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      Respiratory modulation of human autonomic function on Earth

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          Abstract

          Key points

          • We studied healthy supine astronauts on Earth with electrocardiogram, non‐invasive arterial pressure, respiratory carbon dioxide concentrations, breathing depth and sympathetic nerve recordings.

          • The null hypotheses were that heart beat interval fluctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs.

          • R‐R interval fluctuations at usual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea.

          • The subjects’ responses to apnoea could not be attributed to changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve burst areas, frequencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pulmonary stretch receptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympathetic activity). Apnoea responses of healthy subjects may result from changes of central respiratory motoneurone activity.

          Abstract

          We studied eight healthy, supine astronauts on Earth, who followed a simple protocol: they breathed at fixed or random frequencies, hyperventilated and then stopped breathing, as a means to modulate and expose to view important, but obscure central neurophysiological mechanisms. Our recordings included the electrocardiogram, finger photoplethysmographic arterial pressure, tidal volume, respiratory carbon dioxide concentrations and peroneal nerve muscle sympathetic activity. Arterial pressure, vagal tone and muscle sympathetic outflow were comparable during spontaneous and controlled‐frequency breathing. Compared with spontaneous, 0.1 and 0.05 Hz breathing, however, breathing at usual frequencies (∼0.25 Hz) lowered arterial baroreflex gain, and provoked smaller arterial pressure and R‐R interval fluctuations, which were separated by intervals that were likely to be too short and variable to be attributed to baroreflex physiology. R‐R interval fluctuations at usual breathing frequencies disappear during apnoea, and thus cannot provide evidence for the existence of a central respiratory oscillation. Apnoea sets in motion a continuous and ever changing reorganization of the relations among stimulatory and inhibitory inputs and autonomic outputs, which, in our study, could not be attributed to altered chemoreceptor, baroreceptor, or pulmonary stretch receptor activity. We suggest that responses of healthy subjects to apnoea are driven importantly, and possibly prepotently, by changes of central respiratory motoneurone activity. The companion article extends these observations and asks the question, Might terrestrial responses to our 20 min breathing protocol find expression as long‐term neuroplasticity in serial measurements made over 20 days during and following space travel?

          Key points

          • We studied healthy supine astronauts on Earth with electrocardiogram, non‐invasive arterial pressure, respiratory carbon dioxide concentrations, breathing depth and sympathetic nerve recordings.

          • The null hypotheses were that heart beat interval fluctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, and that autonomic responses to apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs.

          • R‐R interval fluctuations at usual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea.

          • The subjects’ responses to apnoea could not be attributed to changes of central chemoreceptor activity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve burst areas, frequencies and probabilities increased, even as arterial pressure climbed to new levels); or altered pulmonary stretch receptor activity (major breathing frequency and tidal volume changes did not alter vagal tone or sympathetic activity). Apnoea responses of healthy subjects may result from changes of central respiratory motoneurone activity.

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          Author and article information

          Contributors
          deckberg@ekholmen.com
          Journal
          J Physiol
          J. Physiol. (Lond.)
          10.1111/(ISSN)1469-7793
          TJP
          jphysiol
          The Journal of Physiology
          John Wiley and Sons Inc. (Hoboken )
          0022-3751
          1469-7793
          26 July 2016
          01 October 2016
          : 594
          : 19 ( doiID: 10.1113/tjp.2016.594.issue-19 )
          : 5611-5627
          Affiliations
          [ 1 ] Departments of Medicine and Physiology Hunter Holmes McGuire Department of Veterans Affairs Medical Center and Virginia Commonwealth University School of Medicine Richmond VA USA
          [ 2 ] Department of Kinesiology, Health, and Nutrition University of Texas at San Antonio San Antonio TX USA
          [ 3 ] Department of Medicine Division of Clinical Pharmacology Autonomic Dysfunction Center Vanderbilt University School of Medicine Vanderbilt University Nashville TN USA
          [ 4 ] Dartmouth Hitchcock Medical Center Lebanon NH USA
          [ 5 ] Department of Physiology Pennsylvania State University University Park and Hershey PA USA
          [ 6 ] Department of Physics University of Turku Turku Finland
          [ 7 ] Department of Clinical Physiology and Nuclear Medicine South Karelia Central Hospital Lappeenranta Finland
          [ 8 ] Gifu University of Medical Science 795‐1 Nagamine Ichihiraga Seki Gifu 501‐3892 Japan
          [ 9 ] Department of Physiology Aichi Medical University Aichi Japan
          [ 10 ] DLR‐Institute for Aerospace Medicine Cologne Germany
          [ 11 ] Department of Medicine University of Texas Southwestern Medical Center at Dallas Dallas TX USA
          [ 12 ] Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas TX USA
          [ 13 ] University of Texas Southwestern Dallas TX USA
          Author notes
          [* ] Corresponding author D. L. Eckberg: Ekholmen, 8728 Dick Woods Road, Afton, VA 22920, USA. Email: deckberg@ 123456ekholmen.com
          [†]

          Deceased

          Article
          PMC5043049 PMC5043049 5043049 TJP7229
          10.1113/JP271654
          5043049
          27028958
          Published 2016. This article is a U.S. Government work and is in the public domain in the USA.
          Page count
          Figures: 8, Tables: 1, Pages: 17, Words: 10251
          Funding
          Funded by: National Aeronautics and Space Administration
          Award ID: NAS0‐19541
          Award ID: NAG2‐408
          Funded by: National Heart, Lung, and Blood Institute
          Award ID: UO1HL‐56417
          Categories
          Autonomic Nervous System
          Developmental Neuroscience
          Respiratory Physiology
          Research Paper
          Neuroscience ‐ Development/Plasticity/Repair
          Custom metadata
          2.0
          tjp7229
          1 October 2016
          Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:29.09.2016

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