Acute hypoxia increases plasma BDNF but not NGF in healthy young men

Background: Neurotrophins like brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are neuroprotective and prevent cell death during ischemic conditions. BDNF and NGF expression have been shown to increase after hypoxia in animal studies. However, the effect of hypoxia on systemic release of BDNF and NGF in vivo has not been thoroughly studied. We investigated the impact of acute hypoxia on plasma concentrations of BDNF and NGF in healthy men. Methods: Hypoxia versus normoxia was examined in 14 healthy men participating in a double-blind cross-over study over 6h. Hypoxia was induced for 30min by decreasing oxygen saturation to 75%. On the control condition, oxygen saturation was left at the normal level of 96%. The time course of plasma BDNF and NGF concentration was determined by sandwich-ELISA. Activation of the hormonal stress systems was evaluated by measurement of catecholamine and cortisol levels as well as by monitoring heart rate and blood pressure. Neurocognitive performance and anxiety were also tested using stroop task, memory task and self rated symptom scale. Results: Hypoxia increased plasma concentration of BDNF but not of NGF, as compared to the normoxic control (P<0.05). Epinephrine concentration (P<0.01) as well as symptoms of anxiety (P<0.05) increased upon hypoxia, whereas levels of norepinephrine and cortisol remained unaffected. Except for slowed reading (P<0.05), neurocognitive performance was not impaired by hypoxia. Conclusions: Findings show that acute hypoxia is accompanied by a brisk increase in circulating BDNF concentration and are consistent with previous studies also demonstrating an increase of circulating BDNF but not of NGF in response to stressful stimuli. The BDNF increase during hypoxia fits to a compensatory stress response probably for neuroprotection, but the meaning and origin of circulating BDNF remains unanswered and requires further examination.