Significance Sensory stimulation generates a robust decrease in oxygen concentration (pO 2 initial dip) in brain tissue of anesthetized cats and rodents. This dip reports local activation of neurons much better than the delayed pO 2 increase associated with functional hyperemia. Here, we reinvestigated the issue in animals that recovered from acute surgery using two-photon lifetime microscopy. Targeting a distinct neuronal network that is the site of strong activation and energy consumption, we show that in anesthetized animals the pO 2 initial dip is present but extremely small in juxtasynaptic capillaries. In awake animals, it is no longer detectable in vessels or in the neuropil. This demonstrates that in healthy animals, neurovascular coupling is too fast and efficient to reveal a pO 2 initial dip.