Controlled Hypoxia Acutely Prevents Physical Inactivity-Induced Peripheral BDNF Decline

Author:

Duderstadt Yves123ORCID,Schreiber Stefanie24567ORCID,Burtscher Johannes8ORCID,Schega Lutz3ORCID,Müller Notger G.29,Brigadski Tanja1011,Braun-Dullaeus Rüdiger C.1ORCID,Leßmann Volkmar46710ORCID,Müller Patrick1247

Affiliation:

1. Division of Cardiology and Angiology, University Hospital Magdeburg, 39120 Magdeburg, Germany

2. German Center for Neurodegenerative Diseases (DZNE), 39120 Magdeburg, Germany

3. Department of Sports Science, Chair of Health and Physical Activity, Otto-von-Guericke University, 39104 Magdeburg, Germany

4. Center for Intervention and Research on Adaptive and Maladaptive Brain Circuits Underlying Mental Health (C-I-R-C), 39120 Magdeburg, Germany

5. Division of Neurology, University Hospital Magdeburg, 39120 Magdeburg, Germany

6. Center for Behavioral Brain Sciences (CBBS), 39120 Magdeburg, Germany

7. German Center for Mental Health (DZPG), 39120 Magdeburg, Germany

8. Institute of Sports Science, University Innsbruck, 6020 Innsbruck, Austria

9. Faculty of Health Sciences Brandenburg, University of Potsdam, 14476 Potsdam, Germany

10. Institute of Physiology, Otto-von-Guericke University, 39120 Magdeburg, Germany

11. Department of Informatics and Microsystems Technology, University of Applied Sciences, 67659 Kaiserslautern, Germany

Abstract

Brain-derived neurotrophic factor (BDNF) is a crucial mediator of neuronal plasticity. Here, we investigated the effects of controlled normobaric hypoxia (NH) combined with physical inactivity on BDNF blood levels and executive functions. A total of 25 healthy adults (25.8 ± 3.3 years, 15 female) were analyzed in a randomized controlled cross-over study. Each intervention began with a 30 min resting phase under normoxia (NOR), followed by a 90 min continuation of NOR or NH (peripheral oxygen saturation [SpO2] 85–80%). Serum and plasma samples were collected every 15 min. Heart rate and SpO2 were continuously measured. Before and after each exposure, cognitive tests were performed and after 24 h another follow-up blood sample was taken. NH decreased SpO2 (p < 0.001, ηp2 = 0.747) and increased heart rate (p = 0.006, ηp2 = 0.116) significantly. The 30-min resting phase under NOR led to a significant BDNF reduction in serum (p < 0.001, ηp2 = 0.581) and plasma (p < 0.001, ηp2 = 0.362). Continuation of NOR further significantly reduced BDNF after another 45 min (p = 0.018) in serum and after 30 min (p = 0.040) and 90 min (p = 0.005) in plasma. There was no significant BDNF decline under NH. A 24 h follow-up examination showed a significant decline in serum BDNF, both after NH and NOR. Our results show that NH has the potential to counteract physical inactivity-induced BDNF decline. Therefore, our study emphasizes the need for a physically active lifestyle and its positive effects on BDNF. This study also demonstrates the need for a standardized protocol for future studies to determine BDNF in serum and plasma.

Funder

Federal Ministry of Education and Research

Medical Faculty of the Otto von Guericke University Magdeburg

Deutsche Forschungsgemeinschaft

Publisher

MDPI AG

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