This study offers evidence suggesting the inheritance of DCS resistance. Future research will focus on genetic and physiological comparisons between the initial strain and the new resistant population.

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, SpO 2 , 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. ResultsThe 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 SpO 2 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. ConclusionThe 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.

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.

Decompression sickness (DCS) is a complex and poorly understood systemic disease with wide inter-individual resistance variability. We selectively bred rats with a 3-fold greater resistance to DCS than standard ones. To investigate possible physiological mechanisms underlying the resistance to DCS, including sex-related differences in these mechanisms, 15 males and 15 females resistant to DCS were compared with aged-matched standard Wistar males (n=15) and females (n=15). None of these individuals had been previously exposed to hyperbaric treatment. Comparison of the allelic frequencies of SNPs showed a difference of one SNP located on the X chromosome. Compared with non-resistant rats, the neutrophil-to-lymphocyte ratio and the plasmatic activity of coagulation Factor X were significantly higher in DCS-resistant individuals regardless of their sex. The maximal relaxation elicited by sodium nitroprusside was lower in DCS-resistant individuals regardless of their sex. Males but not females resistant to DCS exhibited higher neutrophil and lymphocyte counts, higher prothrombin time whereas lower mitochondrial basal O2 consumption and citrate synthase activity. Principal Components Analysis showed that two principal components discriminate the DCS-resistant males but not females from the non-resistant ones. These components were loaded with aPTT, MLR, PT, FX, Fib, for PC1, and ARBC and ANC for PC2. In conclusion, the mechanisms which drive the resistance to DCS appear different between males and females; lower coagulation tendency and enhanced inflammatory response to decompression stress might be key for resistance in males. The involvement of these physiological adaptations in resistance to DCS must now be confirmed.