Oxidative Stress Response Kinetics after 60 Minutes at Different (1.4 ATA and 2.5 ATA) Hyperbaric Hyperoxia Exposures.

Hyperbaric oxygen therapy (HBOT) is a therapeutical approach based on exposure to pure oxygen in an augmented atmospheric pressure. Although it has been used for years, the exact kinetics of the reactive oxygen species (ROS) between different pressures of hyperbaric oxygen exposure are still not clearly evidenced. In this study, the metabolic responses of hyperbaric hyperoxia exposures for 1 h at 1.4 and 2.5 ATA were investigated. Fourteen healthy non-smoking subjects (2 females and 12 males, age: 37.3 ± 12.7 years old (mean ± SD), height: 176.3 ± 9.9 cm, and weight: 75.8 ± 17.7 kg) volunteered for this study. Blood samples were taken before and at 30 min, 2 h, 24 h, and 48 h after a 1 h hyperbaric hyperoxic exposure. The level of oxidation was evaluated by the rate of ROS production, nitric oxide metabolites (NOx), and the levels of isoprostane. Antioxidant reactions were assessed through measuring superoxide dismutase (SOD), catalase (CAT), cysteinylglycine, and glutathione (GSH). The inflammatory response was measured using interleukine-6, neopterin, and creatinine. A short (60 min) period of mild (1.4 ATA) and high (2.5 ATA) hyperbaric hyperoxia leads to a similar significant increase in the production of ROS and antioxidant reactions. Immunomodulation and inflammatory responses, on the contrary, respond proportionally to the hyperbaric oxygen dose. Further research is warranted on the dose and the inter-dose recovery time to optimize the potential therapeutic benefits of this promising intervention.

Oxidative Stress Response Kinetics after 60 Minutes at Different Levels (10% or 15%) of Normobaric Hypoxia Exposure.

In this study, the metabolic responses of hypoxic breathing for 1 h to inspired fractions of 10% and 15% oxygen were investigated. To this end, 14 healthy nonsmoking subjects (6 females and 8 males, age: 32.2 ± 13.3 years old (mean ± SD), height: 169.1 ± 9.9 cm, and weight: 61.6 ± 16.2 kg) volunteered for the study. Blood samples were taken before, and at 30 min, 2 h, 8 h, 24 h, and 48 h after a 1 h hypoxic exposure. The level of oxidative stress was evaluated by considering reactive oxygen species (ROS), nitric oxide metabolites (NOx), lipid peroxidation, and immune-inflammation by interleukin-6 (IL-6) and neopterin, while antioxidant systems were observed in terms of the total antioxidant capacity (TAC) and urates. Hypoxia abruptly and rapidly increased ROS, while TAC showed a U-shape pattern, with a nadir between 30 min and 2 h. The regulation of ROS and NOx could be explained by the antioxidant action of uric acid and creatinine. The kinetics of ROS allowed for the stimulation of the immune system translated by an increase in neopterin, IL-6, and NOx. This study provides insights into the mechanisms through which acute hypoxia affects various bodily functions and how the body sets up the protective mechanisms to maintain redox homeostasis in response to oxidative stress.

Physiology of repeated mixed gas 100-m wreck dives using a closed-circuit rebreather: a field bubble study.

PURPOSE: Data regarding decompression stress after deep closed-circuit rebreather (CCR) dives are scarce. This study aimed to monitor technical divers during a wreck diving expedition and provide an insight in venous gas emboli (VGE) dynamics. METHODS: Diving practices of ten technical divers were observed. They performed a series of three consecutive daily dives around 100 m. VGE counts were measured 30 and 60 min after surfacing by both cardiac echography and subclavian Doppler graded according to categorical scores (Eftedal-Brubakk and Spencer scale, respectively) that were converted to simplified bubble grading system (BGS) for the purpose of analysis. Total body weight and fluids shift using bioimpedancemetry were also collected pre- and post-dive. RESULTS: Depth-time profiles of the 30 recorded man-dives were 97.3 ± 26.4 msw [range: 54-136] with a runtime of 160 ± 65 min [range: 59-270]. No clinical decompression sickness (DCS) was detected. The echographic frame-based bubble count par cardiac cycle was 14 ± 13 at 30 min and 13 ± 13 at 60 min. There is no statistical difference neither between dives, nor between time of measurements (P = 0.07). However, regardless of the level of conservatism used, a high incidence of high-grade VGE was detected. Doppler recordings with the O'dive were highly correlated with echographic recordings (Spearman r of 0.81, P = 0.008). CONCLUSION: Although preliminary, the present observation related to real CCR deep dives questions the precedence of decompression algorithm over individual risk factors and pleads for an individual approach of decompression.

