Serum brain-derived neurotrophic factor response to acute aerobic exercise: implications of plasma volume correction

Damian Bailey, P Fernandez, Julien Brugniaux, Christopher Marley, Danielle Hodson, Yves Barde

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review


Background and Aims: The neurotrophin brain-derived neurotrophic factor (BDNF) is widely discussed as a potential molecular mediator associated with post-exercise enhancement of mood and cognitive function in humans (Chang et al., 2012). In support, emerging evidence suggests a dose-response relationship between exercise intensity and the peripheral concentration of circulating BDNF (Knaepen et al., 2010). However, exercise can also contract plasma volume (PV) due to the combination of increased capillary hydrostatic and interstitial osmotic pressures forcing fluid from the intravascular to the extravascular space. Thus, to what extent the increase in circulating BDNF is due to exercise per se or is simply a reflection of haemoconcentration remains to be established.

Methods: To examine this, 23 physically active participants (19 males/4 females) aged 27 (mean) ± 7 (SD) years old were assessed at rest and during a standardised incremental semi-recumbent cycling test to volitional exhaustion (Bailey et al., 2013). Exactly 30 min following cannulation, blood samples were obtained without stasis from the cephalic vein. Haemoglobin (Hb) was assessed via photometry and haematocrit (Hct) by ultracentrifugation with plasma volume (PV) shifts calculated according to established methods (Dill and Costill, 1974). Following centrifugation, serum was flash frozen in liquid nitrogen and stored at -80 oC. BDNF was measured with an enzyme-linked immunosorbent assay using BDNF monoclonal antibodies (Kolbeck et al., 1999). Breath-by-breath online respiratory gas analysis was employed for the determination of maximal oxygen uptake (VO2MAX) and associated cardiorespiratory parameters. Given that BDNF data were not normally distributed (Shapiro W Wilk tests), differences were analysed using Wilcoxon Matched Pairs Signed Ranks tests and relationships via a Spearman's Rank Correlation. Significance was established at P < 0.05.

Results: All participants achieved a maximal effort according to established criteria recording a VO2MAX of 35 ± 8 ml/kg/min (P < 0.05). Exercise was shown to increase serum BDNF (P < 0.05, see Figure A) and decrease PV by 15 ± 5% (P < 0.05). Adjustment for this apparent haemoconcentration attenuated the exercise-induced increase in BDNF by ~42% (P < 0.05, see Figure B). In contrast, we failed to observe a relationship between exercise-induced changes in PV and BDNF (r = 0.08, P > 0.05).

Conclusions: The present findings emphasise the significance of adjusting for PV contraction when assessing the "true" magnitude of the peripheral BDNF response to acute exercise.
Original languageEnglish
Title of host publicationProceedings of The Physiological Society
Volume 34, PC081
Publication statusPublished - 2015
EventPhysiological Society 2015 Annual Meeting - Motorpoint Arena, Cardiff, United Kingdom
Duration: 6 Jul 20158 Jul 2015


ConferencePhysiological Society 2015 Annual Meeting
Abbreviated titlePhysiology 2015
Country/TerritoryUnited Kingdom


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