Effects of hyperventilation on repeated breath-holding while in a fasting state: do risks outweigh the benefits?

Breath-holding preceded by either an overnight fast or hyperventilation has been shown to potentiate the risk of a hypoxic blackout. However, no study has explored the combined effects of fasting and hyperventilation on apneic performance and associated physiological responses. Nine nondivers (8 males) attended the laboratory on two separate occasions (≥48 h apart), both after a 12-h overnight fast. During each visit, a hyperoxic rebreathing trial was performed followed by three repeated maximal static apneas preceded by either normal breathing (NORM) or a 30-s hyperventilation (HYPER). Splenic volume, hematology, cardiovascular, and respiratory variables were monitored. There were no interprotocol differences at rest or during hyperoxic rebreathing for any variable (P ≥ 0.09). On nine occasions (8 in HYPER), the subjects reached our safety threshold (oxygen saturation 65%) and were asked to abort their apneas, with the preponderance of these incidents (6 of 9) occurring during the third repetition. Across the sequential attempts, longer apneas were recorded in HYPER [median(range), 220(123-324) s vs. 185(78-296) s, P ≤ 0.001], with involuntary breathing movements occurring later [134(65-234) s vs. 97(42-200) s, P ≤ 0.001] and end-apneic partial end-tidal pressures of oxygen (PETO2) being lower (P ≤ 0.02). During the final repetition, partial end-tidal pressure of carbon dioxide [(PETCO2), 6.53 ± 0.46 kPa vs. 6.01 ± 0.45 kPa, P = 0.005] was lower in HYPER. Over the serial attempts, preapneic tidal volume was gradually elevated [from apnea 1 to 3, by 0.26 ± 0.24 L (HYPER) and 0.28 ± 0.30 L (NORM), P ≤ 0.025], with a correlation noted with preapneic PETCO2 (r = -0.57, P < 0.001) and PETO2 (r = 0.76, P < 0.001), respectively. In a fasted state, preapnea hyperventilation compared with normal breathing leads to longer apneas but may increase the susceptibility to a hypoxic blackout.NEW & NOTEWORTHY This study shows that breath-holds (apneas) preceded by a 12-h overnight fast coupled with a 30-s hyperventilation as opposed to normal breathing may increase the likelihood of a hypoxic blackout through delaying the excitation of hypercapnic ventilatory sensory chemoreflexes. Evidently, this risk is exacerbated over a series of repeated maximal attempts, possibly due to a shift in preapneic gas tensions facilitated by an unintentional increase in tidal volume breathing.

Combined effects of mild hypothermia and nitrous-oxide-induced narcosis on manual and cognitive performance.

Divers are at enhanced risk of suffering from acute cognitive deterioration because of the low ambient temperatures and the narcotic action of inert gases inspired at high pressures. Yet, the behavioral effects of cold and inert gas narcosis have commonly been assessed in isolation and during short-term provocations. We therefore evaluated the interactive influence of mild hypothermia and narcosis engendered by a subanesthetic dose of nitrous oxide (N2O; a normobaric intervention analog of hyperbaric nitrogen) on cognitive function during prolonged iterative exposure. Fourteen men partook in two ∼12-h sessions (separated by ≥4 days), wherein they performed sequentially three 120-min cold (20°C) water immersions (CWIs), while inhaling, in a single-blinded manner, either normal air or a normoxic gas mixture containing 30% N2O. CWIs were separated by a 120-min rewarming in room-air breathing conditions. Before the first CWI and during each CWI, subjects performed a finger dexterity test, and the Spaceflight Cognitive Assessment Tool for Windows (WinSCAT) test assessing aspects of attention, memory, learning, and visuospatial ability. Rectal and skin temperatures were, on average, reduced by ∼1.2 °C and ∼8 °C, respectively (P < 0.001). Cooling per se impaired (P ≤ 0.01) only short-term memory (∼37%) and learning (∼18%); the impairments were limited to the first CWI. N2O also attenuated (P ≤ 0.02) short-term memory (∼37%) and learning (∼35%), but the reductions occurred in all CWIs. Furthermore, N2O invariably compromised finger dexterity, attention, concentration, working memory, and spatial processing (P < 0.05). The present results demonstrate that inert gas narcosis aggravates, in a persistent manner, basic and higher-order cognitive abilities during protracted cold exposure.

