Electroencephalographic evidence for pre-motor cortex activation during inspiratory loading in humans

• Published in: The Journal of physiology 2007-01, Vol.578 (2), p.569-578
• Main Authors: Raux, Mathieu, Straus, Christian, Redolfi, Stefania, Morelot‐Panzini, Capucine, Couturier, Antoine, Hug, François, Similowski, Thomas
• Format: Article
• Language: English
• Subjects: Adult; Carbon Dioxide - pharmacology; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Electroencephalography - methods; Electromyography - methods; Female; Humans; Inhalation - physiology; Male; Motor Cortex - physiology; Reproducibility of Results; Respiration, Artificial; Respiratory; Respiratory Mechanics - physiology; Tidal Volume - physiology
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2006.120246

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 19–34 years, three men) were studied during quiet breathing, CO 2 -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 CO 2 -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.