The impact of unpredictability of dyspnea offset on dyspnea perception, fear, and respiratory neural gating.

Dyspnea is a debilitating and threatening symptom in various diseases. Affected patients often report the unpredictability of dyspnea episodes being particularly anxiety-provoking and amplifying the perception of dyspnea. Experimental studies testing dyspnea unpredictability together with related neural processes, physiological fear responses, and dyspnea-related personality traits are sparse. Therefore, we investigated the impact of unpredictability of dyspnea offset on dyspnea perception and fear ratings, respiratory neural gating and physiological fear indices, as well as the influence of interindividual differences in fear of suffocation (FoS). Forty healthy participants underwent a task manipulating the offset predictability of resistive load-induced dyspnea including one unloaded safety condition. Respiratory variables, self-reports of dyspnea intensity, dyspnea unpleasantness, and fear were recorded. Moreover, respiratory neural gating was measured in a paired inspiratory occlusion paradigm using electroencephalography, while electrodermal activity, startle eyeblink, and startle probe N100 were assessed as physiological fear indices. Participants reported higher dyspnea unpleasantness and fear when dyspnea offset was unpredictable compared to being predictable. Individuals with high levels of FoS showed the greatest increase in fear and overall higher levels of fear and physiological arousal across all conditions. Respiratory neural gating, startle eyeblink, and startle probe N100 showed general reductions during dyspnea conditions but no difference between unpredictable and predictable dyspnea conditions. Together, the current results suggest that the unpredictable offset of dyspnea amplifies dyspnea perception and fear, especially in individuals with high levels of FoS. These effects were unrelated to respiratory neural gating or physiological fear responses, requiring future studies on underlying mechanisms.