Figure 1.
Acute molecular effects of exercise on blood vessels. During exercise, increased arterial blood flow leads to an elevation of blood pressure (greater hydrostatic pressure), luminal shear stress, and arterial wall stress. The consequence is a vasodilation predominantly in the resistance arteries (mainly due to a greater release of nitric oxide (NO) and prostacyclin (PGI2) from the endothelial cells and dilation of the smooth muscle cells). In addition, during exercise, changes in neural, metabolic, and humoral factors take place in both the micro- and macrovascular circulation. All these changes contribute to acute adaptations in arterial function, diameter, and wall thickness. NO: nitric oxide, PGI2: prostacyclin I2, NPY: neuropeptide Y, GABA: Gamma-aminobutyric acid, ATP/AMP: Adenosine triphosphate/Adenosine monophosphate; [Ca2+]: intracellular calcium.