Imbalanced cortisol/BDNF signals and oxidative stress underscore temporary cognitive impairment in deep divers after in water/surface decompression: proof of concept.

内容摘要

Military deep divers experience extreme environmental stressors, particularly with prolonged diving. Alterations such as hyperbaric conditions and variable O2 levels can prompt systemic/local oxidative stress (OxS) and elevated nitric oxide (NO.) post-dive release, heightening the risk of inflammation and cardiovascular events. Yet, deep diving (e.g. saturation diving) can also lead to cognitive impairment, whose mechanisms remain largely elusive but relevant to determine. Three Deep Divers (Italian Navy-Comsubin), with an average age of 31.00 ± 2.64 years, carried out a technical surface-supplied bounce diving in open water (-89m) in the Mediterranean Sea. From them, we collected saliva and urine samples before diving (T0), after deep diving followed by water-surface decompression (T1), and after complete subemersion (T2). To assess for pro-inflammatory and stress conditions, we evaluated reactive oxygen species (ROS) production, DNA oxidation (8-OHdG), total antioxidant capacity (TAC), nitric oxide (NO.) oxidation products, and the levels of interleukin-6, cortisol, brain-derived neurotrophic factor (BDNF), dopamine, and glutamate. At T1, ROS production increased (+ 121%) and continued to increase just to T2, coupled to a continuous rise in 8-OHdG, and a contemporary decline in TAC. Simultaneously, cortisol levels increased while those of dopamine decreased (-27%). BDNF levels were also sizably elevated (+ 175%). Conversely, no changes in pro-inflammatory markers and NO concentrations were evident. Oxidative stress and neurotransmitter increase and/or decrease (according to biomarkers evaluated) occur post-deep diving, suggesting preventative strategies to mitigate cognitive impairment.