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Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans
BACKGROUND: Breathing in humans is dually controlled for metabolic (brainstem commands) and behavioral purposes (suprapontine commands) with reciprocal modulation through spinal integration. Whereas the ventilatory response to chemical stimuli arises from the brainstem, the compensation of mechanica...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2006
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1555603/ https://www.ncbi.nlm.nih.gov/pubmed/16875504 http://dx.doi.org/10.1186/1472-6793-6-7 |
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author | Locher, Chrystèle Raux, Mathieu Fiamma, Marie-Noelle Morélot-Panzini, Capucine Zelter, Marc Derenne, Jean-Philippe Similowski, Thomas Straus, Christian |
author_facet | Locher, Chrystèle Raux, Mathieu Fiamma, Marie-Noelle Morélot-Panzini, Capucine Zelter, Marc Derenne, Jean-Philippe Similowski, Thomas Straus, Christian |
author_sort | Locher, Chrystèle |
collection | PubMed |
description | BACKGROUND: Breathing in humans is dually controlled for metabolic (brainstem commands) and behavioral purposes (suprapontine commands) with reciprocal modulation through spinal integration. Whereas the ventilatory response to chemical stimuli arises from the brainstem, the compensation of mechanical loads in awake humans is thought to involve suprapontine mechanisms. The aim of this study was to test this hypothesis by examining the effects of inspiratory resistive loading on the response of the diaphragm to transcranial magnetic stimulation. RESULTS: Six healthy volunteers breathed room air without load (R0) and then against inspiratory resistances (5 and 20 cmH(2)O/L/s, R5 and R20). Ventilatory variables were recorded. Transcranial magnetic stimulation (TMS) was performed during early inspiration (I) or late expiration (E), giving rise to motor evoked potentials (MEPs) in the diaphragm (Di) and abductor pollicis brevis (APB). Breathing frequency significantly decreased during R20 without any other change. Resistive breathing had no effect on the amplitude of Di MEPs, but shortened their latency (R20: -0.903 ms, p = 0.03) when TMS was superimposed on inspiration. There was no change in APB MEPs. CONCLUSION: Inspiratory resistive breathing facilitates the diaphragm response to TMS while it does not increase the automatic drive to breathe. We interpret these findings as a neurophysiological substratum of the suprapontine nature of inspiratory load compensation in awake humans. |
format | Text |
id | pubmed-1555603 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-15556032006-09-02 Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans Locher, Chrystèle Raux, Mathieu Fiamma, Marie-Noelle Morélot-Panzini, Capucine Zelter, Marc Derenne, Jean-Philippe Similowski, Thomas Straus, Christian BMC Physiol Research Article BACKGROUND: Breathing in humans is dually controlled for metabolic (brainstem commands) and behavioral purposes (suprapontine commands) with reciprocal modulation through spinal integration. Whereas the ventilatory response to chemical stimuli arises from the brainstem, the compensation of mechanical loads in awake humans is thought to involve suprapontine mechanisms. The aim of this study was to test this hypothesis by examining the effects of inspiratory resistive loading on the response of the diaphragm to transcranial magnetic stimulation. RESULTS: Six healthy volunteers breathed room air without load (R0) and then against inspiratory resistances (5 and 20 cmH(2)O/L/s, R5 and R20). Ventilatory variables were recorded. Transcranial magnetic stimulation (TMS) was performed during early inspiration (I) or late expiration (E), giving rise to motor evoked potentials (MEPs) in the diaphragm (Di) and abductor pollicis brevis (APB). Breathing frequency significantly decreased during R20 without any other change. Resistive breathing had no effect on the amplitude of Di MEPs, but shortened their latency (R20: -0.903 ms, p = 0.03) when TMS was superimposed on inspiration. There was no change in APB MEPs. CONCLUSION: Inspiratory resistive breathing facilitates the diaphragm response to TMS while it does not increase the automatic drive to breathe. We interpret these findings as a neurophysiological substratum of the suprapontine nature of inspiratory load compensation in awake humans. BioMed Central 2006-07-29 /pmc/articles/PMC1555603/ /pubmed/16875504 http://dx.doi.org/10.1186/1472-6793-6-7 Text en Copyright © 2006 Locher et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Locher, Chrystèle Raux, Mathieu Fiamma, Marie-Noelle Morélot-Panzini, Capucine Zelter, Marc Derenne, Jean-Philippe Similowski, Thomas Straus, Christian Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
title | Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
title_full | Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
title_fullStr | Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
title_full_unstemmed | Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
title_short | Inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
title_sort | inspiratory resistances facilitate the diaphragm response to transcranial stimulation in humans |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1555603/ https://www.ncbi.nlm.nih.gov/pubmed/16875504 http://dx.doi.org/10.1186/1472-6793-6-7 |
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