Orthostatic stress and radial acceleration (+Gz) exposure are associated with cerebral hypoperfusion, which is believed to cause syncope or G-induced loss of consciousness (G-LOC). This study aimed to investigate the relationship between hemodynamic responses to Squat-Stand Test (SST) and +Gz tolerance as cerebral oxygenation debt measured by near-infrared spectroscopy (NIRS). Ten healthy male pilots participated in Japan Air Self-Defense Force centrifuge training and volunteered for the study. Subjects performed SST before the 4 consecutive centrifuge training days. Continuous finger arterial pressure and frontal cortical oxyhemoglobin concentration (O₂Hb) changes were recorded during SST. The centrifuge profiles include gradual onset run (GOR: onset rate of 0.1 G・s^-1) with a maximum of up to 8 G, and rapid onset runs (ROR) with the onset rate varying from 1 to 6 G･s^-1. Maximum +Gz and sustaining duration varied from 4 to 8 G, and from 8 s to 30 s respectively in these RORs. Cerebral O₂Hb was also monitored during the first day profiles including GOR and ROR without anti-G system. All the subjects completed SST without any symptoms, however six subjects terminated the ROR profile at 6 or 7 G with G-LOC. In the posture change from squatting to standing during SST, O₂Hb and mean arterial pressure (MAP) decreased by -7.7 ± 2.5 μmol･L^-1 (Mean ± SD) and -46.2 ± 7.8 mmHg respectively from 4 min seated baseline levels. In the recovery phase (20-30 s after stand), O₂Hb and MAP increased by 4.7 ± 3.4 μmol･L^-1 and 34.4 ± 11.6 mmHg respectively from the stand nadir. The recovery MAP was significantly less in G-LOC subjects (27.4 ± 8.7 mmHg, n = 6) than in the complete group (44.9 ± 5.82 mmHg, n = 4). The significant linear correlation was observed between recovery MAP and O₂Hb decrement at 5 G exposure in ROR (r = 0.66, p < 0.05). The stand nadir O₂Hb was significantly correlated with O ₂Hb decrement at 5 G (r = 0.65, p < 0.05). These parameters were also correlated with the +Gz levels at peripheral light loss (gray out) with straining in GOR. The results showed that higher cerebral oxygenation debt and delayed blood pressure recovery during SST caused lower G-tolerance. Cerebral oxygenation changes and hemodynamic responses during SST may provide valuable information on +Gz tolerance.

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