Nitrous oxide consistently attenuates thermogenic and thermoperceptual responses to repetitive cold stress in humans.

Divers are at enhanced risk of hypothermia, due to the independent action of the inspired inert gases on thermoregulation. Thus, narcosis induced by acute (≤2 h) exposure to either hyperbaric nitrogen or normobaric nitrous oxide (N2O) impairs shivering thermogenesis and accelerates body core cooling. Animal-based studies, however, have indicated that repeated and sustained N2O administration may prevent N2O-evoked hypometabolism. We, therefore, examined the effects of prolonged intermittent exposure to 30% N2O on human thermoeffector plasticity in response to moderate cold. Fourteen men participated in two ∼12-h sessions, during which they performed sequentially three 120-min cold-water immersions (CWIs) in 20°C water, separated by 120-min rewarming. During CWIs, subjects were breathing either normal air or a normoxic gas mixture containing 30% N2O. Rectal and skin temperatures, metabolic heat production (via indirect calorimetry), finger and forearm cutaneous vascular conductance (CVC; laser-Doppler fluxmetry/mean arterial pressure), and thermal sensation and comfort were monitored. N2O aggravated the drop in rectal temperature (P = 0.01), especially during the first (by ∼0.3°C) and third (by ∼0.4°C) CWIs. N2O invariably blunted the cold-induced elevation of metabolic heat production by ∼22%-25% (P < 0.001). During the initial ∼30 min of the first and second CWIs, N2O attenuated the cold-induced drop in finger (P ≤ 0.001), but not in forearm CVC. N2O alleviated the sensation of coldness and thermal discomfort throughout (P < 0.001). Thus, the present results demonstrate that, regardless of the cumulative duration of gas exposure, a subanesthetic dose of N2O depresses human thermoregulatory functions and precipitates the development of hypothermia.NEW & NOTEWORTHY Human thermoeffector plasticity was evaluated in response to prolonged iterative exposure to 30% N2O and moderate cold stress. Regardless of the duration of gas exposure, N2O-induced narcosis impaired in a persistent manner shivering thermogenesis and thermoperception.

Eccentric exercise 24 h prior to hypobaric decompression increases decompression strain.

PURPOSE: Animal studies have shown that recent musculoskeletal injuries increase the risk of decompression sickness (DCS). However, to date no similar experimental study has been performed in humans. The aim was to investigate if exercise-induced muscle damage (EIMD)-as provoked by eccentric work and characterized by reduced strength and delayed-onset muscle soreness (DOMS)-leads to increased formation of venous gas emboli (VGE) during subsequent hypobaric exposure. METHODS: Each subject (n = 13) was on two occasions exposed to a simulated altitude of 24,000 ft for 90 min, whilst breathing oxygen. Twenty-four hours prior to one of the altitude exposures, each subject performed 15 min of eccentric arm-crank exercise. Markers of EIMD were reduction in isometric m. biceps brachii strength and DOMS as assessed on the Borg CR10 pain scale. The presence of VGE was measured in the right cardiac ventricle using ultrasound, with measurements performed at rest and after three leg kicks and three arm flexions. The degree of VGE was evaluated using the six-graded Eftedal-Brubakk scale and the Kisman integrated severity score (KISS). RESULTS: Eccentric exercise induced DOMS (median 6.5), reduced the biceps brachii strength (from 230 ± 62 N to 151 ± 8.8 N) and increased the mean KISS at 24,000 ft, both at rest (from 1.2 ± 2.3 to 6.9 ± 9.2, p = 0.01) and after arm flexions (from 3.8 ± 6.2 to 15.5 ± 17.3, p = 0.029). CONCLUSION: EIMD, induced by eccentric work, provokes release of VGE in response to acute decompression.

Decompression strain in parachute jumpmasters during simulated high-altitude missions: a special reference to preoxygenation strategies.

