Competitive apnea and its effect on the human brain: Focus on the redox regulation of blood-brain barrier permeability and neuronal-parenchymal integrity

Static apnea provides a unique model that combines transient hypertension, hypercapnia, and severe hypoxemia. With apnea durations exceeding 5 min, the purpose of the present study was to determine how that affects cerebral free-radical formation and the corresponding implications for brain structure and function. Measurements were obtained before and following amaximal apnea in 14 divers with transcerebral exchange kinetics, measured as the product of global cerebral blood flow (duplex ultrasound) and radial arterial to internal jugular venous concentration differences (a-vD).Apnea increased the systemic (arterial) and, to a greater extent, the regional (jugular venous) concentration of the ascorbate free radical, resulting in a shift from net cerebral uptake to output (P < 0.05). Peroxidation (lipid hydroperoxides, LDL oxidation), NO bioactivity, and S100b were correspondingly enhanced (P < 0.05), the latter interpreted as minor and not a pathologic disruption of the blood-brain barrier. However, those changeswere insufficient to cause neuronal-parenchymal damage confirmed by the lack of change in the a-vD of neuron-specific enolase and human myelin basic protein (P > 0.05). Collectively, these observations suggest that increased cerebral oxidative stress following prolonged apnea in trained diversmay reflect a functional physiologic response, rather than a purely maladaptive phenomenon.