Oxidative Stress Response's Kinetics after 60 Minutes at Different (30% or 100%) Normobaric Hyperoxia Exposures.

Oxygen is a powerful trigger for cellular reactions and is used in many pathologies, including oxidative stress. However, the effects of oxygen over time and at different partial pressures remain poorly understood. In this study, the metabolic responses of normobaric oxygen intake for 1 h to mild (30%) and high (100%) inspired fractions were investigated. Fourteen healthy non-smoking subjects (7 males and 7 females; age: 29.9 ± 11.1 years, height: 168.2 ± 9.37 cm; weight: 64.4 ± 12.3 kg; BMI: 22.7 ± 4.1) were randomly assigned in the two groups. Blood samples were taken before the intake at 30 min, 2 h, 8 h, 24 h, and 48 h after the single oxygen exposure. The level of oxidation was evaluated by the rate of reactive oxygen species (ROS) and the levels of isoprostane. Antioxidant reactions were observed by total antioxidant capacity (TAC), superoxide dismutase (SOD), and catalase (CAT). The inflammatory response was measured using interleukin-6 (IL-6), neopterin, creatinine, and urates. Oxidation markers increased from 30 min on to reach a peak at 8 h. From 8 h post intake, the markers of inflammation took over, and more significantly with 100% than with 30%. This study suggests a biphasic response over time characterized by an initial "permissive oxidation" followed by increased inflammation. The antioxidant protection system seems not to be the leading actor in the first place. The kinetics of enzymatic reactions need to be better studied to establish therapeutic, training, or rehabilitation protocols aiming at a more targeted use of oxygen.

Physiological effects of mixed-gas deep sea dives using a closed-circuit rebreather: a field pilot study.

PURPOSE: Deep diving using mixed gas with closed-circuit rebreathers (CCRs) is increasingly common. However, data regarding the effects of these dives are still scarce. This preliminary field study aimed at evaluating the acute effects of deep (90-120 msw) mixed-gas CCR bounce dives on lung function in relation with other physiological parameters. METHODS: Seven divers performed a total of sixteen open-sea CCR dives breathing gas mixture of helium, nitrogen and oxygen (trimix) within four days at 2 depths (90 and 120 msw). Spirometric parameters, SpO2, body mass, hematocrit, short term heart rate variability (HRV) and critical flicker fusion frequency (CFFF) were measured at rest 60 min before the dive and 120 min after surfacing. RESULTS: The median [1st-3rd quartile] of the forced vital capacity was lower (84% [76-93] vs 91% [74-107] of predicted values; p = 0.029), whereas FEV1/FVC was higher (98% [95-99] vs 95% [89-99]; p = 0.019) after than before the dives. The other spirometry values and SpO2 were unchanged. Body mass decreased from 73.5 kg (72.0-89.6) before the dives to 70.0 kg (69.2-85.8) after surfacing (p = 0.001), with no change of hematocrit or CFFT. HRV was increased as indicated by the higher SDNN, RMSSD and pNN50 after than before dives. CONCLUSION: The present observation represents the first original data regarding the effects of deep repeated CCR dives. The body mass loss and decrease of FVC after bounce dives at depth of about 100 msw may possibly impose an important physiological stress for the divers.

Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction.

