Hypobaric hypoxia does not induce different physiological responses ...

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“underdog back into the game” with 6 commentaries pro-. Millet et al. vs. 7 pro-Mounier and Brugniaux (plus the re- maining neutral contribution). Even if a basic ...

J Appl Physiol 112: 1796, 2012; doi:10.1152/japplphysiol.00355.2012.

Letter To The Editor

Last Word on Counterpoint: Hypobaric hypoxia does not induce different physiological responses from normobaric hypoxia Remi Mounier1 and Julien V. Brugniaux2 1

Institut Cochin, INSERM U1016, CNRS UMR8104, Université Paris Descartes, France; and 2University of Glamorgan, HESAS/Division of Sport, Health and Exercise Science, Glyntaff Campus, Pontypridd, United Kingdom

First, we would like to thank all the authors who contributed to make this a rigorous and thorough debate (see Ref. 2). As expected, we can note some very strong opinions and diverging points of view among the contributors even from the same institution or within members of the same family!!! We believe this diversity in the commentaries reflects the complexity of the question and the urge for further research. Trying to summarize the contributions, our point is outnumbered by Millet et al.’s (3) supporters by 8 commentaries vs. 5 (⫹1 remaining fairly neutral!). Shall we, therefore, conclude that we have it totally wrong? To address this question, we will bring back memories from a previous Point:Counterpoint between Prs. Wagner and Saltin and Calbet about the limiting ˙ O2max (5) published in the Journal of Applied factors of V Physiology during which Pr. Wagner rightfully pointed out that to answer a question we have to agree on the terms of the question. For instance, if we go back to the origin of this debate the question to be addressed was “is there a physiological difference between hypoxia induced by a change in inspired O2 partial pressure (PIO2) vs. an alteration in the inspired O2 fraction (FIO2)?” Two commentaries are (rightfully) highlighting differences in air density between hypobaric hypoxia (HH) and normobaric hypoxia (NH) as explaining at least part of the discrepancies between the two paradigms; in so doing they are actually arguing for our stance as we mentioned confounding factors associated with HH in the first instance (4). Fueling our argument further, the only commentary, proposed by Conkin and Wessel (see Ref. 2), focusing on the heart of the debate, i.e., PIO2 vs. FIO2, is indeed arguing in our favor. However, we acknowledge that to interpret a full body physiological response one has to look at the broad picture. Bearing this in mind, it therefore seems difficult to accurately compare HH and NH because they appear to be two different stimuli. A very clear illustration of this is the mitigating effect of hypocapnia induced by hyperventilation has on the hypoxiainduced increase in cerebral blood flow when compared with isocapnic hypoxia (1). TO THE EDITOR:

Address for reprint requests and other correspondence: R. Mounier, Institut Cochin, INSERM U1016, CNRS UMR8104, Universite Paris Descartes, France (e-mail: [email protected]).


Overall, a more detailed reading of the available contributions to the present Point:Counterpoint actually brings the “underdog back into the game” with 6 commentaries proMillet et al. vs. 7 pro-Mounier and Brugniaux (plus the remaining neutral contribution). Even if a basic mathematical addition of the commentaries pros or cons Mounier and Brugniaux is somewhat simplistic, because the majority is not always right, we believe there is strong evidence allowing us to stand by our original point stating that (at least) in terms of O2 sensing HH does not induce different physiological responses from NH. Nevertheless, as physiology is very integrative in nature, maybe future debates should move from the topical opposition between PIO2 and FIO2 to focus on a more integrative approach. Being able to address this latter point will, indeed, require further research. DISCLOSURES No conflicts of interest, financial or otherwise, are declared by the authors. AUTHOR CONTRIBUTIONS Author contributions: J.V.B. and R.M. conception and design of research; J.V.B. and R.M. interpreted results of experiments; J.V.B. and R.M. drafted manuscript; J.V.B. and R.M. edited and revised manuscript; J.V.B. and R.M. approved final version of manuscript. REFERENCES 1. Brugniaux JV, Hodges AN, Hanly PJ, Poulin MJ. Cerebrovascular responses to altitude. Respir Physiol Neurobiol 158: 212–223, 2007. 2. Girard O, Koehle MS, MacInnis MJ, Richard N, Guenette JA, Koehle MS, Verges S, Rupp T, Jubeau M, Perrey S, Millet GY, Chapman RF, Levine BD, Conkin J, Wessell JH III, Nespoulet H, Wuyam B, Tamisier R, Verges S, Levy P, Casey DP, Taylor BJ, Snyder EM, Johnson BD, Laymon AS, Stickford JL, Weavil JC, Loeppky JA, Pun M, Schommer K, Bartsch P, Vagula MC, Nelatury CF. Comments on Point:Counterpoint: Hypobaric hypoxia induces/does not induce different responses from normobaric hypoxia. J Appl Physiol; doi:10.1152/japplphysiol.00356.2012. 3. Millet GP, Faiss R, Pialoux V. Point: Hypobaric hypoxia induces different physiological responses from normobaric hypoxia. J Appl Physiol; doi: 10.1152/japplphysiol.00067.2012. 4. Mounier R, Brugniaux JV. Counterpoint: Hypobaric hypoxia does not induce different physiological responses from normobaric hypoxia. J Appl Physiol doi:10.1152/japplphysiol.00067.2012a. ˙ O2max 5. Wagner PD. Counterpoint: In health and in normoxic environment V is limited primarily by cardiac output and locomotor muscle blood flow. J Appl Physiol 100: 745–747; discussion 747–748, 2006.

8750-7587/12 Copyright © 2012 the American Physiological Society


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