Current models of cerebral blood flow (CBF) regulation at the onset of exercise suggests more than a ~50 second delay in the CBF response (1). When compared to other autoregulatory challenges [thigh cuff release and sit-to-stand test], CBF is restored within 20 seconds (2,3). Rest-to-exercise transition induces a brief hypotensive response due to rapid vasodilation of the periphery. Within this context, an investigation into the early blood flow adaptation during the onset of exercise is warranted as previous monoexponential modeling may have omitted these potentially important responses. PURPOSE: The purpose of this study was to identify if exercise-onset-induced hypotension activates a cerebrovascular response prior to monoexponential increases in CBF. METHODS: 7 healthy adults (24 ± 4.1 yrs) completed 2 minutes of quiet rest (baseline, BLN) then cycled for 3-min at 50W on a recumbent cycle ergometer. Middle cerebral artery velocity, a surrogate for CBF (MCAv; transcranial Doppler ultrasound) and mean arterial pressure (MAP; finger photoplethysmography), were measured on a beat-by-beat basis to calculate CVCi = (MCAv/MAP)*100mmHg. End-tidal CO2 was measured using breath-by-breath capnography (ETCO2). Results were analyzed using a paired samples t-test, significance was set at p≤0.05. RESULTS: Data are mean ± S.D. Both MCAv and MAP significantly decreased from BLN (MCAvNADIR -4.4 ± 4.4 cm/s Δ from MCAvBLN, p=0.01; MAPNADIR-10.7 ± 6.3 mmHg Δ from MAPBLN, p=0.001). The MAPNADIR occurred at 10.3 ± 2.6 sec. The CVCi at MCAvNADIR was not different than BLN (73.4 ± 7.6 vs. 72.4 ± 12, p=0.7). However, CVCi at MAPNADIR was elevated compared to BLN (84.7 ± 8.5 VS. 73.4 ± 7.6, p=0.02). ETCO2 did not change within the same timeframe. DISCUSSION: These results indicate the drop in CBF at the onset of exercise is primarily due to exercise-onset-induced hypotension, as opposed to changes in end-tidal CO2. Further, there is activation of vasoregulatory mechanisms that blunt cerebral hypoperfusion at exercise onset. Therefore, monoexponential models overlook potentially significant cerebrovascular countermeasures occurring prior to model predicted blood flow increase.