(888.18) Cerebrovascular Dynamics During Light Exercise

Poster Board Number: E356

John Ashley (University of Oklahoma), Joe Shelley (University of Oklahoma), Jiwon Song (University of Oklahoma), Jongjoo Sun (University of Oklahoma), Courtney Adler (University of Oklahoma), J. Mikhail Kellawan (University of Oklahoma)

Cerebral blood flow (CBF) dynamic response to moderate-intensity exercise has a time delay (TD) of ~ 40s. This is dramatically longer compared to other physiological responses to exercise (e.g. skeletal muscle blood flow lt;10 s) and CBF response to other stimuli (e.g. hypercapnia, thigh cuff occlusion, ~ 10-20 s). A possible explanation is that a rest-to-exercise transition induces a brief hypotensive response due to intensity dependent rapid vasodilation of the periphery (exercise-onset hypotension, EoH).

Purpose: To determine if the magnitude and timing of EoH, effectively reduces CBF at exercise onset causing the longer observed TD. To test this, we modelled CBF kinetic response to light-intensity exercise to mitigate the magnitude of EoH and determine if components of the CBF response were quickened in young healthy adults.

Methods: 26 young healthy adults (13 Women, 23.8 ± 4 yrs; 23.9 ± 2.9 kg/m2) completed a rest (2min seated quietly, BL) to exercise (3 minutes at 50W, EX) transition on a recumbent cycle ergometer. Middle cerebral artery velocity (MCAv; transcranial doppler) and mean arterial pressure (MAP; finger photoplethysmography) were measured on a heartbeat-by-heartbeat basis. End-tidal CO2 (EtCO2) was measured using breath-by-breath capnography. Cerebral vascular conductance index (CVCi) was calculated as (CVCi = MCAv/MAP *100 mmHg). Change in MCAv data (ΔMCAv = MCAvEX-MCAvBL) were averaged into 2 s bins and fit to a monoexponential model (ΔMCAv(t)= Amp(1-e-(t-TD)/ τ)). Time delay (TD), tau (τ), and mean response time (MRT = TD + τ) were obtained from the model. Several subjects (N=11) exhibited little to no TD (TD lt; 1 s), these subjects (FAST) were separated out and compared to individuals with longer TDs (TD ≥ 3 s; SLOW). Comparisons were made using an independent t-test.

Results: All data is mean±SD. In total, subjects exhibited a TD of 15.4 ± 18.2 s, τ of 79.8 ± 139.7, and MRT of 95.3 ± 134.9 s. This coincided with a ΔMAPNADIR (-14.5 ± 8.2 mmHg), ΔMCAvNADIR (-5.7 ± 5.8 cm/s) which occurred at similar times (14.0 ± 17.2 vs. 18.6 ± 14.4 s; p=0.30 MAPNADIR vs. MCAvNADIR), and ΔCVCiMAX (25.3 ± 34.0 cm/s/100mmHg). When data were split, the FAST group experienced a faster TD compared to SLOW (0.01 ± 0.01 vs. 26.8 ± 16.4 s; plt;0.001). ΔMCAvNADIR although different (-1.0 ± 4.0 vs. -9.1 ± 4.2 cm/s; plt;0.001, FAST vs. SLOW), occurred at similar times (20.5 ± 17.3 vs. 17.3 ± 12.5 s; p=0.59, FAST vs. SLOW). ΔMAPNADIR (-14.4 ± 10.4 vs. -14.6 ± 6.5 mmHg; p=0.97) and CVCiMAX (22.1 ± 25.4 vs. 27.6 ± 39.9 cm/s/100mmHg; p=0.56 FAST vs. SLOW) were not different between groups. There were no other differences between groups regrading demographic, EtCO2, or other kinetic variables.

Discussion: Our data indicates EoH is related to the initial drop in CBF and TD during light-exercise is faster (15.9 s) when compared to previous research during moderate-intensity exercise (~40 s). However, our data identifies fast responders who have minimal TD and MCAvNADIR responses without differing EoH at the same absolute exercise intensity. Therefore, these data reveal monoexponential CBF models ignore initial perturbances to CBF and disregard potentially important cerebrovascular mechanisms occurring prior to model predicted blood flow increases.