The Effects of Hypoxia and Core Temperature on Ventilation During Low Intensity Exercise
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THE EFFECTS OF HYPOXIA AND CORE TEMPERATURE ON VENTILATION DURING LOW INTENSITY EXERCISE Aaron L. Chu B.Sc., (Hons.), University of Waterloo, 2000 THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE In the School of Kinesiology O Aaron L. Chu 2004 SIMON FRASER UNIVERSITY Fall 2004 All rights reserved. This work may not be reproduced in whole or in part, by photocopy or other means, without permission of the author. APPROVAL Name: Aaron L. Chu Degree: Masters of Science Title of Thesis: The effects of hypoxia and core temperature on ventilation during exercise Examining Committee: Chair: John Dickinson, Ph.D. Professor and Director, School of Kinesiology, S.F.U. Senior Supervisor: Matthew D. White, Ph.D. Assistant Professor, School of Kinesiology, S.F.U. Supervisor: Don C. McKenzie, M.D., Ph.D. Professor, School of Human Kinetics, U.B.C. Supervisor : Andrew P. Blaber, Ph.D. Assistant Professor, School of Kinesiology, S.F.U. External Examiner : A. William Sheel, Ph.D. Assistant Professor, School of Human Kinetics, U.B.C. Date DefendedIApproved: SIMON FRASER UNIVERSITY PARTIAL COPYRIGHT LICENCE The author, whose copyright is declared on the title page of this work, has granted to Simon Fraser University the right to lend this thesis, project or extended essay to users of the Simon Fraser University Library, and to make partial or single copies only for such users or in response to a request from the library of any other university, or other educational institution, on its own behalf or for one of its users. The author has further granted permission to Simon Fraser University to keep or make a digital copy for use in its circulating collection. The author has further agreed that permission for multiple copying of this work for scholarly purposes may be granted by either the author or the Dean of Graduate Studies. It is understood that copying or publication of this work for financial gain shall not be allowed without the author's written permission. \ Permission for public performance, or limited permission for private scholarly use, of any multimedia materials forming part of this work, may have been granted by the author. This information may be found on the separately catalogued multimedia material and in the signed Partial Copyright Licence. The original Partial Copyright Licence attesting to these terms, and signed by this author, may be found in the original bound copy of this work, retained in the Simon Fraser University Archive. W. A. C. Bennett Library Simon Fraser University Burnaby, BC, Canada Simon Fraser University Ethics Approval The author, whose name appears on the title page of this work, has obtained human research ethics approval from the Simon Fraser University Office of Research Ethics for the research described in this work, or has conducted the research as a member of a project or course approved by the Ethics Office. A copy of the approval letter has been filed at the Theses Office of the University Library at the time of submission of this thesis or project. The original application for ethics approval and letter of approval is filed with the Office of Research Ethics. Inquiries may be directed to that Office. Bennett Library Simon Fraser University Burnaby, BC, Canada ABSTRACT The independent and combined effects of hypoxia and elevated esophageal temperature (T,,) were investigated for their effects on the level and lunetics of exercise ventilation (VE). In either a 'hyperthermic' T,, or a 'normothermic' Tessession, 11 college-aged, healthy males were immersed to the shoulders and pedalled on an underwater cycle ergometer at a steady-state oxygen consumption (V02)of 0.87 ~.min-' (SD 0.07). Following a 30-min rest and 20-min warm-up, a 30-min steady-state cycling period was divided into three 10 min gas phases when participants inhaled: air (Euoxia 1 (El)), hypoxic gas (12 % 02and 88 % N2 (HI)), and air (Euoxia 2 (E2)). End-tidal C02 (PETC02)was maintained at an isocapnic level of 5.19 kPa (SD 0.71) throughout the exercise. Venous blood samples were drawn at rest and 5 min into all gas phases. Results showed a significant increase in \jEduring all hyperthermia conditions (0.0kP c 0.048), however, during hyperthermic hypoxia there was a disproportionate and significant (P = 0.017) increase in VE relative to normothermic hypoxia. This was the main explanation for a significant core temperature and gas type interaction (P = 0.012) for VE. A main effect of core temperature (P = 0.007) was evident on ventilation frequency (f,) with an increased rate of breathing in hyperthennic relative to the normothermic exercise. This gave evidence of a thermally-induced tachypnea which corresponded to significant decreases in inspiratory time (TI) (P = 0.035) and expiratory time (P = 0.014) and was independent of any changes in tidal volume (VT) (P = 0.801). As such inspiratory flow (vT.