Mechanisms governing cerebral blood velocity during cycling and running : the role of arterial CO₂ and blood pressure

During most forms of exercise, changes in middle cerebral artery velocity (MCAv) are primarily driven by alterations in arterial carbon dioxide (PaCO₂); however, there may be an uncoupling between MCAv and PaCO₂ during running. The mechanisms driving this response could relate to brain sensitivity to changes in PaCO₂, mean arterial pressure (MAP), or exercise modality. Therefore, I investigated two questions 1) wheather the MCAv increases proportionally with PaCO₂ and MAP during cycling and running; and 2) wheather the MCAv-PaCO₂ relationship differs among rest and moderate-intensity cycling and running? Twelve participants (7M/5F) completed cycling (52.3±6.7 mL/min/kg) and running (54.5±6.8 mL/min/kg) maximal oxygen consumption tests (VO₂max). Bilateral MCAv and intra-arterial pressure were measured during a hypocapnia sensitivity test at rest and ~57% of steady-state VO₂max. Additionally, participants completed staged cycling and running targeting 35%, 50%, 65%, 80%, and 95% of VO₂max. MCAv increased from rest to 35% of VO₂max and remained stable within ~2 cm s⁻¹ for both cycling (58.3±8.1 to 67.5±11.3 cm s⁻¹, p<0.001) and running (56.3±6.8 to 62.2±7.8 cm s⁻¹, p=0.006). The change in PaCO₂ peaked at 35% in cycling (+1.7±2.1 mmHg, p=0.13) and 50% in running (+1.4±1.4 mmHg, p=0.04), before declining below resting levels at 95% of VO₂max (cycling: -3.8±2.7 mmHg, p=0.016; running: -2.1±3.5 mmHg, p=0.44) and the absolute PaCO₂ response was significantly different between cycling and running (p=0.01). Meanwhile, MAP increased by ~33% in cycling (89.5±7.3 to 119.2±10.8 mmHg, p<0.001) and ~ 28% in running (94.2±6.3 to 120.4±10.0 mmHg, p<0.001) from rest to 95% VO₂max. A mediation analysis was used to evaluate the effects of workload on changes in PaCO₂ and MAP, revealing that their combined indirect effect on changes in MCAv accounted for ~20% and ~-4% of the total change during cycling and running. The MCAv-PaCO₂ slope increased similarly from rest to exercise in both cycling (1.29±0.30 to 1.76±0.40 cm s⁻¹/mmHg, p=0.001) and running (1.25±0.30 to 2.09±0.90 cm s⁻¹/mmHg, p=0.008). Dynamic exercise augments cerebrovascular PaCO₂ sensitivity and increases MCAv independent of PaCO₂. We speculate that the additional, unaccounted-for elevations in MCAv during cycling and running are mediated by increases in cerebral metabolic demand.