Increased serum brain-derived neurotrophic factor protein upon hypoxia in healthy young men.

Exposing animals to brief hypoxic periods leads to neuroprotective ischemic tolerance termed preconditioning. This phenomenon is well documented in the brain, but the underlying mechanisms require further elucidation. As nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are important mediators of maintaining homeostatic conditions in the adult nervous system in terms of physiological and pathophysiological processes, we hypothesized that hypoxic preconditioning might modulate serum neurotrophin concentrations. Hypoxia was induced for 30 min in 14 healthy young men resulting in a constant blood oxygen saturation of 75%. Hyperinsulinemic euglycemic clamps were performed and serum concentrations of BDNF and NGF were measured at baseline, directly after the intervention, and at the end of the session. Overall, serum BDNF concentrations decreased over time by maximally 35% (P = 0.001) while in contrast NGF concentrations remained unchanged. Acute hypoxia alleviated the decrease of BDNF resulting in higher BDNF concentrations as compared to normoxic control (P < 0.01). Our findings show that acute hypoxia results in significantly higher serum BDNF concentrations pointing to a potential role of BDNF in the underlying mechanism of hypoxic preconditioning. Based on its neuroprotective properties, BDNF may be of high clinical relevance for therapeutic options in ischemic neurovascular diseases.