~fl)was significantly increased in hyperthermic- relative to normothermic (P = 0.003) exercise, an increase that was pronounced (P = 0.013) during hyperthermic hypoxia. A significant reduction of the time constants (z) for vEwas evident (P = 0.032) during the onset of exercise under the hyperthermic as compared to the normothermic condition. This reduction in z was associated with an increase in T,, (R' =0.829, P = 0.01 1) but not in skin temperature. Between core temperature levels there were no significant changes in z for the VE response from euoxic to hypoxic steady-state exercise. From normothermic to hyperthermic exercise increases of VE in El were 9.4 % (SD 9.7) and not significantly different than the 6.9 % (SD 10.7) increase in V02. However in HI, vEand VO~increased by 29.2 % (SD 25.5) and 13.5 % (SD 10.I), respectively, which bordered a significant difference (P = 0.056). No changes in lactate or potassium (K') levels were evident across all gas type and core temperature conditions. In conclusion, these results suggest the following: 1) During low intensity, steady-state exercise an elevated Tes caused an increased vE,which was mediated by an increased f,. 2) The addition of hypoxia during hyperthermic exercise caused a multiplicative increase in VEwhich corresponded with a multiplicative increase in V~.T~-'.This would suggest the possibility of a core temperature mediated stimulation of the peripheral chemoreceptors. 3) An increased Tesduring the onset of exercise but not during the transition from low intensity euoxic to hypoxic exercise shortened the time course of the VEresponse. 4) Oxygen consumption, K+ and lactate did not appear to be significant mediators of the augmented hyperthermic hypoxic VEresponse. Overall the results support the hypothesis that temperature plays a significant role in the control of ventilation, particularly during hypoxic exercise. ACKNOWLEDGEMENTS The work presented in this thesis has been carried out at the Laboratory of Exercise and Environmental Physiology in the School of Kinesiology of The Faculty of Applied Sciences, Simon Fraser University. My research was financially supported in part by funding provided from the Canadian Foundation for Innovation and the National Sciences and Engineering Research Council. I would first of all like to thank my committee members and in particular my senior supervisor Dr. Matthew White for his guidance, effort and time on this project. I would also like to thank him for giving me the opportunity to work in this area. I would like to extend my gratitude to all of my fellow students and staff, past and present, both of the Laboratory of Exercise and Environmental Physiology and the School of Kinesiology, all of which have provided support and enjoyment throughout my time as a research student. Thanks to all of the participants in my study, without whom, my research would not be possible. Special thanks to Dr. Ollie Jay who was invaluable to me as a subject, an assistant, but more importantly as a good friend during my work. Last of all thanks to my family and closest friends, who have given me unwavering encouragement throughout my education. TABLE OF CONTENTS .. Approval ...........................................................................................................................11 ... Abstract ......................................................................................................................... 111 Acknowledgements ..........................................................................................................vi .. Table of Contents ............................................................................................................vii List of Tables ......................................................................................................................x List of Figures .................................................................................................................. xi ... Abbreviations and Acronyms .......................................................................................xu1 Terms and Definitions .....................................................................................................xv Chapter 1 Thesis Overview ..............................................................................................1 1.1 References ......................................................................................................-3 Chapter 2 Literature Review ............................................................................................4 Temperature Regulation ..................................................................................4