83.5% (P < 0.05 from baseline) and after dive three 82.5% (P < 0.01 from baseline). SpO2 had returned to baseline within 20 s after all dives. CONCLUSIONS: We speculate that the enhanced rate of arterial oxygen desaturation across the serial dives may be attributed to a remaining 'oxygen debt', leading to progressively increased oxygen extraction by desaturated muscles. Despite being twice the dive duration, the recovery period may be too short to allow full recovery and to sustain prolonged serial diving, thus does not guarantee safe diving. Copyright: This article is the copyright of the authors who grant Diving and Hyperbaric Medicine a non-exclusive licence to publish the article in electronic and other forms.

Purpose: To examine the effect of freediving depth on risk for hypoxic blackout by recording arterial oxygen saturation (SpO2) and heart rate (HR) during deep and shallow dives in the sea. Methods: Fourteen competitive freedivers conducted open-water training dives wearing a water-/pressure proof pulse oximeter continuously recording HR and SpO2. Dives were divided into deep (&gt; 35 m) and shallow (10–25 m) post-hoc and data from one deep and one shallow dive from 10 divers were compared. Results: Mean ± SD depth was 53 ± 14 m for deep and 17 ± 4 m for shallow dives. Respective dive durations (120 ± 18 s and 116 ± 43 s) did not differ. Deep dives resulted in lower minimum SpO2 (58 ± 17%) compared with shallow dives (74 ± 17%; P = 0.029). Overall diving HR was 7 bpm higher in deep dives (P = 0.002) although minimum HR was similar in both types of dives (39 bpm). Three divers desaturated early at depth, of which two exhibited severe hypoxia (SpO2 ≤ 65%) upon resurfacing. Additionally, four divers developed severe hypoxia after dives. Conclusions: Despite similar dive durations, oxygen desaturation was greater during deep dives, confirming increased risk of hypoxic blackout with increased depth. In addition to the rapid drop in alveolar pressure and oxygen uptake during ascent, several other risk factors associated with deep freediving were identified, including higher swimming effort and oxygen consumption, a compromised diving response, an autonomic conflict possibly causing arrhythmias, and compromised oxygen uptake at depth by lung compression possibly leading to atelectasis or pulmonary edema in some individuals. Individuals with elevated risk could likely be identified using wearable technology.