PURPOSE: Previous studies have shown vascular dysfunction of main conductance arteries and microvessels after diving. We aim to evaluate the impact of bubble formation on vascular function and haemostasis. To achieve this, we used a vibration preconditioning to influence bubble levels without changing any other parameters linked to the dive. METHODS: Twentty-six divers were randomly assigned to one of three groups: (1) the "vibrations-dive" group (VD; n = 9) was exposed to a whole-body vibration session 30 min prior the dive; (2) the "diving" group (D; n = 9) served as a control for the effect of the diving protocol; (3) The "vibration" protocol (V; n = 8) allowed us to assess the effect of vibrations without diving. Macro- and microvascular function was assessed for each subject before and after the dive, subsequently. Bubble grades were monitored with Doppler according to the Spencer grading system. Blood was taken before and after the protocol to assess any change of platelets or endothelial function. RESULTS: Bubble formation was lower in the VD than the diving group. The other measured parameters remained unchanged after the "vibration" protocol alone. Diving alone induced macrovascular dysfunction, and increased PMP and thrombin generation. Those parameters were no longer changed in the VD group. Conversely, a microvascular dysfunction persists despite a significant decrease of circulating bubbles. CONCLUSIONS: Finally, the results of this study suggest that macro- but not microvascular impairment results at least partly from bubbles, possibly related to platelet activation and generation of pro-coagulant microparticles.

Physiology of deep closed circuit rebreather mixed gas diving: vascular gas emboli and biological changes during a week-long liveaboard safari.

Introduction: Diving decompression theory hypothesizes inflammatory processes as a source of micronuclei which could increase related risks. Therefore, we tested 10 healthy, male divers. They performed 6-8 dives with a maximum of two dives per day at depths ranging from 21 to 122 msw with CCR mixed gas diving. Methods: Post-dive VGE were counted by echocardiography. Saliva and urine samples were taken before and after each dive to evaluate inflammation: ROS production, lipid peroxidation (8-iso-PGF2), DNA damage (8-OH-dG), cytokines (TNF-α, IL-6, and neopterin). Results: VGE exhibits a progressive reduction followed by an increase (p < 0.0001) which parallels inflammation responses. Indeed, ROS, 8-iso-PGF2, IL-6 and neopterin increases from 0.19 ± 0.02 to 1.13 ± 0.09 µmol.min-1 (p < 0.001); 199.8 ± 55.9 to 632.7 ± 73.3 ng.mg-1 creatinine (p < 0.0001); 2.35 ± 0.54 to 19.5 ± 2.96 pg.mL-1 (p < 0.001); and 93.7 ± 11.2 to 299 ± 25.9 µmol·mol-1 creatinine (p = 0.005), respectively. The variation after each dive was held constant around 158.3% ± 6.9% (p = 0.021); 151.4% ± 5.7% (p < 0.0001); 176.3% ± 11.9% (p < 0.0001); and 160.1% ± 5.6% (p < 0.001), respectively. Discussion: When oxy-inflammation reaches a certain level, it exceeds hormetic coping mechanisms allowing second-generation micronuclei substantiated by an increase of VGE after an initial continuous decrease consistent with a depletion of "first generation" pre-existing micronuclei.

Dark chocolate reduces endothelial dysfunction after successive breath-hold dives in cool water.

OBJECTIVE: The aim of this study is to observe the effects of dark chocolate on endothelial function after a series of successive apnea dives in non-thermoneutral water. METHODS: Twenty breath-hold divers were divided into two groups: a control group (8 males and 2 females) and a chocolate group (9 males and 1 female). The control group was asked to perform a series of dives to 20 m adding up to 20 min in the quiet diving pool of Conflans-Ste-Honorine (Paris, France), water temperature was 27 °C. The chocolate group performed the dives 1 h after ingestion of 30 g of dark chocolate. Flow-mediated dilatation (FMD), digital photoplethysmography, nitric oxide (NO), and peroxynitrite ONOO−) levels were measured before and after each series of breath-hold dives. RESULTS: A significant decrease in FMD was observed in the control group after the dives (95.28 ± 2.9 % of pre-dive values, p < 0.001) while it was increased in the chocolate group (104.1 ± 2.9 % of pre-dive values, p < 0.01). A decrease in the NO level was observed in the control group (86.76 ± 15.57 %, p < 0.05) whereas no difference was shown in the chocolate group (98.44 ± 31.86 %, p > 0.05). No differences in digital photoplethysmography and peroxynitrites were observed between before and after the dives. CONCLUSION: Antioxidants contained in dark chocolate scavenge free radicals produced during breath-hold diving. Ingestion of 30 g of dark chocolate 1 h before the dive can thus prevent endothelial dysfunction which can be observed after a series of breath-hold dives.