PURPOSE: Military parachute operations are often executed at high altitude, from an unpressurized aircraft compartment. Parachute jumpmasters (JM) are thus regularly exposed to 29,500 ft for 60 min. The aim was to investigate the decompression strain during a simulated JM mission at high altitude and to compare two strategies of preoxygenation, conducted either at sea-level or below 10,000 ft, during ascent to mission altitude. METHODS: Ten JM completed, on separate occasions, a 45-min preoxygenation either at sea-level (normobaric: N) or 8200ft (hypobaric: H), followed by exposure to 28,000 ft for 60 min, whilst laying supine and breathing 100% oxygen. At min 45 of the exposure to 28,000 ft, the JM performed 10 weighted squats. Decompression strain was determined from ultrasound assessment of venous gas emboli (VGE) during supine rest (5-min intervals), after three unloaded knee-bends (15-min intervals) and immediately following the weighted squats. The VGE were scored using a six-graded scale (0-5). RESULTS: In condition H, two JM experienced decompression sickness (DCS), whereas no DCS incidents were reported in condition N. The prevalence of VGE was higher in the H than the N condition, at rest [median(range), 3(0-4) vs 0(0-3); p = 0.017], after unloaded knee-bends [3(0-4) vs 0(0-3); p = 0.014] and after the 10 weighted squats [3(0-4) vs 0(0-3); p = 0.014]. VGE were detected earlier in the H (28 ± 20 min, p = 0.018) than the N condition (50 ± 19 min). CONCLUSIONS: A preoxygenation/altitude procedure commonly used by JM, with a 60-min exposure to 28,000 ft after pre-oxygenation for 45 min at 8200 ft is associated with high risk of DCS. The decompression strain can be reduced by preoxygenating at sea level.

The effect of dietary intake on apneic performance, cardiovascular and splenic responses during repeated breath holds.

Static apneas performed after an overnight fast as opposed to postprandially have been evinced to improve apneic performance. However, no study has explored the effect of dietary intake on apneic performance, cardiovascular or splenic responses over a series of repeated apneas. Ten healthy adults attended the laboratory on three separate occasions (≥48-h apart): after a 14-h fast (F14), 1 h postconsumption of a high-calorie, high-carbohydrate (HCHC) meal, or 1 h postconsumption of a low-calorie, low-carbohydrate (LCLC)-based meal. During each visit, the subjects performed a hyperoxic rebreathing trial and a series of three repeated maximal static apneas. Heart rate, peripheral oxyhemoglobin saturation ([Formula: see text]), and gas exchange were monitored continuously, whereas splenic volume (SV) and hematology were assessed after the rebreathing and apneas. At rest, after HCHC, the respiratory exchange ratio (0.87 ± 0.17, P ≤ 0.043), expired minute volume of carbon dioxide (CO2; HCHC, 0.35 ± 0.09 L/min, P ≤ 0.014), and SV (227 ± 45 mL, P ≤ 0.031) were higher compared with F14 (0.71 ± 0.08; 0.23 ± 0.04 L/min; 204 ± 49 mL) and LCLC (0.72 ± 0.07; 0.25 ± 0.03 L/min; 199 ± 49 mL). A faster CO2 accumulation was recorded during the HCHC (96 ± 35 s) rebreathing trial (F14, 162 ± 42 s, P = 0.001; LCLC, 151 ± 23 s, P = 0.002). Longer apneas were reported in F14 compared with HCHC (apneas 1-3, P ≤ 0.046) and LCLC (apneas 2-3, P ≤ 0.006). After the first apnea, SV was lower in F14 (141 ± 43 mL, P = 0.015) compared with HCHC (180 ± 34 mL). Moreover, after the third apnea, end-tidal partial pressure of oxygen and nadir [Formula: see text] were lower in F14 (8.6 ± 2.2 kPa, P = 0.028; 77 ± 13%, P = 0.009) compared with HCHC (10.1 ± 1.7 kPa; 84 ± 9%). No differences were measured in end-apneic end-tidal partial pressure of CO2, heart rate nor hematology across diets. Fasting improved apneic performance with apneas being terminated at lower oxygen levels through altering the rate of CO2 accumulation but without affecting the cardiovascular responses.

