Analgesic effects of dyspnoea: “Air hunger” does not inhibit the spinal nociception reflex in humans

• Dyspnoea has antinociceptive effects in humans.
• This is true for both air hunger and the sensation of excessive respiratory work/effort.
• Spinal inhibition (diffuse nociceptive inhibitory controls) is one of the mechanisms of dyspnoea-pain counter-irritation.
• Yet spinal inhibition does not occur in response to experimental air hunger in normal humans (this study).
• The analgesic effects of air hunger therefore probably proceed from central phenomena.

Dyspnoea 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.