PMID- 31644554 OWN - NLM STAT- MEDLINE DCOM- 20200320 LR - 20231014 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 14 IP - 10 DP - 2019 TI - Acute normobaric hypoxia does not affect the simultaneous exercise-induced increase in circulating BDNF and GDNF in young healthy men: A feasibility study. PG - e0224207 LID - 10.1371/journal.pone.0224207 [doi] LID - e0224207 AB - Physical exercise has a neuromodulatory effect on the central nervous system (CNS) partially by modifying expression of neuropeptides produced and secreted by neurons and glial cells, among which the best examined are brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). Because both neurotrophins can cross the brain-blood barrier (BBB), their blood levels indirectly reflect their production in the CNS. Moreover, both neuropeptides are involved in modulation of dopaminergic and serotoninergic system function. Because limited information is available on the effects of exercise to volition exhaustion and acute hypoxia on CNS, BDNF and GDNF formation, the aims of the present study were to verify whether 1) acute exercise to exhaustion in addition to neurons also activates glial cells and 2) additional exposure to acute normobaric moderate hypoxia affects their function. In this feasibility study we measured blood concentrations of BDNF, GDNF, and neuropeptides considered as biomarkers of brain damage (bFGF, NGF, S100B, GFAP) in seven sedentary healthy young men who performed a graded exercise test to volitional exhaustion on a cycle ergometer under normoxic (N) and hypoxic conditions: 2,000 m (H2; FiO2 = 16.6%) and 3,000 m altitude (H3; FiO2 = 14.7%). In all conditions serum concentrations of both BDNF and GDNF increased immediately after cessation of exercise (p<0.01). There was no effect of condition or interaction (condition x time of measurement) and exercise on any of the brain damage biomarkers: bFGF, NGF, S100B, GFAP. Moreover, in N (0<0.01) and H3 (p<0.05) exercise caused elevated serum 5-HT concentration. The results suggest that a graded effort to volitional exhaustion in normoxia, as well as hypoxia, simultaneously activates both neurons and astrocytes. Considering that s100B, GFAP, bFGF, and NGF (produced mainly by astrocytes) are markers of brain damage, it can be assumed that a maximum effort in both conditions is safe for the CNS. FAU - Piotrowicz, Zofia AU - Piotrowicz Z AUID- ORCID: 0000-0002-7302-6442 AD - Institute of Sport Sciences, The Jerzy Kukuczka Academy of Physical Education, Katowice, Poland. FAU - Chalimoniuk, Malgorzata AU - Chalimoniuk M AD - Department of Tourism and Health in Biala Podlaska, The Jozef Pilsudski University of Physical Education, Warsaw, Poland. FAU - Ploszczyca K, Kamila AU - Ploszczyca K K AUID- ORCID: 0000-0003-3516-9124 AD - Department of Kinesiology, Institute of Sport, Warsaw, Poland. FAU - Czuba, Milosz AU - Czuba M AD - Department of Kinesiology, Institute of Sport, Warsaw, Poland. AD - Department of Sports Theory, The Jerzy Kukuczka Academy of Physical Education, Katowice, Poland. FAU - Langfort, Jozef AU - Langfort J AD - Institute of Sport Sciences, The Jerzy Kukuczka Academy of Physical Education, Katowice, Poland. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20191023 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (GDNF protein, human) RN - 0 (Glial Cell Line-Derived Neurotrophic Factor) RN - 7171WSG8A2 (BDNF protein, human) SB - IM MH - Adult MH - Brain-Derived Neurotrophic Factor/*blood MH - Cells, Cultured MH - Exercise/*physiology MH - Feasibility Studies MH - Glial Cell Line-Derived Neurotrophic Factor/*blood MH - Humans MH - Hypoxia/*physiopathology MH - Male MH - Neuroglia/cytology/*metabolism MH - Neurons/cytology/*metabolism MH - Young Adult PMC - PMC6808427 COIS- The authors have declared that no competing interests exist. EDAT- 2019/10/24 06:00 MHDA- 2020/03/21 06:00 PMCR- 2019/10/23 CRDT- 2019/10/24 06:00 PHST- 2019/08/09 00:00 [received] PHST- 2019/10/08 00:00 [accepted] PHST- 2019/10/24 06:00 [entrez] PHST- 2019/10/24 06:00 [pubmed] PHST- 2020/03/21 06:00 [medline] PHST- 2019/10/23 00:00 [pmc-release] AID - PONE-D-19-22522 [pii] AID - 10.1371/journal.pone.0224207 [doi] PST - epublish SO - PLoS One. 2019 Oct 23;14(10):e0224207. doi: 10.1371/journal.pone.0224207. eCollection 2019.