• Capucine Morélot-Panzini, Julien Mayaux, François Hug, Jean-Claude Willer, and Thomas Similowski.
• Assistance Publique - Hôpitaux de Paris, Service de Pneumologie et Réanimation Médicale, Groupe Hospitalier Pitié Salpétrière, Paris, France; Université Paris 6, ER10UPMC, Paris, France. Electronic address: capucine.morelot@psl.ap-hop-paris.fr.
• Respir Physiol Neurobiol. 2014 Jan 1; 190: 81-5.

AbstractDyspnoea has distinct sensory modalities, including air hunger and the sensation of excessive breathing "work/effort". Both have analgesic properties. In the case of work/effort, spinal mechanisms have been documented (inhibitory effect on the spinal nociceptive flexor reflex, RIII). This mechanism involves C-fibres. As C-fibres are unlikely to play a major role in air hunger, we hypothesised that inducing this type of dyspnoea would not result in RIII inhibition. Eight healthy volunteers were exposed to a hypercapnic hyperoxic gas mixture (5% CO2 and 95% O2) and asked to voluntarily fight the corresponding ventilatory reflex response by reducing tidal volume below its spontaneous level. Ventilatory variables and dyspnoea intensity (ordinal scale) were measured. Electromyography of the biceps femoris was used to record the amplitude of RIII in response to painful electrical sural nerve stimulation. Air hunger failed to inhibit the RIII reflex. We conclude that the mechanisms of air hunger induced analgesia do not include a spinal contribution and are therefore mostly central.Copyright © 2013 Elsevier B.V. All rights reserved.

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