Effect of exercise intensity and apnea on splenic contraction and hemoglobin increase in well-trained cross-country skiers.

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 [Formula: see text]O2max test (day 1), followed by three submaximal exercise intensities on a roller skiing treadmill corresponding to 55, 70, and 85% of [Formula: see text]O2max (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 [Formula: see text]O2max 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.

Differential splenic responses to hyperoxic breathing at high altitude in Sherpa and lowlanders.

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 = âˆ¼430 torr; P O 2 ${P_{{{\mathrm{O}}_{\mathrm{2}}}}}$  = âˆ¼90 torr). Throughout the test, we measured spleen volume using ultrasonography and monitored oxygen saturation ( S p O 2 ${S_{{\mathrm{p}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ). 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].

First Real-Life Data on the Diving Response in Healthy Children.

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.

Unlocking the depths: multiple factors contribute to risk for hypoxic blackout during deep freediving.

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 (> 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.

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

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.

Underwater pulse oximetry reveals increased rate of arterial oxygen desaturation across repeated freedives to 11 metres of freshwater.

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.

Case Studies in Physiology: Is blackout in breath-hold diving related to cardiac arrhythmias?

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.

Test-retest reliability of splenic volume assessment by ultrasonography.

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.

Illness Incidence, Psychological Characteristics, and Sleep in Dogsled Drivers During the Iditarod Trail Sled Dog Race.

INTRODUCTION: Every March, dogsled drivers (mushers) compete in a 1569-km race across Alaska, involving physical exertion, mental exertion, and sleep deprivation for up to 2 wk. These factors may increase mushers' vulnerability to illness, making them a relevant study population for acute infection risk factors. Specifically, the influence of psychological factors on illness risk during prolonged physical exertion has rarely been investigated. The aim of this study was to examine the relationship between psychological characteristics, sleep deprivation, and illness incidence in Iditarod mushers. METHODS: Fourteen mushers completed 4 psychological instruments to assess state and trait anxiety, resilience and perceived stress, and self-reported upper respiratory symptoms (URS) in the month before the race. Mushers self-reported sleep duration and URS during the race. RESULTS: State and trait anxiety, resilience, and perceived stress did not differ between mushers with and without pre- and in-race URS (P>0.05). However, all mushers who reported in-race URS had reported URS ≤9 d before the race, and the onset of symptoms during the race typically occurred shortly after a rest period. Sleep duration was higher in mushers who reported in-race URS, both before (4.9±0.3 h, P=0.016) and during illness (5.9±1.3 h, P=0.006), vs mushers without in-race URS (3.4±0.8 h). CONCLUSIONS: This study highlights recent illness, rest periods, and greater sleep requirements as potential risk factors for URS onset during a multiday endurance challenge, whereas psychological factors were not associated with URS.

Effects of dynamic apnea training on diving bradycardia and short distance swimming performance.

BACKGROUND: Apnea training enhances bradycardia and improves competitive apnea performance and has been proposed as a training method for other sports, such as swimming. We evaluated the effects of apneic underwater swimming, i.e., dynamic apnea (DYN), in 9 competitive swimmers (TR) who completed ten DYN sessions over 2 weeks. METHODS: TR performed pre- and post-training tests including a static apnea test with continuous heart rate (HR) and peripheral oxygen saturation measurements, all-out 50m and 100m freestyle tests and an all-out DYN test. Control groups were competitive swimmers (SC; N.=10) that trained swimming without DYN, and a non-swimmer group (AC; N.=10) performing only static apnea tests. RESULTS: Post-training, TR mean±SD time for 50 m freestyle improved from 25.51±2.01 s to 24.64±2.02 s (P<0.01) and for 100m from 55.5±4.2 s to 54.1±4.4 s (P<0.05). SC also improved their 100m time from 56.7±3.3 s to 56.0±3.1 s (P<0.01; P=0.07 between groups). Only TR performed DYN tests; DYN distance increased from 62.1±11.5 m to 70.9±18.9 m (P<0.05) while DYN speed decreased from 0.74±0.14m/s to 0.64±0.18 m/s (P<0.01). Static apnea duration did not change in any of the groups, but HR-reduction was enhanced post-training only in TR (24.8±14.8% to 31.1±10.9%, P<0.01; P<0.001 between groups). CONCLUSIONS: We conclude that 2 weeks of DYN training enhanced DYN performance, which may be caused by the enhanced apnea-induced diving bradycardia. Further research is required to determine whether DYN training enhances short distance freestyle swimming performance.

