M.Sc. [Human and applied physiology] (King’s College London)
Ph.D. [Exercise physiology and metabolism] (Liverpool John Moores University)
Professor, School of Health and Exercise Sciences, University of British Columbia Okanagan
Canada Research Chair in Cerebrovascular Physiology
Co-Director, Centre for Heart, Lung & Vascular Health, University of British Columbia Okanagan
Research InterestsCardiovascular health; cerebral blood flow regulation; cerebrovascular function
Dr. Philip Ainslie’s research is focused on the integrated mechanisms that regulate human cerebral blood flow in health and disease, the influence of environmental stress, and the effects of exercise training on cerebrovascular function.
Dr. Philip Ainslie is a Professor in the School of Health and Exercise Sciences at UBC Okanagan, the Co-Director of the Centre for Heart, Lung & Vascular Health, and an ICORD Investigator. His Ph.D. (in exercise physiology & metabolism) was a collaborative project between the Liverpool John Moores University, University of Manchester and University of Oxford. Following completion of a post-doctoral research fellowship at the University of Calgary he began a faculty position in 2005, as Lecturer and Principal Investigator in the Department of Physiology at the University of Otago, New Zealand. Here, he established his independent research program, focusing on the integrative mechanisms that regulate human cerebral blood flow. In 2009, he returned to Canada, taking a faculty post in School of Health and Exercise Sciences at the UBC Okanagan.
Over the last five years, Dr. Ainslie’s most significant themes of research contributions include:
- How blood pressure (BP) influences cerebral blood flow (CBF): The traditional concept of cerebral autoregulation (CA) was constructed from data taken across different groups and included drugs known to affect CBF , and warranted further investigation. By incrementally lowering and rising BP, Dr. Ainslie discovered that the healthy human cerebral pressure-flow relationship resembled a finite slope [2,3] rather than a flat plateau  and that: 1) the brain can buffer rising BP much better than falling BP , and 2) larger extra-cranial arteries assist in CA . New evidence indicates that vascular properties (e.g., compliance) influence CA , therefore, his lab developed a new mathematical models to assess CA [5,6,7]. Dr. Ainslie’s research has partly transformed the canonized views of CA, and he has published methodological guidelines in this area [7,8].
- The link between respiration, CO2 and CBF: Dr. Ainslie’s lab is the first to document the relationship between hypocapnia and hypercapnia and regional change in CBF at rest , during heat  and orthostatic stress . We have found in humans that: 1) the prevailing level of BP can markedly influence the brains reactivity to both hypocapnia and hypercapnia ; 2) CBF is a function of extravascular pH rather than just arterial pH or PaCO2 ; and 3) the brain can effectively extract more O2 to compensate for the hypocapnia-induced reductions in CBF . His lab’s methodological guidelines on the correct assessment for interpretation of CBF measures and chemoreflex reactivity  has been cited >200 times.
- Oxygen and the brain: For the first time, Dr. Ainslie showed that at sea level and at high altitude that: 1) for a given level of hypoxemia, there is a preferential increase in brainstem blood flow [5,14] to ensure a well-maintained cerebral oxygen delivery; and 2) at high altitude cerebral metabolism is supported almost exclusively by carbohydrate oxidation during severe levels of hypoxemia , however, during exercise, the brain appears to increase non-oxidative metabolism during exercise and recovery . Dr. Ainslie has highly cited review articles on this topic [16,17].
- Development of innovative techniques: Dr. Ainslie’s lab [5,18] and others  have challenged the assumption that the diameter of the middle cerebral artery (MCA) does not change during changes in CO2 and O2. Dr. Ainslie has adapted duplex vascular ultrasound  and colour-coded Doppler ultrasound  approaches to assess dilation of larger extra-cranial neck vessels and the MCA respectively, during hypoxia, as a means to monitor reactivity and vessel dilation not viable via TCD . These new approaches, combined with MRI, will provide new insight into the mechanisms regulating CBF.
References: 1. Physiol Rev 39,183(1959); 2. Hypertension 55,698 (2010); 3. Med Eng Phys 36,1487 (2014); 4. Hypertension 56,268 (2010); 5. J Physiol 590,3261 (2012); 6. J Physiol 589,3263 (2011); 7. Am J Physiol Heart Circ Physiol 303,658 (2012); 8. Med Eng Phys 36,620(2014); 9. J Appl Physiol 115,653 (2013); 10. J Physiol 592,5203 (2014); 11. J Appl Physiol 113,1058 (2012); 12. J Cereb Blood Flow and Metab 35,66 (2015); 13. Am J Physiol Regul Integr Comp Physiol 296,1473 (2009); 14. Clin Sci (Lond) 126,661 (2014); 15. J Physiol 592,5507 (2014); 16. Exp Physiol 95,251 (2010); 17. High Alt Med Biol 15,133 (2014); 18. J Appl Physiol 116,905 (2014); 19. J Cereb Blood Flow and Metab 31,2019 (2011).
Techniques Employed in the Lab
- Duplex ultrasound
- End-tidal forcing
- Vascular function testing
- Brain arterial-venous difference measures
- Molecular quantification of free radicals
- Canada Research Chair
- CSEP Young Investigator (2011)
- UBC Researcher of the Year (2012)
Current Lab Members
|Undergraduate Students||Master Students||Ph.D. Students||Postdoctoral Fellows|
|Connor Howe||Matt Reiger||Ryan Hoiland||Nia Lewis|
|Hannah Caldwell||Alex Hansen||Mike Tymko||Chris Willie|
|Geoff Coombs||Katelyn Wood|
|Myp Sekhon (MSD)|
- Bain, AR et al.. 2017. Forced vital capacity and not central chemoreflex predicts maximal hyperoxic breath-hold duration in elite apneists.. Respir Physiol Neurobiol. doi: 10.1016/j.resp.2017.02.015.
- Brassard, P et al.. 2017. Evidence for Hysteresis in the Cerebral Pressure-Flow Relationship in Healthy Men.. Am. J. Physiol. Heart Circ. Physiol. doi: 10.1152/ajpheart.00790.2016.
- Bain, AR et al.. 2016. Role of cerebral blood flow in extreme breath holding.. Transl Neurosci. doi: 10.1515/tnsci-2016-0003.
- Hoiland, RL et al.. 2017. Adenosine receptor dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans.. J. Appl. Physiol. doi: 10.1152/japplphysiol.00840.2016.
- Bain, AR et al.. 2017. Hypercapnia is essential to reduce the cerebral oxidative metabolism during extreme apnea in humans.. J. Cereb. Blood Flow Metab. doi: 10.1177/0271678X16686093.