Proceedings of The Physiological Society

University College London December 2005 (2006) Proc Physiol Soc 1, PC28

Poster Communications

Cerebral haemodynamics and neurovascular headache: modulation by exercise and hypoxia

Ainslie, Philip N; Evans, Kevin A; Fall, Lewis; Martins, Pedro; Kewley, Emily; Bailey, Ben; Bailey, Damian M;

1. Department of Physiology, University of Otago, Dunedin, New Zealand. 2. Department of Physiology, University of Glamorgan, Pontypridd, United Kingdom.


  • Table 1. Cerebrovascular responses during hypoxia and exercise
    Values are means

Inspiratory hypoxia and exercise independently increase perfusion of cerebral capillaries which may result in 'autoregulatory breakthrough' similar to that encountered in hypertensive encephalopathy. In the present study, we tested the hypothesis that these stimuli would act synergistically to increase intracranial pressure (ICP) and impair cerebral autoregulation (CA) in those individuals susceptible to hypoxic headache (HHS). In 18 males, CA and estimated ICP (eICP) were assessed at rest in normoxia (N-REST), after 6h passive exposure to 12% oxygen (H-REST), and immediately following a cycling test to exhaustion (H-EXERCISE). A dynamic rate of CA was calculated from continuous recordings of blood flow velocity in the middle cerebral artery (MCAv; transcranial Doppler) and arterial blood pressure (ABP; plethysmography) during transiently induced hypotension. Estimated cerebral perfusion pressure (eCPP) was calculated from the formula: eCPP = mean MCAv x (mean ABP  diastolic ABP)/ (mean MCAv  diastolic MCAv). eICP was calculated from: mean ABP - eCPP. Headache was diagnosed using a clinically validated visual analogue scale. Nine subjects were clinically diagnosed as HHS during passive exposure to hypoxia whilst eight subjects remained resistant to HH (HHR). As highlighted in Table 1, CA was moderately impaired in the HHS group during hypoxia which was related to the severity of headache (r = 0.77; P < 0.05). In contrast, CA was unchanged in the HHR group. Hypoxia and exercise did not influence eICP in either group and there were no relationships observed between the changes in eICP, CA or headache symptoms. In conclusion, passive exposure to hypoxia resulted in a moderate impairment of CA which may have increased susceptibility to HH independently of eICP.

Where applicable, experiments conform with Society ethical requirements