Spleen Contraction During Sudden Eupneic Hypoxia Elevates Hemoglobin Concentration.

The spleen contracts progressively during moderate normobaric hypoxia exposure of 20 min, which elevates hemoglobin concentration (Hb). However, acute hypoxia exposure could be shorter and more severe when oxygen systems fail during, e.g., high-altitude sky diving, aircraft cabin pressure drop, balloon flights, extreme altitude climbing, and in some maladies. We aimed to evaluate the speed and magnitude of spleen contraction during short exposure to extreme eupneic hypoxia and its subsequent recovery on oxygen. Eight female and seven male volunteers were exposed to normobaric hypoxia (10% oxygen) for 10 min during sitting rest, followed by 10 min on 100% oxygen. Heart rate (HR), arterial oxygen saturation (SpO2), and mean arterial blood pressure (MAP) were measured continuously. The spleen was measured via ultrasonic imaging every minute for volume calculations, and venous blood samples were drawn before and after exposure for hemoglobin concentration (Hb). Mean (SD) spleen volume was 279 (115) mL before exposure, 219 (75) mL (21% reduction; P = 0.005) at 3 min of exposure, and 201 (93) mL after 10 min exposure to hypoxia (28% reduction; P < 0.001). Hb was 138.8 (7.6) g·L-1 before and 142.9 (8.1) g·L-1 after 10 min of exposure (2.9% increase; P < 0.001). SpO2 was 96.4 (1.7)% before exposure and 74.7 (8.4)% during the last minute of exposure (22.5% reduction; P < 0.001). HR increased from 80 (14) to 90 (17) bpm during exposure (12% increase, P < 0.05). MAP remained unchanged. After 10 min recovery on oxygen, values had been restored for spleen volume and Hb, while SpO2 was higher and HR lower compared with before hypoxia exposure. We concluded that acute normobaric hypoxia of only 10 min caused significant spleen volume contraction with Hb increase. This rapid spleen response, evident already after 3 min of exposure, could have a protective effect during sudden exposure to severe hypoxia.

Association Between Arterial Oxygen Saturation and Lung Ultrasound B-Lines After Competitive Deep Breath-Hold Diving.

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 (r s = -0.491; p = 0.002) and mean SpO2 (r s = -0.335; p = 0.046). B-line scores were positively correlated with depth (r s = 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 < 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.

Corrigendum: Using Underwater Pulse Oximetry in Freediving to Extreme Depths to Study Risk of Hypoxic Blackout and Diving Response Phases.

[This corrects the article DOI: 10.3389/fphys.2021.651128.].

When the human brain goes diving: using near-infrared spectroscopy to measure cerebral and systemic cardiovascular responses to deep, breath-hold diving in elite freedivers.

Continuous measurements of haemodynamic and oxygenation changes in free living animals remain elusive. However, developments in biomedical technologies may help to fill this knowledge gap. One such technology is continuous-wave near-infrared spectroscopy (CW-NIRS)-a wearable and non-invasive optical technology. Here, we develop a marinized CW-NIRS system and deploy it on elite competition freedivers to test its capacity to function during deep freediving to 107 m depth. We use the oxyhaemoglobin and deoxyhaemoglobin concentration changes measured with CW-NIRS to monitor cerebral haemodynamic changes and oxygenation, arterial saturation and heart rate. Furthermore, using concentration changes in oxyhaemoglobin engendered by cardiac pulsation, we demonstrate the ability to conduct additional feature exploration of cardiac-dependent haemodynamic changes. Freedivers showed cerebral haemodynamic changes characteristic of apnoeic diving, while some divers also showed considerable elevations in venous blood volumes close to the end of diving. Some freedivers also showed pronounced arterial deoxygenation, the most extreme of which resulted in an arterial saturation of 25%. Freedivers also displayed heart rate changes that were comparable to diving mammals both in magnitude and patterns of change. Finally, changes in cardiac waveform associated with heart rates less than 40 bpm were associated with changes indicative of a reduction in vascular compliance. The success here of CW-NIRS to non-invasively measure a suite of physiological phenomenon in a deep-diving mammal highlights its efficacy as a future physiological monitoring tool for human freedivers as well as free living animals. This article is part of the theme issue 'Measuring physiology in free-living animals (Part II)'.