Effect of a single, open-sea, air scuba dive on human micro- and macrovascular function.

PURPOSE: Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function. METHODS: Nine divers took part in a SCUBA dive at 30 msw (400 kPa), for 30 min of bottom time. Pre- and post-dive, they underwent an assessment of endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) microvascular function (laser Doppler flowmetry), as well as endothelial-dependent (flow-mediated dilation) and endothelial-independent (nitroglycerin-mediated dilation) function. Bubble grades were monitored with Doppler according to the Spencer grade. RESULTS: The mean KISS bubble score ranged from 21.10 ± 4.7 at rest to 55.03 ± 8.8 after knee flexion. The increase in cutaneous vascular conductance elicited by either acetylcholine (25.34 ± 6.71 to 7.63 ± 1.25 %, p = 0.021) or sodium nitroprusside (35.24 ± 8.75 to 7.61 ± 1.86 %, p = 0.017) was significantly reduced after diving. Similarly, both flow-mediated dilation (10.8 ± 0.9 to 5.4 ± 1.5 %, p = 0.002) and nitroglycerin-mediated dilation (15 ± 1.1 to 6.5 ± 1.6 %, p = 0.002) were also significantly decreased. There were no correlations between vascular parameters and bubble formation. CONCLUSIONS: There appears to be a reduction in endothelium-dependent and endothelium-independent, macro- and microvascular function associated with diving. Our results suggest that in the process of vascular dysfunction during diving, functional changes in the vessel wall may not be limited to the endothelium and may be mediated by alterations in vascular smooth muscle.

Diving under a microscope--a new simple and versatile in vitro diving device for fluorescence and confocal microscopy allowing the controls of hydrostatic pressure, gas pressures, and kinetics of gas saturation.

How underwater diving effects the function of the arterial wall and the activities of endothelial cells is the focus of recent studies on decompression sickness. Here we describe an in vitro diving system constructed to achieve real-time monitoring of cell activity during simulated dives under fluorescent microscopy and confocal microscopy. A 1-mL chamber with sapphire windows on both sides and located on the stage of an inverted microscope was built to allow in vitro diving simulation of isolated cells or arteries in which activities during diving are monitored in real-time via fluorescent microscopy and confocal microscopy. Speed of compression and decompression can range from 20 to 2000 kPa/min, allowing systemic pressure to range up to 6500 kPa. Diving temperature is controlled at 37°C. During air dive simulation oxygen partial pressure is optically monitored. Perfusion speed can range from 0.05 to 10 mL/min. The system can support physiological viability of in vitro samples for real-time monitoring of cellular activity during diving. It allows regulations of pressure, speeds of compression and decompression, temperature, gas saturation, and perfusion speed. It will be a valuable tool for hyperbaric research.

Skin temperature influence on transcutaneous carbon dioxide (CO2) conductivity and skin blood flow in healthy human subjects at the arm and wrist.