Profound hypercapnia but only moderate hypoxia found during underwater rugby play.

Background: Underwater rugby is a team sport where players try to score points with a negatively buoyant ball while submerged in a swimming pool. Reports of syncope incidents at the Swedish Championships led to us to investigate end-tidal oxygen and carbon dioxide levels during simulated match play. Methods: Eight male underwater rugby club players of varying experience participated. Repetitive measurements were made while players were defending during simulated match play. Each time a player surfaced they exhaled through a mouthpiece connected to a flow meter and a gas analyzer to measure tidal volume, PETO2 and PETCO2. Results: Measurements were made over 12 dives, with an average dive duration of 18.5 seconds. The mean maximal PETCO2 across the eight participants was 10.0 kPa (~75 mmHg) (range, 9.1-11.7 [~68-88]). The corresponding mean minimum PETO2 was 7.6 kPa (~57 mmHg) (6.3-10.4 [~47-78)). PETCO2 drifted upward, with the mean upward change from the first to last dive for each participant being +1.8 (~13.5 mmHg) (SD 1.74) kPa. A similar trend for PETO2 was not detected, with a mean change of -0.1 (~0.75 mmHg) (SD 3.79) kPa. Conclusion: Despite high PETCO2 values that were close to narcotic being recorded, these players seemed to regulate their urge to breathe based on hypoxia rather than hypercapnia.

Protein tau concentration in blood increases after SCUBA diving: an observational study.

PURPOSE: It is speculated that diving might be harmful to the nervous system. The aim of this study was to determine if established markers of neuronal injury were increased in the blood after diving. METHODS: Thirty-two divers performed two identical dives, 48 h apart, in a water-filled hyperbaric chamber pressurized to an equivalent of 42 m of sea water for 10 min. After one of the two dives, normobaric oxygen was breathed for 30 min, with air breathed after the other. Blood samples were obtained before and at 30-45 and 120 min after diving. Concentrations of glial fibrillary acidic, neurofilament light, and tau proteins were measured using single molecule array technology. Doppler ultrasound was used to detect venous gas emboli. RESULTS: Tau was significantly increased at 30-45 min after the second dive (p < 0.0098) and at 120 min after both dives (p < 0.0008/p < 0.0041). Comparison of matching samples showed that oxygen breathing after diving did not influence tau results. There was no correlation between tau concentrations and the presence of venous gas emboli. Glial fibrillary acidic protein was decreased 30-45 min after the first dive but at no other point. Neurofilament light concentrations did not change. CONCLUSIONS: Tau seems to be a promising marker of dive-related neuronal stress, which is independent of the presence of venous gas emboli. Future studies could validate these results and determine if there is a quantitative relationship between dive exposure and change in tau blood concentration.

Intra-Individual Test-Retest Variation Regarding Venous Gas Bubble Formation During High Altitude Exposures.

INTRODUCTION: Hypobaric decompression sickness remains a problem during high-altitude aviation. The prevalence of venous gas emboli (VGE) serves as a marker of decompression stress and has been used as a method in evaluating the safety/risk associated with aviation profiles and/or gas mixtures. However, information is lacking concerning the variability of VGE formation when exposed to the same hypobaric profile on different occasions. In this paper, intra-individual test-retest variation regarding bubble formation during repeated hypobaric exposures is presented. The data can be used to determine the sample size needed for statistical power.METHOD: A total of 19 male, nonsmoking subjects volunteered for altitude exposures to 24,000 ft (7315 m). VGE was measured using ultrasound scanning and scored according to the Eftedal-Brubakk (EB) scale. Intraindividual test-retest variation in bubble formation (maximum VGE) was evaluated in subjects exposed more than once to hypobaric pressure. The statistical reliability was examined between paired exposures using the Intraclass Correlation test. G*Power version 3.1.9.6 was used for power calculations.RESULTS: During repeated 20-30 and 70-min exposures to 24,000 ft, 42% (N = 19, CI 23-67%) and 29% (N = 7, CI 5-70%) of the subjects varied between maximum EB scores < 3 and ≥ 3. The sample size needed to properly reject statistical significance of 1 EB step nominal difference between two paired exposures varied between 29-51 subjects.CONCLUSION: The large intraindividual test-retest variations in bubble grades during repeated hypobaric exposures highlight the need for relatively large numbers of subjects to reach statistical power when there are no or small differences in decompression stress between the exposures.Ånell R, Grönkvist M, Eiken O, Elia A, Gennser M. Intra-individual test-retest variation regarding venous gas bubble formation during high altitude exposures. Aerosp Med Hum Perform. 2022; 93(1):46-49.

