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 five minutes, the purpose of the present study was to determine how this impacts cerebral free radical formation and corresponding implications for brain structure/function. Measurements were obtained before and following a maximal apnea in fourteen divers with trans-cerebral 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 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, low density lipoprotein oxidation), nitric oxide bioactivity (nitrite) and S100β were correspondingly enhanced (P < 0.05), the latter interpreted as minor and not pathological disruption of the blood-brain barrier. However, these changes were 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 a prolonged apnea in trained divers may reflect a functional physiologic response rather than a purely maladaptive phenomenon.