To clarify the role of O2 stores in the fluctuations in VO2 observed with changing posture, O2 intake (Veo2) and pulmonary capillary O2 transfer (Vpco2) were calculated breath by breath with a box-balloon sprometer and mass spectrometer. Changes in O2 stores of the lungs (O2L) and blood (O2b) were computed assuming metabolic rate (Vco2) constant (O2L = Veo2 - Vpco2; O2b = Vpco2 - Vco2). Measurements were made before, during, and after passive tilt to 60 degrees and on return to recumbency after 10 min erect. From supine to upright O2L increased rapidly and O2b dropped slowly, creating a net deficit in Veo2 of 130 ml in 10 min. Return to supine caused rapid loss in O2L and gain in O2b with a net Veo2 excess of 117 ml. Shifts in O2b were 2.5 times greater but opposite to shifts in O2L. Changes in O2b result from shifts in blood volume and flow more than from changes in cardiac output. Refilling of O2b, matching loss while upright, caused transient hypoxia with significant hyperpnea.