Inter- and Intra-Rater Level of Agreement in Ultrasonic Video Grading of Venous Gas Emboli.

INTRODUCTION: This study aimed to evaluate whether a short familiarization session is sufficient for individuals with no prior experience of sonography to both reliably and consistently evaluate the prevalence of venous gas emboli (VGE) from precordial ultrasonic videos.METHODS: A total of 10 adults with no prior experience of sonography were introduced to the Eftedal-Brubakk 6-grade scale and were shown 6 video sequences, each of a maximum of 10 heartbeats, representing each grading level. Thereafter, they independently evaluated the prevalence of VGE in 70 ultrasonic videos before and after a 14-d interval (test-retest; intra-rater), with these being compared to an experienced sonographer's grading (inter-rater).RESULTS: A significant inter-rater level of agreement was found between the naïve and experienced sonographers' bubble grading both during the first (W = 0.945) and second (W = 0.952) round of bubble evaluation. The naïve observers' evaluations were on average 79% (range: 61-95%) and 75% (range: 48-95%) in complete agreement with the experienced sonographer's gradings, while the level of agreement was 99% and 98% within 1 grade unit. There was a significant intra-rater level of agreement (κ = 0.845) during the test-retest series, with a mean percentage level of agreement of 87% (range: 72-93%).CONCLUSION: This study demonstrates that a short familiarization session enables individuals with no prior sonography experience to consistently evaluate VGE prevalence from precordial ultrasonic videos.Elia A, Ånell R, Eiken O, Grönkvist M, Gennser M. Inter- and intra-rater level of agreement in ultrasonic video grading of venous gas emboli. Aerosp Med Hum Perform. 2022; 93(1):54-57.

High-altitude decompression strain can be reduced by an early excursion to moderate altitude while breathing oxygen.

Recent observations suggest that development of venous gas emboli (VGE) during high-altitude flying whilst breathing hyperoxic gas will be reduced by intermittent excursions to moderate altitude. The present study aimed to investigate if an early, single excursion from high to moderate altitude can be used as an in-flight means to reduce high-altitude decompression strain. Ten healthy men were investigated whilst breathing oxygen in a hypobaric chamber under two conditions, once during a 90-min continuous exposure to a simulated cabin altitude of 24,000 ft (High; H) and once during 10 min at 24,000 ft, followed by 30 min at 15,000 ft and by 80 min at 24,000 ft (high-low-high; H-L-H). VGE scores were assessed by cardiac ultrasound, using a 6-graded scale. In H, VGE increased throughout the course of the sojourn at 24,000 ft to attain peak value [median (range)] of 3 (2-4) at min 90, just prior to descent. In H-L-H, median VGE scores were 0 throughout the trial, except for at min 10, just prior to the excursion to 15,000 ft, whence the VGE score was 1.5 (0-3). Thus, an early, single excursion from high to moderate cabin altitude holds promise as an in-flight means to reduce the risk of altitude decompression sickness during long-duration high-altitude flying in aircraft with limited cabin pressurization. Presumably, such excursion acts by facilitating the gas exchange in decompression bubbles from a predomination of nitrogen to that of oxygen.

Whole-body vibration preconditioning reduces the formation and delays the manifestation of high-altitude-induced venous gas emboli.

