Why the study?
During aerobic exercise, the extent to which central hemodynamics and CO2 partial pressure contribute to middle cerebral artery blood velocity response was unknown.
Central hemodynamics and end-tidal CO2 primarily contribute to middle cerebral artery blood velocity during the steady-state phase of aerobic exercise, but not during the initial dynamic response.
Modeling indicates PETCO2 drives MCAv kinetics more than MAP during exercise transitions; leaves open whether CO2 modulation alters cerebral perfusion in patients.
During aerobic exercise, central hemodynamics and CO2 partial pressure are central to middle cerebral artery blood velocity (MCAv) response. Still, the extent of their contribution is unknown. The purpose of this study was to characterize and utilize statistical modeling to determine the contribution of heart rate (HR), mean arterial pressure (MAP), and end-tidal CO 2 (P ET CO 2 ) dynamics to MCAv dynamics. Three randomized exercise bouts were completed on a recumbent stepper at 30-40% (Low), 45-55% (Mod1), and 60-70% (Mod2) of estimated HRmax. A 90-s resting period was followed by 6-min of continuous exercise within the estimated HR ranges. HR, MAP, P ET CO 2 , and MCAv exercise dynamics were modeled with a monoexponential curve. From this modeling, the baseline ( BL ), time delay ( TD ), time constant (τ), and steady-state ( SS ) responses were determined. Backward AIC linear regression models determined contributing dynamics. Seventeen healthy adults completed all exercise bouts (28 ± 6 yrs, 8 females). The time from initiation of exercise to an exponential increase in HR (HR TD ) was significantly longer for Low than Mod2 (p=0.047). The time constant for the rise in HR (HRτ) was significantly shorter for Low than Mod1 and Mod2 (p=0.01). The absolute change in HR from baseline to steady-state (HR SS ) was significantly lower for Low than Mod1 and Mod2 (p<0.001), and Mod1 was significantly lower than Mod2 (p<0.001). MAP SS was significantly lower for Low than Mod1 (p=0.01) and Mod2 (p<0.001). Exercise intensity, HR TD , and MAP TD accounted for 17% of variation for MCAv TD (p=0.01). HR TD , P ET CO 2TD , and MCAv TD accounted for 21% of variation MCAvτ (p<0.01). MCAvτ, MAP SS , and P ET CO 2SS accounted for 60% of variation for MCAv SS (p<0.001). Throughout the MCAv dynamic response pathway central hemodynamics and end-tidal CO 2 do not account for most MCAv response until the steady-state phase. Thus, other physiological factors should be considered with assessing cerebrovascular function during aerobic exercise.
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Aaron et al. (2023) studied this question.
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