Breath-hold diving results in significant changes in blood gases’ levels. Challenging variations in oxygen partial pressures may induce reactive oxygen species (ROS) production that exacerbate oxidative stress and, consequently, affect endothelial function. The aim of this study was to investigate the effects of breath-hold diving on oxidative stress damage, assessing ROS production. Nitric oxide metabolites, inducible nitric oxide synthase (iNOS), aminothiols, and renal function were evaluated too as markers of redox status and renal damage.

ROS production was assessed with electron paramagnetic resonance. Oxidative status values were measured at pre- and post-40 m dive in a deep swimming pool (Y-40) from six divers (mean age 46.6 ± 9.3 years; height 176 ± 4 cm; BMI 25 ± 2.9 kg/m²).

Significant (p < 0.05) increases at post-dive of ROS production rate (0.158 ± 0.003 vs 0.195 ± 0.006 μmol min⁻¹), lipid peroxidation (8-isoprostane: 375.67 ± 195.62 vs 420.49 ± 232.31 pg mg⁻¹ creatinine), nitrate (27.91 ± 19.71 vs 30.80 ± 20.44 μM), iNOS (31.30 ± 4.52 vs 35.68 ± 6.72 IU mL⁻¹) and neopterin concentration (96.20 ± 40.41 vs 118.76 ± 27.84 μmol mol⁻¹ creatinine) were recorded. Conversely, the antioxidant capacity significantly decreased (3.423 ± 0.089 vs 3.015 ± 0.284 mM) after immersion.

Overproduction of ROS and consequent oxidative damage to lipids of membrane and antioxidant capacity decreasing reflect also a hypoxic condition, which in the breath-hold diving typically occurs in the last few meters below the surface. iNOS produces NO in large quantities under the examined extreme conditions. Neopterin and creatinine concentration level increased, suggesting an “impairment of renal function” as a likely physiological response to PaO₂ variations during dive activity.