Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate.
Level 5 - mechanism / opinion, no new human data
Preclinical animal and bench research
PubMed 27253067 · doi:10.7554/eLife.15092
What was done
Investigated the molecular pathway linking exercise to brain-derived neurotrophic factor (Bdnf) induction in mice (Mus musculus). The authors assessed the effect of the exercise metabolite beta-hydroxybutyrate on Bdnf promoters (focusing on promoter I) and histone deacetylases HDAC2 and HDAC3, evaluated hippocampal Bdnf expression following direct intraventricular administration of beta-hydroxybutyrate, and measured synaptic neurotransmitter release via electrophysiology with TrkB receptor dependency testing.
What was found
The abstract provides no exact numerical data or effect sizes. Qualitatively, beta-hydroxybutyrate selectively inhibited HDAC2 and HDAC3 to activate Bdnf promoters (particularly promoter I), direct ventricular delivery increased hippocampal Bdnf expression, and electrophysiological testing showed an increase in neurotransmitter release that was dependent on the TrkB receptor.
Why it matters
The study identifies an endogenous biochemical link between peripheral exercise metabolism and central neuroplasticity, demonstrating that exercise-induced ketone bodies can directly trigger hippocampal BDNF expression via HDAC inhibition.
Limits
All findings are from rodent and in vitro models, limiting direct translation to humans. The abstract does not report sample sizes, concentrations tested, statistical comparisons, or numerical outcomes.
Cited by
- supports Ketone bodies, such as beta-hydroxybutyrate, activate brain-derived neurotrophic factor (BDNF) in the brain.