Neurovascular Responses Following Acute Hypoxia Open Access
- Other title
Sympathetic Nervous System
- Type of item
- Degree grantor
University of Alberta
- Author or creator
Skow, Rachel J
- Supervisor and department
Steinback, Craig (Faculty of Physical Education and Recreation)
- Examining committee member and department
Kennedy, Michael (Faculty of Physical Education and Recreation)
Delorey, Darren (Faculty of Physical Education and Recreation)
Physical Education and Recreation
- Date accepted
- Graduation date
Master of Science
- Degree level
Introduction: The sympathetic nervous system is the primary regulator of the "fight or flight" response, with muscle sympathetic nerve activity (MSNA) increasing in response to various stressors, including low oxygen (hypoxia; HX). MSNA is an important regulator of cardiovascular function, whereby an acute increase in MSNA constricts blood vessels and increases arterial blood pressure (ABP). Previous work from our lab and others has shown that MSNA increases during HX and remains elevated following hypoxic exposure for a period beyond the original exposure. However, it is unknown if and how the elevation in MSNA affects vascular function following acute HX.
Hypothesis: We hypothesize that the increase in MSNA that persists following an acute HX exposure will be associated with acute changes in vascular function measured as increases in arterial stiffness and femoral vascular resistance (FVR).
Methodology: We recruited 16 healthy volunteers (8 female) who were 24 ± 3 years old and instrumented them to continuously measure ABP, heart rate, arterial stiffness (pulse wave velocity; PWV), FVR and MSNA. Participants breathed through a mask that allowed for changes in inspired gases (room air vs. HX). Following ten minutes of rest, participants underwent a ten minute poikilocapnic HX exposure (~80% oxygen saturation), followed by a twenty min recovery period
Results: ABP was not increased during HX, but systolic blood pressure was increased at 15 minutes of recovery. Cardiac output was increased during, but not following HX and, similarly, total peripheral resistance (TPR) was decreased during, but not following HX. Additionally, FVR was decreased during HX and remained decreased up to ten minutes following HX. Neither central (aortic) nor peripheral (upper or lower limb) PWV were changed during or following HX. Lastly, MSNA burst frequency (burst per minute) and burst amplitude were increased following HX.
Discussion: This study adds to the current knowledge in that it is the first to comprehensively analyze both sympathetic and cardiovascular responses during and during and following acute poikilocapnic HX. Specifically, the augmented burst amplitude may imply that the peripheral chemoreflex gain is increased following poikilocapnic HX and that this may contribute to the overall increase in MSNA following HX. Further the differences in the TPR and FVR responses highlight the differential regulation of blood flow during and following acute HX. We believe these data are important for understanding the physiological consequences of environments, activities and clinical disorders associated with poikilocapnic HX (i.e. travel to altitude).
- Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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