No abstract

Plasma gelsolin (pGSN) levels fall in association with diverse inflammatory conditions. We hypothesized pGSN would decrease due to the stresses imposed by high pressure and subsequent decompression, and repletion would ameliorate injuries in a murine decompression sickness (DCS) model. Research subjects were found to exhibit a modest decrease in pGSN level while at high pressure and a profound decrease after decompression. Changes occurred concurrent with elevations of circulating microparticles (MPs) carrying interleukin (IL)-1β. Mice exhibited a comparable decrease in pGSN after decompression along with elevations of MPs carrying IL-1β. Infusion of recombinant human (rhu)-pGSN into mice before or after pressure exposure abrogated these changes and prevented capillary leak in brain and skeletal muscle. Human and murine MPs generated under high pressure exhibited surface filamentous (F-) actin to which pGSN binds, leading to particle lysis. Additionally, human neutrophils exposed to high air pressure exhibit an increase in surface F-actin that is diminished by rhu-pGSN resulting in inhibition of MPs production. Administration of rhu-pGSN may have benefit as prophylaxis or treatment for DCS.

Production of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.

The seasonal extremes of photoperiod in the high Arctic place particular strain on the human circadian system, which leads to trouble sleeping and increased feelings of negative affect in the winter months. To qualify for our study, potential participants had to have been at Canadian Forces Station (CFS) Alert (82° 30' 00″ N) for at least 2 weeks. Subjects filled out questionnaires regarding sleep difficulty, psychological well-being and mood and wore Actigraphs to obtain objective sleep data. Saliva was collected at regular intervals on two occasions, 2 weeks apart, to measure melatonin and assess melatonin onset. Individuals with a melatonin rhythm that was in disaccord with their sleep schedule were given individualized daily light treatment interventions based on their pretreatment salivary melatonin profile. The light treatment prescribed to seven of the twelve subjects was effective in improving sleep quality both subjectively, based on questionnaire results, and objectively, based on the actigraphic data. The treatment also caused a significant reduction in negative affect among the participants. Since the treatment is noninvasive and has minimal associated side effects, our results support the use of the light visors at CFS Alert and other northern outposts during the winter for individuals who are experiencing sleep difficulty or low mood.

(Sadler C, Brett K, Heerboth A, Swisher AR, Mehregani N, Touriel R, Cannon DT. Safety proposals for freediving time limits should consider the metabolic-rate dependence of oxygen stores depletion. Diving and Hyperbaric Medicine. 2020 December 20;50(4):356–362. doi: 10.28920/dhm50.4.356-362. PMID: 33325016.) Introduction: There is no required training for breath-hold diving, making dissemination of safety protocols difficult. A recommended breath-hold dive time limit of 60 s was proposed for amateur divers. However, this does not consider the metabolic-rate dependence of oxygen stores depletion. We aimed to measure the effect of apnoea time and metabolic rate on arterial and tissue oxygenation. Methods: Fifty healthy participants (23 (SD 3) y, 22 women) completed four periods of apnoea for 60 s (or to tolerable limit) during rest and cycle ergometry at 20, 40, and 60 W. Apnoea was initiated after hyperventilation to achieve PETCO2 of approximately 25 mmHg. Pulse oximetry, frontal lobe oxygenation, and pulmonary gas exchange were measured throughout. We defined hypoxia as SpO2 < 88%. Results: Static and exercise (20, 40, 60 W) breath-hold break times were 57 (SD 7), 50 (11), 48 (11), and 46 (11) s (F [2.432, 119.2] = 32.0, P < 0.01). The rise in PETCO2 from initiation to breaking of apnoea was dependent on metabolic rate (time × metabolic rate interaction; F [3,147] = 38.6, P < 0.0001). The same was true for the fall in SpO2 (F [3,147] = 2.9, P = 0.03). SpO2 fell to < 88% on 14 occasions in eight participants, all of whom were asymptomatic. Conclusions: Independent of the added complexities of a fall in ambient pressure on ascent, the effect of apnoea time on hypoxia depends on the metabolic rate and is highly variable among individuals. Therefore, we contend that a universally recommended time limit for breath-hold diving or swimming is not useful to guarantee safety.

Introduction: Faults or errors during use of closed-circuit rebreathers (CCRs) can cause hypoxia. Military aviators face a similar risk of hypoxia and undergo awareness training to determine their ‘hypoxia signature’, a personalised, reproducible set of symptoms. We aimed to establish a hypoxia signature among divers, and to investigate their ability to detect hypoxia and self-rescue while cognitively overloaded. Methods: Eight CCR divers and 12 scuba divers underwent an initial unblinded hypoxia exposure followed by three trials; a second hypoxic trial and two normoxic trials in randomised order. Hypoxia was induced by breathing on a CCR with no oxygen supply. Subjects pedalled on a cycle ergometer while playing a neurocognitive computer game to simulate real world task loading. Subjects identified hypoxia symptoms by pointing to a board listing common hypoxia symptoms, and were instructed to perform a ‘bailout’ procedure to mimic self-rescue if they perceived hypoxia. Divers were prompted to bailout if peripheral oxygen saturation fell to 75%, or after six minutes during normoxic trials. Subsequently we interviewed subjects to determine their ability to distinguish hypoxia from normoxia. Results: Ninety-five percent of subjects (19/20) showed agreement between unblinded and blinded hypoxia symptoms. Subjects correctly identified the gas mixture in 85% of the trials. During unblinded hypoxia, only 25% (5/20) of subjects performed unprompted bailout. Fifty-five percent of subjects (11/20) correctly performed the bailout but only when prompted, while 15% (3/20) were unable to bailout despite prompting. During blinded hypoxia 45% of subjects (9/20) performed the bailout unprompted while 15% (3/20) remained unable to bailout despite prompting. Conclusions: Although our data support a normobaric hypoxia signature among both CCR and scuba divers under experimental conditions, most subjects were unable to recognise hypoxia in real time and perform a self-rescue unprompted, although this improved in the second hypoxia trial. These results do not support hypoxia exposure training for CCR divers.

Introduction: While otic barotrauma (OBT) is a common condition experienced by divers, data related to military divers is limited. This study aimed to determine the incidence of OBT in Canadian armed forces (CAF) shallow-water diver (SWD) students trained through the Fleet Dive Unit (Atlantic) (FDU[A]) between 2011-2015. Methods: A retrospective cohort evaluation was performed. The study group consisted of all SWD candidates who embarked on an SWD course through FDU(A) between 2011-2015. A total of 241 subjects comprised the final data analysis. Results: A total of 56 individuals (23.2%) suffered 60 instances of OBT, yielding an incidence density rate of 8.68 per 1,000 person-days on course. A total of 73 diving days (10.44 per 1,000 planned person-course days, or 4.87 diving days per course) were lost due to OBT. Of the reported OBT cases, 18% resulted in cessation of training, 72% in temporary removal from diving. There was no statistically significant association between sex, history of environmental allergies, previous dive qualification, age or rank and the development of OBT. Conclusion: This study reveals that OBT is prevalent among CAF SWD candidates, with operational impact due to missed diving days. This study is limited, and further prospective study is recommended.

No abstract