The goal of this study was to evaluate inflammatory and oxidative stress responses in human subjects (9 females and 15 males) (age [29.6 ± 11.5 years old (mean ± SD)], height [172.0 ± 10.05 cm], and weight [67.8 ± 12.4 kg]) exposed to 1.45 ATA of helium (He) or nitrogen (N2) without concurrent hyperoxia.

The “normobaric oxygen paradox” (NOP) describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as an oxygen shortage, up-regulating redox-sensitive transcription factors. We have previously characterized the time trend of oxygen-sensitive transcription factors in human PBMCs, in which the return to normoxia after 30% oxygen is sensed as a hypoxic trigger, characterized by hypoxia-induced factor (HIF-1) activation.

Purpose: Breath-hold divers (BHDs) often undergo repeated depth training, but the cumulative physiological consequences of such routines remain poorly established. This study aimed to determine whether repeated deep breath-hold dives (DBHDs) induce oxidative, inflammatory, and pulmonary stress responses in the absence of decompression-related mechanisms. The primary objective was to assess changes in salivary inflammatory markers, with secondary objectives including the evaluation of gas microbubbles, lung aeration loss, and hydration status.

Background: SCUBA diving involves exposure to a hyperbaric environment that can induce oxidative stress and inflammation. This study investigates the evolution of oxy-inflammation status in divers who performed repetitive dives in cold water.

Introduction: Diving induced immersion diuresis predisposes divers to dehydration. Dehydration is considered a risk factor for decompression sickness (DCS) but there is very little evidence to prove it. Dehydration also potentially modifies venous gas emboli (VGE) formation and impairs endothelial function. The purpose of this study was to report the effects of fluid loss during a dive on the diver's physiology.