Faced with mechanical inspiratory loading, awake animals and anaesthetised 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 premotor representation of inspiratory muscles in this behaviour. Ten healthy subjects (age 19-34, 3 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 premotor activity. Premotor potentials were present during voluntary sniffs in all subjects (average latency +/- SD: 1325 +/- 521 ms), but also during inspiratory threshold loading (1427 +/- 537 ms) and during inspiratory resistive loading (1109 +/- 465 ms). Premotor potentials were systematically followed by motor potentials during inspiratory loading. Premotor 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 3 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.