Objective: present transcutaneous carbon dioxide (CO2)-tcpCO2-monitors suffer from limitations which hamper their widespread use, and call for a new tcpCO2 measurement technique. However, the progress in this area is hindered by the lack of knowledge in transcutaneous CO2 diffusion. To address this knowledge gap, this study focuses on investigating the influence of skin temperature on two key skin properties: CO2 permeability and skin blood flow. Methods: a monocentric prospective exploratory study including 40 healthy adults was undertaken. Each subject experienced a 90 min visit split into five 18 min sessions at different skin temperatures-Non-Heated (NH), 35, 38, 41, and 44°C. At each temperature, custom sensors measured transcutaneous CO2 conductivity and exhalation rate at the arm and wrist, while Laser Doppler Flowmetry (LDF) assessed skin blood flow at the arm. Results: the three studied metrics sharply increased with rising skin temperature. Mean values increased from the NH situation up to 44°C from 4.03 up to 8.88 and from 2.94 up to 8.11 m·s-1 for skin conductivity, and from 80.4 up to 177.5 and from 58.7 up to 162.3 cm3·m-2·h-1 for exhalation rate at the arm and wrist, respectively. Likewise, skin blood flow increased elevenfold for the same temperature increase. Of note, all metrics already augmented significantly in the 35-38°C skin temperature range, which may be reached without active heating-i.e. only using a warm clothing. Conclusion: these results are extremely encouraging for the development of next-generation tcpCO2 sensors. Indeed, the moderate increase (× 2) in skin conductivity from NH to 44°C tends to indicate that heating the skin is not critical from a response time point of view, i.e. little to no skin heating would only result in a doubled sensor response time in the worst case, compared to a maximal heating at 44°C. Crucially, a skin temperature within the 35-38°C range already sharply increases the skin blood flow, suggesting that tcpCO2 correlates well with the arterial paCO2 even at such low skin temperatures. These two conclusions further strengthen the viability of non-heated tcpCO2 sensors, thereby paving the way for the development of wearable transcutaneous capnometers.

Scientific shallow saturation dive expedition using diving rebreathers and a specific dry habitat: medical management of the "Capsule" programme.

BACKGROUND: Scientific underwater exploration could benefit from professional diving facilities. This could allow marine research for durations far exceeding anything currently possible. The closed-circuit rebreather expansion provides new perspectives by unleashing divers and their diving bell. "Under the Pole Expeditions" developed an innovative compact underwater habitat for this purpose. MATERIALS AND METHODS: The habitat's depth was fixed at 20 m. Saturation lasted 3 days and was followed by a 245 min long decompression procedure with mandatory in-water phase. Isolation and environmental constraints will require specific medical and safety procedures. "In situ" medical concerns were considered, and a specific evacuation plan was established. This report describes the medical management of this atypical project and the systematic clinical follow-up mostly targeted on the cardiovascular system, fatigue and psychological tolerance. RESULTS: Seventeen individual saturation exposures were performed. All selected divers were professional. Neither severe illness nor decompression sickness was observed. These short-term saturation exposures appeared to be well tolerated. There was a relatively low bubble grade after decompression. Psychological tolerance appeared good. However, a transient moderate orthostatic hypotension suggested cardiovascular deconditioning after dive. CONCLUSIONS: This first experiment demonstrates the interest and feasibility of a shallow revisited saturation dive with rebreather use. This isolation requires medical accompaniment and rigorous preparation. Medical and physiological risks assessment is essential in this context and must be consolidated by new experiences.

Does Decreased Diffusing Capacity of the Lungs for Carbon Monoxide Constitute a Risk of Decompression Sickness in Occupational Divers?

Long-term alterations of pulmonary function (mainly decreased airway conductance and capacity of the lungs to diffuse carbon monoxide (DLCO)) have been described after hyperbaric exposures. However, whether these alterations convey a higher risk for divers' safety has never been investigated before. The purpose of the present pilot study was to assess whether decreased DLCO is associated with modifications of the physiological response to diving. In this case-control observational study, 15 "fit-to-dive" occupational divers were split into two groups according to their DLCO measurements compared to references values, either normal (control) or reduced (DLCO group). After a standardized 20 m/40 min dive in a sea water pool, the peak-flow, vascular gas emboli (VGE) grade, micro-circulatory reactivity, inflammatory biomarkers, thrombotic factors, and plasmatic aldosterone concentration were assessed at different times post-dive. Although VGE were recorded in all divers, no cases of decompression sickness (DCS) occurred. Compared to the control, the latency to VGE peak was increased in the DLCO group (60 vs. 30 min) along with a higher maximal VGE grade (p < 0.0001). P-selectin was higher in the DLCO group, both pre- and post-dive. The plasmatic aldosterone concentration was significantly decreased in the control group (-30.4 ± 24.6%) but not in the DLCO group. Apart from a state of hypocoagulability in all divers, other measured parameters remained unchanged. Our results suggest that divers with decreased DLCO might have a higher risk of DCS. Further studies are required to confirm these preliminary results.

