Proceedings of The Physiological Society

University of Oxford (2011) Proc Physiol Soc 23, PC213

Poster Communications

Neurovascular coupling and distribution of cerebral blood flow during exercise

C. K. Willie1, E. C. Cowan2, P. N. Ainslie1, C. E. Taylor3, K. J. Smith1, P. Y. Sin4, Y. Tzeng4

1. Human Kinetics, University of British Columbia Okanagan, Kelowna, British Columbia, Canada. 2. School of Medicine and Dentistry, University of Aberdeen, Aberdeen, United Kingdom. 3. Research Institute for Sport and Exercise Science, Liverpool John Moore's University, Liverpool, United Kingdom. 4. Cardiovascular systems laboratory, University of Otago, Wellington, New Zealand.


There is a ~20% increase in global cerebral blood flow (CBF) during exercise that is thought to be principally due to increases in neural activation. There is evidence, however, that the increased CBF may be different between the anterior and posterior cerebral territories, perhaps because neuronal activation is locally coupled to changes in blood flow. This neuro-metabolic coupling is termed neurovascular coupling (NVC), and can be assessed with simple visual stimulation tasks, such as reading. It is not understood, however, how changes in baseline CBF influence this regional blood supply regulation, and also if exercise-induced CBF increase is a global or regional phenomenon. In ten healthy subjects (5 male; aged 25 ± 7 [mean ± SD]; body mass index 22 ± 2 kg m-2) blood velocities (transcranial Doppler ultrasound) in the posterior and middle cerebral arteries (PCAv and MCAv, respectively) were recorded. The P1 segment of the PCA was located on the right and left hemispheres, and the best signal used for measurement of PCA blood velocity. The MCAv was measured on the contralateral side 10mm distal to the MCA/anterior cerebral artery bifurcation. Arteries were confirmed using ipsilateral carotid compression to verify a velocity reduction in the MCA and increased velocity in the PCA. Heart rate (ECG), beat-to-beat blood pressure (Finipres), and end-tidal PCO2 were recorded throughout. NVC was quantified as the change in systolic PCAv to a visual stimulus. Following 2 minutes of baseline measures, five cycles of 40 seconds reading, 20 seconds eyes-closed with concomitant measurement of PCAv and MCAv were completed during both rest and steady-state exercise on an upright stationary bike at ~60% of estimated maximal oxygen consumption. Although PCAv was shifted to higher velocities during exercise, the relative change in PCAv with visual stimulation, and time to peak response, was not different between exercise and rest (resting delta PCAv: 9.3 ± 4.4 cm/s, 11.5 ± 3.2 s to peak; exercise delta PCAv: 9.2 ± 3.8 cm/s, 9.1 ± 2.4 s to peak). At rest mean MCAv was 55.8 ± 10.3 cm/s and PCAv 38.0 ± 7.3 cm/s. With steady-state exercise, MCAv increased by 15.2 ± 13.6% from baseline versus 26.1 ± 22.5% for PCAv (P<0.05). These data indicate that there is a regionally heterogenous increase in CBF during exercise that does not impose any restriction to a visual-stimulus induced increase in occipital cortex blood flow; exercise does not disrupt neurovascular coupling. Since NVC has been found to be a useful marker of cerebrovascular disease, our findings provide the first documentation of NVC during exercise, and consequently provides a useful point of reference for comparison against pathology.

Where applicable, experiments conform with Society ethical requirements