In some disease conditions, an increase in lung volume (hyperinflation) may contribute to the sensation of dyspnoea. Cortical processing of respiratory-related sensory information can be investigated using transient inspiratory occlusions (TIOs). This afferent stimulation results in respiratory-related sensory evoked potentials (RREPs) which exhibit early (Nf, P1: within 100 ms of stimulus onset) and late (N1, P2, P3: 100 – 350 ms after stimulus) latency components (Davenport et al., 2002). With this context, we hypothesised that the processing of sensory information from the respiratory system may be modulated by changing lung volume and that such changes might contribute to the sensation of dyspnoea. To test this we determined changes in the RREP response to TIO in healthy volunteers induced by increasing lung volume. Surface EEG electrodes were placed to record RREPs at frontal, central and parietal cortical sites. RREPs were elicited using TIOs of 0.3 s in 15 healthy subjects with ethical approval. Subjects were instructed, in response to a tone, to voluntarily inspire from their functional residual capacity to their inspiratory capacity (IC) whilst maintaining a targeted constant flow rate. In each trial, TIOs were presented in a randomised order, either early in the targeted inspiration at a low volume (10.3 ± 1.9 % IC; group mean ± se) or late in the inspiration at a high volume (70.5 ± 1.2 % IC) of the subject’s IC. No significant differences (ANOVA) in amplitude (Table 1; group mean ± se, μV) or latency were observed in the early or late components of the RREP between low and high volumes. This study demonstrates no modulation of respiratory-related sensory information by increasing lung volume and suggests that changes in the processing of sensory information, associated with hyperinflation, may not contribute to the sensation of dyspnoea in lung disease.