Highlighting of the interactions of MYD88 and NFKB1 SNPs in rats resistant to decompression sickness: toward an autoimmune response.

Decompression sickness (DCS) with neurological disorders includes an inappropriate inflammatory response which degenerates slowly, even after the disappearance of the bubbles. There is high inter-individual variability in terms of the occurrence of DCS that could have been mastered by the selection and then the breeding of DCS-resistant rats. We hypothesized the selection of single-nucleotide polymorphisms (SNPs) linked to autoimmunity operated upon a generation of a DCS-resistant strain of rats. We used the candidate gene approach and targeted SNPs linked to the signaling cascade that directly regulates inflammation of innate immunity transiting by the Toll-like receptors. Twenty candidate SNPs were investigated in 36 standard rats and 33 DCS-resistant rats. For the first time, we identify a diplotype (i.e., with matched haplotypes)-when coinherited-that strengthens protection against DCS, which is not strictly homozygous and suggests that a certain tolerance may be considered. We deduced an ideal haplotype of six variants from it (MyD88_50-T, _49-A, _97-C coupled to NFKB_85-T, _69-T, _45-T) linked to the resistant phenotype. Four among the six identified variants are located in pre- and/or post-transcriptional areas regulating MyD88 or NFKB1 expression. Because of missense mutations, the other two variants induce a structural change in the NFKB1 protein complex including one damage alteration according to the Missense3D algorithm. In addition to the MyD88/NFKB1 haplotype providing rats with a strong resistance to DCS, this also highlights the importance that the immune response, here linked to the genetic heritage, can have in the development of DCS and offer a new perspective for therapeutic strategies.

Blood pressure in rats selectively bred for their resistance to decompression sickness.

INTRODUCTION: Susceptibility to decompression sickness (DCS) is characterised by a wide inter-individual variability whose origins are still poorly understood. This hampers reliable prediction of DCS by decompression algorithms. We previously selectively bred rats with a 3-fold greater resistance to DCS than standard rats. Based on its previously reported relation with decompression outcomes, we assessed whether modification in vascular function is associated with resistance to DCS. METHODS: The arterial pressure response to intravenous administration of acetylcholine (ACh, 5 µg.kg-1) and adrenaline (5 and 10 µg.kg-1) was compared in anaesthetised DCS-resistant rats (seven females, seven males) and standard Wistar rats (seven females, 10 males) aged 14-15 weeks. None of these rats had previously undergone hyperbaric exposure. RESULTS: There was a non-significant tendency for a lower diastolic (DBP) and mean blood pressure (MBP) in DCS-resistant rats. After ACh administration, MBP was significantly lower in resistant rats, for both males (P = 0.007) and females (P = 0.034). After administration of adrenaline 10 µg.kg-1, DCS-resistant rats exhibited lower maximal DBP (P = 0.016) and MBP (P = 0.038). Systolic and pulse blood pressure changes did not differ between groups in any of the experiments. CONCLUSIONS: Resistance to DCS in rats is associated to a trend towards a lower vascular tone but not blood pressure reactivity. Whether these differences are a component of the susceptibility to DCS remains to be confirmed.

Effect of occupational exposure to welding fumes and noise on heart rate variability: An exposed-unexposed study on welders and airport workers' population.

