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].

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 V ˙ O2max test (day 1), followed by three submaximal exercise intensities on a roller skiing treadmill corresponding to 55, 70, and 85% of V ˙ 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 V ˙ 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.

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.

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.

The effects of high altitude ascent on splenic contraction and the diving response during voluntary apnoea.

NEW FINDINGS: What is the central question of this study? What is the relative contribution of a putative tonic splenic contraction to the haematological acclimatization process during high altitude ascent in native lowlanders? What is the main finding and its importance? Spleen volume decreased by -14.3% (-15.2 ml) per 1000 m ascent, with an attenuated apnoea-induced [Hb] increase, attesting to a tonic splenic contraction during high altitude ascent. The [Hb]-enhancing function of splenic contraction may contribute to restoring oxygen content early in the acclimatization process at high altitude. ABSTRACT: Voluntary apnoea causes splenic contraction and reductions in heart rate (HR; bradycardia), and subsequent transient increases in haemoglobin concentration ([Hb]). Ascent to high altitude (HA) induces systemic hypoxia and reductions in oxygen saturation ( SpO2 ), which may cause tonic splenic contraction, which may contribute to haematological acclimatization associated with HA ascent. We measured resting cardiorespiratory variables (HR, SpO2 , [Hb]) and resting splenic volume (via ultrasound) during incremental ascent from 1400 m (day 0) to 3440 m (day 3), 4240 m (day 7) and 5160 m (day 10) in non-acclimatized native lowlanders during assent to HA in the Nepal Himalaya. In addition, apnoea-induced responses in HR, SpO2 and splenic volume were measured before and after two separate voluntary maximal apnoeas (A1-A2) at 1400, 3440 and 4240 m. Resting spleen volume decreased -14.3% (-15.2 ml) per 1000 m with ascent, from 140 ± 41 ml (1400 m) to 108 ± 28 ml (3440 m; P > 0.99), 94 ± 22 ml (4240 m; P = 0.009) and 84 ± 28 ml (5160 m; P = 0.029), with concomitant increases in [Hb] from 125 ± 18.3 g l-1 (1400 m) to 128 ± 10.4 g l-1 (3440 m), 138.8 ± 12.7 g l-1 (4240 m) and 157.5 ± 8 g l-1 (5160 m; P = 0.021). Apnoea-induced splenic contraction was 50 ± 15 ml (1400 m), 44 ± 17 ml (3440 m; P > 0.99) and 26 ± 8 ml (4240 m; P = 0.002), but was not consistently associated with increases in [Hb]. The apnoea-induced bradycardia was more pronounced at 3440 m (A1: P = 0.04; A2: P = 0.094) and at 4240 m (A1: P = 0.037 A2: P = 0.006) compared to values at 1400 m. We conclude that hypoxia-induced splenic contraction at rest (a) may contribute to restoring arterial oxygen content through its [Hb]-enhancing contractile function and (b) eliminates further apnoea-induced [Hb] increases in hypoxia. We suggest that tonic splenic contraction may contribute to haematological acclimatization early in HA ascent in humans.

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.

Spleen contraction elevates hemoglobin concentration at high altitude during rest and exercise.

PURPOSE: Hypoxia and exercise are known to separately trigger spleen contraction, leading to release of stored erythrocytes. We studied spleen volume and hemoglobin concentration (Hb) during rest and exercise at three altitudes. METHODS: Eleven healthy lowlanders did a 5-min modified Harvard step test at 1370, 3700 and 4200 m altitude. Spleen volume was measured via ultrasonic imaging and capillary Hb with Hemocue during rest and after the step test, and arterial oxygen saturation (SaO2), heart rate (HR), expiratory CO2 (ETCO2) and respiratory rate (RR) across the test. RESULTS: Resting spleen volume was reduced with increasing altitude and further reduced with exercise at all altitudes. Mean (SE) baseline spleen volume at 1370 m was 252 (20) mL and after exercise, it was 199 (15) mL (P < 0.01). At 3700 m, baseline spleen volume was 231 (22) mL and after exercise 166 (12) mL (P < 0.05). At 4200 m baseline volume was 210 (23) mL and after exercise 172 (20) mL (P < 0.05). After 10 min, spleen volume increased to baseline at all altitudes (NS). Baseline Hb increased with altitude from 138.9 (6.1) g/L at 1370 m, to 141.2 (4.1) at 3700 m and 152.4 (4.0) at 4200 m (P < 0.01). At all altitudes Hb increased from baseline during exercise to 146.8 (5.7) g/L at 1370 m, 150.4 (3.8) g/L at 3700 m and 157.3 (3.8) g/L at 4200 m (all P < 0.05 from baseline). Hb had returned to baseline after 10 min rest at all altitudes (NS). The spleen-derived Hb elevation during exercise was smaller at 4200 m compared to 3700 m (P < 0.05). Cardiorespiratory variables were also affected by altitude during both rest and exercise. CONCLUSIONS: The spleen contracts and mobilizes stored red blood cells during rest at high altitude and contracts further during exercise, to increase oxygen delivery to tissues during acute hypoxia. The attenuated Hb response to exercise at the highest altitude is likely due to the greater recruitment of the spleen reserve during rest, and that maximal spleen contraction is reached with exercise.

