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Protective Effect of Exercise Training Against Age-induced Cerebral Microvascular Rarefaction: VEGF/Flk-1/PI3K/Akt
Sheepsumon Viboolvorakul1, Decha Buranajitpirom2, Suthiluk Patumraj3
1Physiology Unit, Department of Medical Science, Faculty of Science, Rangsit University, Pathum Thani, Thailand; sheepsumon.v@rsu.ac.th.
In Vivo (Athens, Greece)
|February 27, 2026
Summary
Exercise training combats age-related brain microvascular loss by enhancing blood flow and vessel density. Swimming increases vascular endothelial growth factor (VEGF) signaling, promoting brain health in aging rats.
Area of Science:
- Neuroscience
- Gerontology
- Cardiovascular Science
Background:
- Age-related decline in cerebral microvasculature impairs brain function.
- Reduced angiogenesis and vascular endothelial growth factor (VEGF) contribute to this decline.
- Exercise is known to benefit brain health, but mechanisms in aging are unclear.
Purpose of the Study:
- To investigate exercise's impact on aging brain microvessel density.
- To assess exercise effects on cerebral tissue perfusion (CTP).
- To explore exercise's influence on VEGF-mediated angiogenic signaling.
Main Methods:
- Male rats were grouped into age-matched control, sedentary control, and exercise-trained (swimming).
- Cerebral tissue perfusion (CTP) was measured in vivo.
- Immunohistochemistry for GLUT1 and immunoassays for VEGF angiogenic proteins were performed.
Main Results:
- Sedentary aging reduced microvessel density and CTP.
- Exercise training significantly increased microvessel density and CTP.
- Exercise elevated VEGF angiogenic proteins and GLUT1, indicating restored endothelial function.
Conclusions:
- Swimming exercise may prevent age-related cerebral microvascular loss via VEGF signaling.
- Exercise restores structural and metabolic endothelial function in the aging brain.
- Increased GLUT1 suggests improved endothelial metabolic health post-exercise.
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