Table 1.
Relationship between aerobic activity, neurogenesis, and changes in the cerebrovascular architecture.
| Physical activity | Role | Supporting evidence |
|---|---|---|
| ↑ VEGF in circulation | Crosses the BBB | • blocking peripheral VEGF in mice abolishes exercise-induced neurogenesis79 |
| ↑ angiogenesis | ||
| ↑ neurogenesis | ||
| ↑ IGF-1 in circulation | Crosses the BBB ↑ angiogenesis | • IGF-1 promotes vessel remodeling via HIF-1α and VEGF81 |
| ↑ neurogenesis | • Blocking peripheral IGF-1 in mice abolishes exercise-induced neurogenesis82 and upregulation of BDNF83 | |
| • Low levels of IGF-1 are a risk factor for cognitive decline66 | ||
| ↑ BDNF in the brain | ↑ neuroplasticity | • Blocking BDNF receptors in mice abolishes exercise-induced increase in cognitive function83 |
| ↑ cognitive function | ||
| • BDNF promotes neurogenesis84 | ||
| ↑ eNOS activity | ↑ endothelial | • eNOS deficient mice do not show exercise-induced increase in EPCs72 |
| progenitor cells | ||
| (EPCs) in circulation | • Blocking NOS in mice abolishes exercise-induced vasculogenesis71 | |
| ↑ vasculogenesis |
Notes: Aerobic activity is linked to increased cognitive function and increased density of microvessels in specific regions of the brain. VEGF, insulin like growth factor 1 (IGF-1), brain-derived neurotrophic growth factor (BDNF), and endothelial nitric oxide synthase (eNOS) are thought to be key regulators of neurogenesis and angiogenesis.
BBB: blood–brain barrier; VEGF: vascular endothelial growth factor.