Introduction: Welding fumes (WF) are a complex mixture of gas and particles. Action of occupational exposure to WF on cardiovascular system has been recently studied as for noise. Research question: The main objectives of our study are therefore to evaluate the impact of exposure to WF, noise, and combined WF and noise on autonomic nervous system as assessed by heart rate variability (HRV). Methods: The study groups were 16 welders and eight airport workers (as a control group). All the participants underwent ambulatory electrocardiogram, personal WF, and noise exposure monitoring, respectively, with dust track and calibrated noise dosimeter during workday. Atmospheric environmental assessments at workplaces have been also performed. HRV parameters were summarized for all the workday and hourly. Correlation tests were used to examine relation between HRV parameters and levels of noise exposure in the two population. Analysis of covariance (ANCOVA) was used for mean of each HRV parameters. Results: For HRV parameters, we found significant higher levels for mean range of high frequency (HF), standard deviation of normal-to-normal R-R interval (SDNN), and root mean square of successive heartbeat interval difference (RMSSD) in welders which suggested an imbalance between sympathetic and parasympathetic nervous system in this population. For relation between noise and HRV parameters, we noted that levels of low frequency (LF), HF, and SDNN were significantly correlated with mean noise levels for welders (respectively, r = 0.62, r = 0.357, r = 0.48), not in control group. Using ANCOVA, we found that working as a welder significantly increases mean of HF (p = 0.01) and RMSSD (p = 0.02) and decreases in LF/HF (p = 0.008). Indeed, the interaction between exposure to WF and mean noise levels for HF (p = 0.005), LF/HF (p = 0.01), and RMSSD (p = 0.007) was significant. Conclusion: This study shows an impact of WF and noise on ANS balance. One hypothesis is WF exposure could increase sensibility to noise exposure on autonomic nervous system or there is a synergic effect.

Comparison of insulation provided by dry or wetsuits among recreational divers during cold water immersion (< 5°C).

BACKGROUND: Divers thermal status influences susceptibility to decompression sickness hence the need for proper insulation during immersion in cold water. However, there is a lack of data on thermal protection provided by diving suits, hence this study. MATERIALS AND METHODS: Two different groups of divers wearing either a wetsuit (n = 15) or a dry suit (n = 15) volunteered for this study. Anthropometric data and dive experience were recorded; skin temperatures at the cervical-supraclavicular (C-SC) area and hands were assessed through high-resolution thermal infrared imaging taken pre- and post-dive. RESULTS: As far as anthropometrics, pre-dive C-SC temperatures (37.0 ± 0.4°C), depth (dry: 43 ± 4.6 mfw vs. wet: 40.3 ± 4.0 mfw) and water temperature exposure (4.3°C) are concerned, both groups were comparable. Total dive time was slightly longer for dry suit divers (39.6 ± 4.0 min vs. 36.5 ± 4.1 min, p = 0.049). Post-dive, C-SC temperature was increased in dry suit divers by 0.6 ± 0.6°C, and significantly decreased in wetsuit divers by 0.8 ± 0.6°C. The difference between groups was highly significant (dry: 37.5 ± 0.7°C vs. wet: 36.2 ± 0.7°C, p = 0.004). Hand's temperature decreased significantly in both groups (dry: 30.3 ± 1.2°C vs. wet: 29.8 ± 0.8°C, p = 0.33). Difference between groups was not significant. CONCLUSIONS: Medium-duration immersion in cold water (< 5°C), of healthy and fully protected subjects was well tolerated. It was demonstrated that proper insulation based on a three-layer strategy allows maintaining or even slightly improve thermal balance. However, from an operational point of view, skin extremities are not preserved.

Evidence of a hormonal reshuffle in the cecal metabolome fingerprint of a strain of rats resistant to decompression sickness.