Blood lactate accumulation during competitive freediving and synchronized swimming.

A number of competitive water sports are performed while breath-holding (apnea). Such performances put large demands on the anaerobic system, but the study of lactate accumulation in apneic sports is limited. We therefore aimed to determine and compare the net lactate accumulation (NLA) during competition events in six disciplines of competitive freediving (FD) and three disciplines of synchronized swimming (SSW). The FD disciplines were: static apnea (STA; n = 14); dynamic apnea (DYN; n = 19); dynamic apnea no fins (DNF; n = 16); constant weight (CWT; n = 12); constant weight no fins (CNF; n = 8); free immersion (FIM; n =10). The SSW disciplines were solo (n = 21), duet (n = 31) and team (n = 34). Capillary blood lactate concentration was measured before and three minutes after competition performances, and apneic duration and performance variables were recorded. In all nine disciplines NLA was observed. The highest mean (SD) NLA (mmol·L-1) was found in CNF at 6.3 (2.2), followed by CWT at 5.9 (2.3) and SSW solo at 5 (1.9). STA showed the lowest NLA 0.7 (0.7) mmol·L-1 compared to all other disciplines (P ⟨ 0.001). The NLA recorded shows that sports involving apnea involve high levels of anaerobic activity. The highest NLA was related to both work done by large muscle groups and long apneic periods, suggesting that NLA is influenced by both the type of work and apnea duration, with lower NLA in SSW due to shorter apneic episodes with intermittent breathing.

Acute dietary nitrate supplementation improves arterial endothelial function at high altitude: A double-blinded randomized controlled cross over study.

INTRODUCTION: Dietary nitrate (NO3-) supplementation serves as an exogenous source of nitrite (NO2-) and nitric oxide (NO) through the NO3- - NO2- - NO pathway, and may improve vascular functions during normoxia. The effects of NO3- supplementation in healthy lowlanders during hypobaric hypoxia are unknown. PURPOSE: Determine the effect of acute oral NO3-supplementation via beetroot juice (BJ) on endothelial function (flow mediated dilation; FMD) in lowlanders at 3700 m. METHODS: FMD was measured using ultrasound and Doppler in the brachial artery of 11 healthy subjects (4 females, age 25 ± 5 yrs; height 1.8 ± 0.1 m, weight 72 ± 10 kg) sojourning to high altitude. In a randomized, double-blinded crossover study design, FMD was measured 3 h after drinking BJ (5.0 mmol NO3-) and placebo (PL; 0.003 mmol NO3-) supplementation at 3700 m, with a 24-h wash out period between tests. FMD was also measured without any BJ supplementation pre-trek at 1370 m, after 5 days at 4200 m and upon return to 1370 m after 4 weeks of altitude exposure (above 2500 m). The altitude exposure was interrupted by a decent to lower altitude where subjects spent two nights at 1370 m before returning to altitude again. RESULTS: Ten subjects completed the NO3- supplementation. FMD (mean ± SD) pre-trek value was 6.53 ± 2.32% at 1370 m. At 3700 m FMD was reduced to 3.84 ± 1.31% (p < 0.01) after PL supplementation but was normalized after receiving BJ (5.77 ± 1.14% (p = 1.00). Eight of the subjects completed the interrupted 4-week altitude stay, and their FMD was lower at 4200 m (FMD 3.04 ± 2.22%) and at post-altitude exposure to 1370 m (FMD 3.91 ± 2.58%) compared to pre-trek FMD at 1370 m. CONCLUSION: Acute dietary NO3-supplementation may abolish altitude-induced reduction in endothelial function, and can serve as a dietary strategy to ensure peripheral vascular function in lowland subjects entering high altitude environments.

Voluntary apnea evokes diving responses in obstructive sleep apnea patients.

PURPOSE: Two potentially protective responses to apnea were studied in obstructive sleep apnea (OSA) patients; the diving response and the increase in Hb concentration [Hb] via spleen contraction. METHODS: Eight OSA patients and ten healthy controls performed apneas in air (A) and apneas with facial immersion in 15 °C water (FIA) after inspiration and without prior hyperventilation. In each condition, subjects performed three apneas of maximal voluntary duration spaced by 2 min of rest. Cardiorespiratory parameters were measured non-invasively, and venous blood samples for [Hb] analysis were drawn before and after apneas. RESULT: Mean (SD) apnea durations were similar between groups (NS). In controls, the heart rate (HR) reduction was 10 ± 10 % at apnea and 19 ± 10 % in FIA (P < 0.05). In OSA patients, however, the fall in HR was the same in both conditions, 13 ± 10 and 14 ± 8 % for A and FIA, respectively (NS). In controls, the [Hb] increase was the same in A and FIA (2.2 ± 2.9 and 2.1 ± 2.2 %), while in OSA the [Hb] increase was greater during FIA compared to A (3.3 ± 2.2 and 1.4 ± 0.9 %; P < 0.05). CONCLUSION: Apnea induces a diving response and [Hb] increase in both groups. OSA patients did not show the typical training effect of the diving response seen in apnea divers despite their frequent nocturnal apneas. However, they also deviated from normal controls in response pattern; face immersion enhanced the cardiovascular diving response in controls but not in OSA, while the hematological response was enhanced by face immersion only in OSA patients.

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.

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.

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.

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.].