Brain aging is associated with reduced vascular reactivity, exacerbated brain energy deficits and cognitive decline. However, it is still unclear how normal aging impacts neurovascular function and its underlying mechanism, especially in the awake brains. It is also unknown whether arteries and capillaries undergo different age-related structural and functional remodeling. Using laser speckle contrast imaging and two-photon imaging in awake, behaving young adult and aged mice, we show that neurovascular coupling (NVC) responses in the aged brain are prolonged, with reduced amplitudes, and this is more pronounced at the capillaries than at the arteries. Compared with anesthetized state, the total flow change of NVC at both arteries and capillaries are preserved in the awake aged brains.  Furthermore, the NVC response is mediated by Ca²⁺ signaling in vascular mural cells, i.e. vascular smooth muscle cells and pericytes. We revealed a different Ca²⁺ kinetics of vascular mural cells in young adult and aged mice. The rate of calcium transport and the calcium sensitivity of vascular mural cells are reduced in aged mice, which explains the reduced and prolonged vasodilation. Structurally, we further revealed the retraction of transitional point from contractile to non-contractile mural cells at aged capillaries. Lastly, the vascular and Ca²⁺ responses triggered by spontaneous behavior such as locomotion also exhibits consistent prolonged characteristics. In all, our data suggests that the altered NVC responses in the aged awake brain is associated with remodeling of Ca²⁺ signals and vascular coverage of contractile mural cells. Novel interventions to delay age-related brain pathology could be based on fully harnessing the power of the vascular remodeling mechanisms with age.