NEW FINDINGS: What is the central question of this study? Is performing a 30-min whole-body vibration (WBV) prior to a continuous 90-min exposure at 24,000 ft sufficient to prevent venous gas emboli (VGE) formation? What is the main finding and its importance? WBV preconditioning significantly reduces the formation and delays the manifestation of high-altitude-induced VGE. This study suggests that WBV is an effective strategy in lowering decompression stress. ABSTRACT: Rapid decompression may give rise to formation of venous gas emboli (VGE) and resultantly, increase the risk of sustaining decompression sickness. Preconditioning aims at lowering the prevalence of VGE during decompression. The purpose of this study was to investigate the efficacy of whole-body vibration (WBV) preconditioning on high-altitude-induced VGE. Eight male subjects performed, on separate days in a randomised order, three preconditioning strategies: 40-min seated-rest (control), 30-min seated-rest followed by 150 knee-squats performed over a 10-min period (exercise) and 30-min WBV proceeded by a 10-min seated-rest. Thereafter, subjects were exposed to an altitude of 24,000 ft (7315 m) for 90 min whilst laying in a supine position and breathing 100% oxygen. VGE were assessed ultrasonically both during supine rest (5-min intervals) and after three fast, unloaded knee-bends (15-min intervals) and were scored using a 5-grade scale and evaluated using the Kisman Integrated Severity Score (KISS). There was a significant difference in VGE grade (P < 0.001), time to VGE manifestation (P = 0.014) and KISS score following knee-bends (P = 0.002) across protocols, with a trend in KISS score during supine rest (P = 0.070). WBV resulted in lower VGE grades (median (range), 1 (0-3)) and KISS score (2.69 ± 4.56 a.u.) compared with control (2 (1-3), P = 0.002; 12.86 ± 8.40 a.u., P = 0.011) and exercise (3 (2-4) , P < 0.001; 22.04 ± 13.45 a.u., P = 0.002). VGE were detected earlier during control (15 ± 14 min, P = 0.024) and exercise (17 ± 24 min, P = 0.032) than WBV (54 ± 38 min). Performing a 30-min WBV prior to a 90-min continuous exposure at 24,000 ft both delays the manifestation and reduces the formation of VGE compared with control and exercise preconditioning.

Hyperoxic Effects on Decompression Strain During Alternating High and Moderate Altitude Exposures.

INTRODUCTION: In fighter aircraft, long-duration high-altitude sorties are typically interrupted by refueling excursions to lower altitude. In normoxia, excursions to moderate cabin altitude may increase the occurrence of venous gas emboli (VGE) at high cabin altitude. The aim was to investigate the effect of hyperoxia on VGE and decompression sickness (DCS) during alternating high and moderate altitude exposure.METHODS: In an altitude chamber, 13 healthy men were exposed to three different conditions: A) 90 min at 24,000 ft (7315 m) breathing normoxic gas (54% O2; H-NOR); B) 90 min at 24,000 ft breathing hyperoxic gas (90% O2; H-HYP); and C) three 30-min exposures to 24,000 ft interspersed by two 30-min exposures to 18,000 ft (5486 m) breathing 90% O2 (ALT-HYP). VGE occurrence was evaluated from cardiac ultrasound imaging. DCS symptoms were rated using a scale.RESULTS: DCS occurred in all conditions and altogether in 6 of the 39 exposures. The prevalence of VGE was similar in H-NOR and H-HYP throughout the exposures. During the initial 30 min at 24,000 ft, the prevalence of VGE was similar in ALT-HYP as in the other two conditions, whereas, after the first excursion to 18,000 ft, the VGE score was lower in ALT-HYP than in H-NOR and H-HYP.DISCUSSION: Hyperoxic excursions from 24,000 to 18,000 ft reduces VGE occurrence, presumably by facilitating diffusive gas exchange across the bubble surfaces, increasing the share of bubble content contributed by oxygen. Still, the excursions did not abolish the DCS risk.Ånell R, Grönkvist M, Gennser M, Eiken O. Hyperoxic effects on decompression strain during alternating high and moderate altitude exposures. Aerosp Med Hum Perform. 2021; 92(4):223230.

Considerations for scuba and breath-hold divers during the COVID-19 pandemic: A call for awareness.