Enhanced splenic volume and contraction in elite endurance athletes.

Splenic contraction, which leads to ejection of stored erythrocytes, is greater in athletes involved in regular freediving or high-altitude activities. As this response facilitates oxygen-carrying capacity, similar characteristics may be expected of elite endurance athletes. Therefore, our aims were to compare resting and apnea-induced splenic volume in endurance athletes and untrained individuals, and to assess the athletes' exercise-induced splenic volume. Twelve elite biathletes (7 women) and 12 controls (6 women) performed a maximal effort apnea in a seated position. In addition, the biathletes completed a maximal roller-skiing time trial. Splenic dimensions were measured by ultrasonic imaging for subsequent volume calculations, whereas Hb was analyzed from capillary blood samples and cardiorespiratory variables were monitored continuously. Baseline splenic volume was larger in the biathletes (214 ± 56 mL) compared with controls (157 ± 39 mL, P = 0.008) and apnea-induced splenic contraction was also greater in the biathletes (46 ± 20 mL vs. 30 ± 16 mL, P = 0.035). Hb increased immediately after apnea in the biathletes (4.5 ± 4.8%, P = 0.029) but not in the controls (-0.7 ± 3.1%, P = 0.999). Increases in exercise-induced splenic contraction (P = 0.008) and Hb (P = 0.001) were greater compared with the apnea-induced responses among the athletes. Baseline splenic volume tended to be correlated with V̇o2max (r = 0.584, P = 0.059). We conclude that elite biathletes have greater splenic volume with a greater ability to contract and elevate Hb compared with untrained individuals. These characteristics may transiently enhance O2-carrying capacity and possibly increase O2 uptake, thereby helping biathletes to cope with high intermittent O2 demands and severe O2 deficits that occur during biathlon training and competition.NEW & NOTEWORTHY This study demonstrates that elite biathletes have larger splenic volume, apnea-induced splenic contraction, and Hb elevation compared with untrained individuals, which is likely functional to cope with high O2 demands and substantial O2 deficits. We believe that enhanced splenic contraction may be of importance during competitions involving cross-country skiing, to regulate circulating Hb and enhance O2-carrying capacity, which may protect [Formula: see text] and increase O2 uptake.

First Evaluation of a Newly Constructed Underwater Pulse Oximeter for Use in Breath-Holding Activities.

Studying risk factors in freediving, such as hypoxic blackout, requires development of new methods to enable remote underwater monitoring of physiological variables. We aimed to construct and evaluate a new water- and pressure proof pulse oximeter for use in freediving research. The study consisted of three parts: (I) A submersible pulse oximeter (SUB) was developed on a ruggedized platform for recording of physiological parameters in challenging environments. Two MAX30102 sensors were used to record plethysmograms, and included red and infra-red emitters, diode drivers, photodiode, photodiode amplifier, analog to digital converter, and controller. (II) We equipped 20 volunteers with two transmission pulse oximeters (TPULS) and SUB to the fingers. Arterial oxygen saturation (SpO2) and heart rate (HR) were recorded, while breathing room air (21% O2) and subsequently a hypoxic gas (10.7% O2) at rest in dry conditions. Bland-Altman analysis was used to evaluate bias and precision of SUB relative to SpO2 values from TPULS. (III) Six freedivers were monitored with one TPULS and SUB placed at the forehead, during a maximal effort immersed static apnea. For dry baseline measurements (n = 20), SpO2 bias ranged between -0.8 and -0.6%, precision between 1.0 and 1.5%; HR bias ranged between 1.1 and 1.0 bpm, precision between 1.4 and 1.9 bpm. For the hypoxic episode, SpO2 bias ranged between -2.5 and -3.6%, precision between 3.6 and 3.7%; HR bias ranged between 1.4 and 1.9 bpm, precision between 2.0 and 2.1 bpm. Freedivers (n = 6) performed an apnea of 184 ± 53 s. Desaturation- and resaturation response time of SpO2 was approximately 15 and 12 s shorter in SUB compared to TPULS, respectively. Lowest SpO2 values were 76 ± 10% for TPULS and 74 ± 13% for SUB. HR traces for both pulse oximeters showed similar patterns. For static apneas, dropout rate was larger for SUB (18%) than for TPULS (<1%). SUB produced similar SpO2 and HR values as TPULS, both during normoxic and hypoxic breathing (n = 20), and submersed static apneas (n = 6). SUB responds more quickly to changes in oxygen saturation when sensors were placed at the forehead. Further development of SUB is needed to limit signal loss, and its function should be tested at greater depth and lower saturation.

