Exercise induces cerebral VEGF and angiogenesis via the lactate receptor HCAR1.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study using mouse models
PubMed 28534495 · doi:10.1038/ncomms15557
What was done
Researchers investigated the localization and vascular function of the lactate receptor HCAR1 in mice. They evaluated cerebral vascular endothelial growth factor A (VEGFA) levels and capillary density in wild-type versus HCAR1-knockout mice following either high-intensity interval exercise (5 days weekly for 7 weeks) or subcutaneous L-lactate injections calibrated to mirror exercise-induced blood lactate elevations. Vascular changes in skeletal muscle were also evaluated.
What was found
HCAR1 was enriched in pial fibroblast-like cells and intracerebral pericyte-like cells along microvessels. Both 7 weeks of interval exercise and L-lactate injections increased brain VEGFA protein and capillary density in wild-type mice, but not in HCAR1 knockout mice. Skeletal muscle showed no vascular HCAR1 expression and no HCAR1-dependent vascularization changes. The abstract does not report numerical data, effect sizes, or variance.
Why it matters
The study identifies a direct molecular mechanism by which muscle-derived lactate acts on brain vascular HCAR1 receptors to promote cerebral angiogenesis.
Limits
The study was conducted entirely in mouse models, meaning human clinical relevance remains unestablished. The abstract does not provide sample sizes, baseline data, quantitative figures, or functional cognitive outcomes.
Cited by
- supports Lactate signals to increase vascular endothelial growth factor (VEGF) at the blood-brain barrier to promote angiogenesis and repair blood vessels.