My interests focus on three interacting areas of human cardiovascular research: i) endothelial function, ii) autonomic function and iii) the physiological effects of psychosocial stress. The vascular endothelium is a single layer of cells that lines all of the blood vessels in the body. It exerts local control over vascular tone and also plays a key role in modulating atherosclerosis development. One branch of my research is aimed at i) improving our understanding of how the endothelium responds to changes in blood flow, ii) improving endothelial function assessment in humans, and iii) understanding how endothelial function changes with disease. The sympathetic branch of the autonomic nervous system increases heart rate and causes vasoconstriction. Acute changes in sympathetic nervous activity occur during exercise and are essential for blood pressure regulation. In contrast, the chronically elevated sympathetic nervous activity observed in some disease states (e.g. congestive heart failure and sleep apnea) contributes to pathological vascular adaptations. My interests lie in understanding how acute and chronic sympathetic nervous activation influence vascular tone, compliance and endothelial function. Psychosocial stress is associated with the development of cardiovascular disease, although the physiological basis of this connection is not fully understood. Initially focused on basic, mechanistic questions, this research will lead to an investigation of the ability of stress reduction interventions (e.g. stress management counselling) to improve physiological measures of cardiovascular function and health.
Laboratory: Cardiovascular Stress Response Laboratory - School of Kinesiology and Health Studies
Accepting students at the master's and PhD level for September 2015-2016.
Canada Foundation for Innovation
Natural Sciences and Engineering Research Council of Canada (NSERC)
F. Jazuli and K.E. Pyke (2011). The impact of baseline artery diameter on flow-mediated vasodilation: A comparison of brachial and radial artery responses to matched levels of shear stress. American Journal of Physiology. 301(4): H1667-77
K.E. Pyke and F. Jazuli (2011). Impact of repeated increases in shear stress via reactive hyperemia and handgrip exercise: No evidence of systematic changes in brachial artery FMD. American Journal of Physiology 300 (3): H1078-1089
D. H.J. Thijssen, M.A. Black, K. E. Pyke, J. Padilla, G. Atkinson, R. A. Harris, B. Parker, M. E. Widlansky, M. E. Tschakovsky, D.J.Green. (2011) Assessment of flow mediated dilation (FMD) in humans: A methodological and physiological guideline. American Journal of Physiology 300(1): H2-12.
K.E.Pyke. Are we still on the fence or can we open the gate? Evidence that QRS-gating in FMD analysis is not essential. Journal of Applied Physiology. 109(4): 945-6 Free link to article
K.E. Pyke, Green, D., Weisbrond, C, Best, M. Dembo, L., O'Driscoll, G. and Tschakovsky, M.E. (2010). Nitric oxide is not obligatory for radial artery flow-mediated dilation following release of 5 or 10 min of distal occlusion. American Journal of Physiology, Heart and Circulatory Physiology. 298(1):H119-26
K.E.Pyke, J.A.Hartnett, and M.E.Tschakovsy. (2008). Are the dynamic response characteristics of brachial artery FMD sensitive to the magnitude of the increase in SS? Journal of Applied Physiology. 105(1): 282-92.
K.E.Pyke, V.Poitras and M.E.Tschakovsky. (2008). Brachial artery flow mediated dilation during handgrip exercise: evidence for endothelial transduction of the mean shear stimulus. American Journal of Physiology, Heart and Circulatory Physiology. 294(6): H2669-79.
K.L. Walker, N.R. Saunders, D. Jensen, J.L. Kuk, S.L. Wong, K.E.Pyke, E.M. Dwyer, M.E. Tschakovsky. (2007). Do vasodilatory mechanisms in human muscle compensate for changes in arterial perfusion pressure? American Journal of Physiology, Heart and Circulatory Physiology. 293(5) H2928-36.
K.E. Pyke and M.E. Tschakovsky. (2007). Peak vs. total reactive hyperemia: which determines the magnitude of flow mediated dilation? Journal of Applied Physiology. 102(4): 1510-1519.
D.J. Green; A.J. Maiorana; M.E. Tschakovsky; K.E. Pyke; C.J. Weisbrod and G. O’Driscoll. (2006). Relationship between changes in brachial artery flow mediated dilation and basal release of nitric oxide in type II diabetic subjects. American Journal of Physiology, Heart and Circulatory Physiology. 291(3) H1193-9.
K.E. Pyke and M.E.Tschakovsky. (2005). The shear stress FMD relationship: Implications for FMD as an assessment of endothelial function. Journal of Physiology. 568(2); 357-69.
M.E. Tschakovsky and K.E. Pyke. (2005). Counterpoint: Flow-mediated dilation does not reflect nitric oxide-mediated endothelial function. Journal of Applied Physiology. 99(3):1235-7.
N.R. Saunders, K.E., Pyke, M.E. Tschakovsky. (2005). Dynamic response characteristics of local blood flow regulatory mechanisms in human forearm exercise. Journal of Applied Physiology. 98(4) 1286-96.
N.R. Saunders, F.A. Dinenno, K.E. Pyke, A.M. Rogers, M.E. Tschakovsky. (2005). Impact of combined NO and PG blockade on rapid vasodilation in a forearm mild to moderate exercise transition in humans. American Journal of Physiology; Heart and Circulatory Physiology. 288(1) H214-20.
K.E. Pyke, E.M. Dwyer and M.E. Tschakovsky. (2004). Impact of controlling shear rate on flow-mediated dilation in the brachial artery of humans. Journal of Applied Physiology. 97(2), 499-508.
M.E. Tschakovsky, A.M.Rogers, K.E.Pyke, N.Glenn, S.J.Lee, T. Weissgerber, and E.M. Dwyer. (2004). Immediate exercise hyperemia in humans is contraction intensity dependent: evidence for rapid vasodilation. Journal of Applied Physiology. 96(2), 639-634.