In late 2019, a highly pathogenic novel coronavirus (CoV), severe acute respiratory syndrome (SARS)-CoV-2 emerged from Wuhan, China and led to a global pandemic. SARS-CoV-2 has a predilection for the pulmonary system and can result in serious pneumonia necessitating hospitalisation. Computed tomography (CT) chest scans of patients with severe symptoms, show signs of multifocal bilateral ground or ground-glass opacities (GGO) associated with consolidation areas with patchy distribution. However, it is less well known that both asymptomatic and mild symptomatic patients may exhibit similar lung changes. Presumably, the various pathological changes in the lungs may increase the risk of adverse events during diving (e.g., lung barotrauma, pulmonary oedema, etc.), thus these lung manifestations need to be considered prior to allowing resumption of diving. Presently, it is not known how the structural changes in the lungs develop and to what extent they resolve, in particular in asymptomatic carriers and patients with mild disease. However, current evidence indicates that a month of recovery may be too short an interval to guarantee complete pulmonary restitution even after COVID-19 infections not demanding hospital care.

Biomarkers of neuronal damage in saturation diving-a controlled observational study.

PURPOSE: A prospective and controlled observational study was performed to determine if the central nervous system injury markers glial fibrillary acidic protein (GFAp), neurofilament light (NfL) and tau concentrations changed in response to a saturation dive. METHODS: The intervention group consisted of 14 submariners compressed to 401 kPa in a dry hyperbaric chamber. They remained pressurized for 36 h and were then decompressed over 70 h. A control group of 12 individuals was used. Blood samples were obtained from both groups before, during and after hyperbaric exposure, and from the intervention group after a further 25-26 h. RESULTS: There were no statistically significant changes in the concentrations of GFAp, NfL and tau in the intervention group. During hyperbaric exposure, GFAp decreased in the control group (mean/median - 15.1/ - 8.9 pg·mL-1, p < 0.01) and there was a significant difference in absolute change of GFAp and NfL between the groups (17.7 pg·mL-1, p = 0.02 and 2.34 pg·mL-1, p = 0.02, respectively). Albumin decreased in the control group (mean/median - 2.74 g/L/ - 0.95 g/L, p = 0.02), but there was no statistically significant difference in albumin levels between the groups. In the intervention group, haematocrit and mean haemoglobin values were slightly increased after hyperbaric exposure (mean/median 2.3%/1.5%, p = 0.02 and 4.9 g/L, p = 0.06, respectively). CONCLUSION: Hyperbaric exposure to 401 kPa for 36 h was not associated with significant increases in GFAp, NfL or tau concentrations. Albumin levels, changes in hydration or diurnal variation were unlikely to have confounded the results. Saturation exposure to 401 kPa seems to be a procedure not harmful to the central nervous system. TRIAL REGISTRATION: ClinicalTrials.gov NCT03192930.

Evolution and Preservation of Venous Gas Emboli at Alternating High and Moderate Altitude Exposures.

INTRODUCTION: The evolution and preservation of venous gas emboli (VGE), as markers of decompression stress, were investigated during alternating high- and moderate altitude exposures, thus, simulating a fighter aircraft high-altitude flight, interrupted by refueling excursions to lower altitudes.METHODS: Eight men served as subjects during three normoxic simulated altitude exposures: High = 90 min at 24,000 ft; High-Low = three × 30 min at 24,000 ft, interspersed by two 30-min intervals at 15,000 ft; Low = 90 min at 15,000 ft. VGE scores were assessed by cardiac ultrasound, using a 5-grade scale. Respiratory nitrogen exchange was measured continuously using a modified closed-circuit electronic rebreather.RESULTS: Both High and High-Low induced persistent VGE, with no inter-condition difference either at rest [median (range): High: 1 (0-3), High-Low: 2 (0-3)] or during unloaded knee-bends [High: 3 (1-4), High-Low: 3 (0-4)], whereas VGE was considerably less in Low, both at rest [0 (0-1)] and during knee-bends [0 (0-2)]. In High-Low, VGE decreased temporarily during the 15,000-ft excursions, but resumed pre-excursion values upon return to 24,000 ft. During the final descent to ground level, VGE were more persistent following High-Low than High. In both High and Low, nitrogen was continuously washed out at altitude, whereas in High-Low, the washout at 24,000 ft was interrupted by nitrogen uptake at 15,000 ft.DISCUSSION: In normoxic conditions, long-duration flying at a cabin altitude of 24,000 ft is associated with substantial VGE occurrence, which is not abolished by intermittent excursions to a cabin altitude of 15,000 ft.Ånell R, Grönkvist M, Gennser M, Eiken O. Evolution and preservation of venous gas emboli at alternating high and moderate altitude exposures. Aerosp Med Hum Perform. 2020; 91(1):11-17.

