Elevated Lactate by High-Intensity Interval Training Regulates the Hippocampal BDNF Expression and the Mitochondrial Quality Control System.
Level 5 - mechanism / opinion, no new human data
Preclinical animal (mouse) and in vitro cell culture study
PubMed 33716776 · doi:10.3389/fphys.2021.629914
What was done
Researchers evaluated the effects of a 6-week high-intensity interval training (HIIT) protocol on peripheral and central lactate levels, mitochondrial function, the mitochondrial quality control system, and brain-derived neurotrophic factor (BDNF) expression in mouse hippocampus. In vitro experiments using primary cultured mouse hippocampal cells were subsequently performed to determine the specific role and mechanisms of lactate in regulating mitochondrial function and BDNF expression.
What was found
The abstract reports qualitative directions of effect without numerical values or effect sizes. In vivo, 6 weeks of HIIT elevated immediate post-exercise peripheral and central lactate levels, increased hippocampal ATP production, upregulated selected mitochondrial oxidative phosphorylation (OXPHOS) genes, promoted mitochondrial fusion and biogenesis, suppressed mitochondrial fission, and stimulated BDNF expression. In vitro, lactate exposure directly regulated mitochondrial quality control and supported mitochondrial function associated with BDNF expression.
Why it matters
This study outlines a mechanistic pathway indicating that lactate generated during high-intensity exercise may act directly as a signaling molecule in the brain to optimize hippocampal mitochondrial dynamics and stimulate neurotrophic factor expression.
Limits
The study was conducted entirely in mice and primary mouse cell cultures; findings cannot be directly generalized to humans. The abstract omits sample sizes, specific exercise intensities, quantitative measurements, and statistical effect estimates.
Cited by
- supports Lactate directly stimulates the production of brain-derived neurotrophic factor (BDNF).