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RESPIRATORY |
1 Université Pierre et Marie Curie-Paris6, UPRES EA 2397, Paris, France
2 Assistance Publique Hôpitaux de Paris, Laboratoire de Physiopathologie Respiratoire, Service de Pneumologie et Réanimation, Groupe Hospitalier Pitié Salpétrière, Paris, France
3 Assistance Publique Hôpitaux de Paris, Service Central d'Explorations Fonctionnelles Respiratoires, Groupe Hospitalier Pitié Salpétrière, Paris, France
4 Servizio di Medicina Interna 1, Spedali Civili, and Universita di Brescia, Brescia, Italy
5 Laboratoire de Biomécanique et Physiologie, Institut National du Sport (INSEP), Paris, France
6 Université de Nantes, Nantes Atlantique Universités, JE2438, Nantes, France
Faced with mechanical inspiratory loading, awake animals and anaesthetized humans develop alveolar hypoventilation, whereas awake humans do defend ventilation. This points to a suprapontine compensatory mechanism instead of or in addition to the traditional brainstem respiratory regulation. This study assesses the role of the cortical pre-motor representation of inspiratory muscles in this behaviour. Ten healthy subjects (age 1934 years, three men) were studied during quiet breathing, CO2-stimulated breathing, inspiratory resistive loading, inspiratory threshold loading, and during self-paced voluntary sniffs. Pre-triggered ensemble averaging of Cz EEG epochs starting 2.5 s before the onset of inspiration was used to look for pre-motor activity. Pre-motor potentials were present during voluntary sniffs in all subjects (average latency (±S.D.): 1325 ± 521 ms), but also during inspiratory threshold loading (1427 ± 537 ms) and during inspiratory resistive loading (1109 ± 465 ms). Pre-motor potentials were systematically followed by motor potentials during inspiratory loading. Pre-motor potentials were lacking during quiet breathing (except in one case) and during CO2-stimulated breathing (except in two cases). The same pattern was observed during repeated experiments at an interval of several weeks in a subset of three subjects. The behavioural component of inspiratory loading compensation in awake humans could thus depend on higher cortical motor areas. Demonstrating a similar role of the cerebral cortex in the compensation of disease-related inspiratory loads (e.g. asthma attacks) would have important pathophysiological implications: it could for example contribute to explain why sleep is both altered and deleterious in such situations.
(Received 1 September 2006;
accepted after revision 14 November 2006;
first published online 16 November 2006)
Corresponding author T. Similowski: Laboratoire de Physiopathologie Respiratoire, Service de Pneumologie et de Réanimation, Groupe Hospitalier Pitié Salpétrière, 4783 boulevard de l'Hôpital, 75651 Paris Cedex 13, France. Email: thomas.similowski{at}psl.ap-hop-paris.fr
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