Serum tau concentration after diving - an observational pilot study.

INTRODUCTION: Increased concentrations of tau protein are associated with medical conditions involving the central nervous system, such as Alzheimer's disease, traumatic brain injury and hypoxia. Diving, by way of an elevated ambient pressure, can affect the nervous system, however it is not known whether it causes a rise in tau protein levels in serum. A prospective observational pilot study was performed to investigate changes in tau protein concentrations in serum after diving and also determine their relationship, if any, to the amount of inert gas bubbling in the venous blood. METHODS: Subjects were 10 navy divers performing one or two dives per day, increasing in depth, over four days. Maximum dive depths ranged from 52-90 metres' sea water (msw). Air or trimix (nitrogen/oxygen/helium) was used as the breathing gas and the oxygen partial pressure did not exceed 160 kPa. Blood samples taken before the first and after the last dives were analyzed. Divers were monitored for the presence of venous gas emboli (VGE) at 10 to15 minute intervals for up to 120 minutes using precordial Doppler ultrasound. RESULTS: Median tau protein before diving was 0.200 pg·mL⁻¹ (range 0.100 to 1.10 pg·mL⁻¹) and after diving was 0.450 pg·mL⁻¹ (range 0.100 to 1.20 pg·mL⁻¹; P = 0.016). Glial fibrillary acidic protein and neurofilament light protein concentrations analyzed in the same assay did not change after diving. No correlation was found between serum tau protein concentration and the amount of VGE. CONCLUSION: Repeated diving to between 52-90 msw is associated with a statistically significant increase in serum tau protein concentration, which could indicate neuronal stress.

Nitrogen Washout and Venous Gas Emboli During Sustained vs. Discontinuous High-Altitude Exposures.

INTRODUCTION: The frequency of long-duration, high-altitude missions with fighter aircraft is increasing, which may increase the incidence of decompression sickness (DCS). The aim of the present study was to compare decompression stress during simulated sustained high-altitude flying vs. high-altitude flying interrupted by periods of moderate or marked cabin pressure increase.METHODS: The level of venous gas emboli (VGE) was assessed from cardiac ultrasound images using the 5-degree Eftedal-Brubakk scale. Nitrogen washout/uptake was measured using a closed-circuit rebreather. Eight men were investigated in three conditions: one 80-min continuous exposure to a simulated cabin altitude of A) 24,000 ft, or four 20-min exposures to 24,000 ft interspersed by three 20-min intervals at B) 20,000 ft or C) 900 ft.RESULTS: A and B induced marked and persistent VGE, with peak bubble scores of [median (range)]: A: 2.5 (1-3); B: 3.5 (2-4). Peak VGE score was less in C [1.0 (1-2), P < 0.01]. Condition A exhibited an initially high and exponentially decaying rate of nitrogen washout. In C the washout rate was similar in each period at 24,000 ft, and the nitrogen uptake rate was similar during each 900-ft exposure. B exhibited nitrogen washout during each period at 24,000 ft and the initial period at 20,000 ft, but on average no washout or uptake during the last period at 20,000 ft.DISCUSSION: Intermittent reductions of cabin altitude from 24,000 to 20,000 ft do not appear to alleviate the DCS risk, presumably because the pressure increase is not sufficient to eliminate VGE. The nitrogen washout/uptake rate did not reflect DCS risk in the present exposures.Ånell R, Grönkvist M, Eiken O, Gennser M. Nitrogen washout and venous gas emboli during sustained vs. discontinuous high-altitude exposures. Aerosp Med Hum Perform. 2019; 90(6):524-530.