Using Underwater Pulse Oximetry in Freediving to Extreme Depths to Study Risk of Hypoxic Blackout and Diving Response Phases.

Deep freediving exposes humans to hypoxia and dramatic changes in pressure. The effect of depth on gas exchange may enhance risk of hypoxic blackout (BO) during the last part of the ascent. Our aim was to investigate arterial oxygen saturation (SpO2) and heart rate (HR) in shallow and deep freedives, central variables, which have rarely been studied underwater in deep freediving. Four male elite competitive freedivers volunteered to wear a newly developed underwater pulse oximeter for continuous monitoring of SpO2 and HR during self-initiated training in the sea. Two probes were placed on the temples, connected to a recording unit on the back of the freediver. Divers performed one "shallow" and one "deep" constant weight dive with fins. Plethysmograms were recorded at 30 Hz, and SpO2 and HR were extracted. Mean ± SD depth of shallow dives was 19 ± 3 m, and 73 ± 12 m for deep dives. Duration was 82 ± 36 s in shallow and 150 ± 27 s in deep dives. All divers desaturated more during deeper dives (nadir 55 ± 10%) compared to shallow dives (nadir 80 ± 22%) with a lowest SpO2 of 44% in one deep dive. HR showed a "diving response," with similar lowest HR of 42 bpm in shallow and deep dives; the lowest value (28 bpm) was observed in one shallow dive. HR increased before dives, followed by a decline, and upon resurfacing a peak after which HR normalized. During deep dives, HR was influenced by the level of exertion across different diving phases; after an initial drop, a second HR decline occurred during the passive "free fall" phase. The underwater pulse oximeter allowed successful SpO2 and HR monitoring in freedives to 82 m depth - deeper than ever recorded before. Divers' enhanced desaturation during deep dives was likely related to increased exertion and extended duration, but the rapid extreme desaturation to below 50% near surfacing could result from the diminishing pressure, in line with the hypothesis that risk of hypoxic BO may increase during ascent. Recordings also indicated that the diving response is not powerful enough to fully override the exercise-induced tachycardia during active swimming. Pulse oximetry monitoring of essential variables underwater may be an important step to increase freediving safety.

Splenic contraction is enhanced by exercise at simulated high altitude.

PURPOSE: Splenic contraction increases circulating hemoglobin (Hb) with advantages during hypoxia. As both hypoxia and exercise have been shown to be important separate triggers of splenic contraction we aimed to investigate if the spleen response to simulated high altitude (HA) is enhanced by superimposing exercise. METHOD: Fourteen healthy volunteers (seven females) performed the following protocol in a normobaric environment sitting on an ergometer cycle: 20 min rest in normoxia; 20 min rest while breathing hypoxic gas simulating an altitude of 3500 m; 10 min exercise at an individually set intensity while breathing the hypoxic gas; 20 min rest in hypoxia; and finally 20 min rest in normoxia. Spleen measurements were collected by ultrasonic imaging and venous Hb measured at the end of each intervention. RESULT: Mean ± SD baseline spleen volume during normoxic rest was 280 ± 107 mL, the volume was reduced by 22% during rest in hypoxia to 217 ± 92 mL (p < 0.001) and by 33% during exercise in hypoxia (189 mL; p < 0.001). Hb was 140.7 ± 7.0 g/L during normoxic rest and 141.3 ± 7.4 g/L during hypoxic rest (NS), but increased by 5.3% during hypoxic exercise (148.6 ± 6.3 g/L; p < 0.001). Spleen volume and Hb were stepwise changed back to baseline at cessation of exercise and return to normoxia. CONCLUSION: Splenic contraction is induced by hypoxia and further enhanced by superimposing exercise, and reduced when exercise ceases, in a step-wise manner, showing that the tonic but partial contraction observed in long-term field expeditions to HA may occur also in the short term. This "graded response" may be beneficial during acclimatization to HA, to cope with moderate chronic hypoxia during rest while allowing additional enhancement of oxygen carrying capacity to overcome short bouts of extreme hypoxia caused by exercise.