On one side, decompression sickness (DCS) with neurological disorders lead to a reshuffle of the fecal metabolome from rat caecum. On the other side, there is high inter-individual variability in terms of occurrence of DCS. One could wonder whether the fecal metabolome could be linked to the DCS-susceptibility. We decided to study male and female rats selected for their resistance to decompression sickness, and we hypothesize a strong impregnation concerning the fecal metabolome. The aim is to verify whether the rats resistant to the accident have a fecal metabolomic signature different from the stem generations sensitive to DCS. 39 DCS-resistant animals (21 females and 18 males), aged 14 weeks, were compared to 18 age-matched standard Wistar rats (10 females and 8 males), i.e., the same as those we used for the founding stock. Conventional and ChemRICH approaches helped the metabolomic interpretation of the 226 chemical compounds analyzed in the cecal content. Statistical analysis shows a panel of 81 compounds whose expression had changed following the selection of rats based on their resistance to DCS. 63 compounds are sex related. 39 are in common. This study shows the spectral fingerprint of the fecal metabolome from the caecum of a strain of rats resistant to decompression sickness. This study also confirms a difference linked to sex in the metabolome of non-selected rats, which disappear with selective breeding. Results suggest hormonal and energetic reshuffle, including steroids sugars or antibiotic compounds, whether in the host or in the microbial community.

Pre-hydration strongly reduces decompression sickness occurrence after a simulated dive in the rat.

INTRODUCTION: Hydration status is considered a parameter likely to influence the risk of decompression sickness (DCS), but scientific evidence is scarce and conflicting. This experiment aimed to analyse the influence of pre-hydration on DCS occurrence in a rat model. METHODS: Intra-peritoneal injections of saline solution were administered to rats (NaCl 0.9% 0 ml (Control), 0.1 ml (Group 1), or 1 ml·100g-1 body mass (Group 2) at each of 24 h, 12 h, and 30 min prior to simulated air dives (45 min at 1,010 kPa; compression and decompression rates 101 kPa·min-1; stops 5 min at 202 kPa, 5 min at 160 kPa, 10 min at 130 kPa). Evaluation of DCS occurrence and severity was made after decompression. RESULTS: Pre-dive hydration reduced severe DCS from 47% (Control) to 29% (Group 1) and 0% (Group 2), and increased the proportion of animals without any signs of DCS from 40 (Control) to 57% (Group 1) and 93% (Group 2); Chi2 P = 0.041. CONCLUSIONS: This experiment demonstrated that pre-hydration can drastically reduce the DCS occurrence in an animal model. In the context of scuba diving, this result highlights the importance of elucidating the mechanisms linking hydration status and DCS risk.

Field study of anthropomorphic and muscle performance changes among elite skippers following a transoceanic race.

BACKGROUND: Ocean racing has become increasingly demanding, both physically and psychologically. The aim of the study was to assess global changes after a transoceanic race. MATERIALS AND METHODS: Eight male sailors were evaluated pre- and post-race through anthropometric measurements (weight, skinfold, girth at different level and estimated body fat percentage), multifrequency tetrapolar bioelectrical impedance, muscular performance, visual analogic scale for perceived fatigue and Critical Flicker Fusion Frequencies for cerebral arousal. RESULTS: Compared to pre-race values, a significant decrease in body weight (-3.6 ± 1.4%, p = 0.0002) and body composition with reduction of body fat percentage (-15.1 ± 3.5%, p < 0.0001) and fat mass (-36.4 ± 31.4%, p = 0.022) was observed. Muscle performance of the upper limb was preserved. In the lower limb, monohulls skippers showed a significant reduction of jump height (-6.6 ± 4.8%, p = 0.022), power (-11.7 ± 7.3%, p = 0.011) and speed (-14.6 ± 7.4%, p = 0.0006) while a multihulls skipper showed a gain in speed (+0.87%), power (+8.52%), force (+11%) resulting in a higher jump height (+1.12%). These changes were inversely correlated with sea days (Pearson r of -0.81, -0.96 and -0.90, respectively, p < 0.01). CONCLUSIONS: Changes in body weight and composition are consistent with previous data indicating a probable negative energy balance. The main finding demonstrates a difference in muscular conditioning between upper and lower limbs that might be explained by differential workload related to boat architecture (trampolines) or handling.