Thesis Defence: Mechanisms Governing Cerebral Blood Velocity During Cycling and Running

Justin Monteleone, supervised by Dr. Philip Ainslie, will defend their thesis titled “Mechanisms Governing Cerebral Blood Velocity During Cycling and Running: The Role of Arterial CO₂ and Blood Pressure” in partial fulfillment of the requirements for the degree of Master of Science in Health and Exercise Sciences.

An abstract for Justin Monteleone’s thesis is included below.

Defences are open to all members of the campus community as well as the general public. Registration is not required for in-person defences.

Abstract

During 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 the sensitivity of the brain to changes in PaCO₂, mean arterial pressure (MAP), or differences in exercise modality. Therefore, we investigated whether 1) does the MCAv increases proportionally with PaCO₂ and MAP during cycling and running, and 2) does 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 both progressively declining to below resting levels at 95% of O2max (cycling: -3.8±2.7 mmHg, p=0.016; running: -2.1±3.5 mmHg, p=0.44). 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. 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. No differences were observed in the MCAv, PaCO2, and MAP responses to staged exercise between cycling and running. We speculate that additional, unaccounted-for elevations in cerebral perfusion during cycling and running are mediated by increases in cerebral metabolic demand.