AbstractBackground and objectiveUpper airway surgery for obstructive sleep apnoea (OSA) is an alternative treatment for patients who are intolerant of continuous positive airway pressure (CPAP). However, upper airway surgery has variable treatment efficacy with no reliable predictors of response. While we now know that there are several endotypes contributing to OSA (i.e., upper airway collapsibility, airway muscle response/compensation, respiratory arousal threshold and loop gain), no study to date has examined: (i) how upper airway surgery affects all four OSA endotypes, (ii) whether knowledge of baseline OSA endotypes predicts response to surgery and (iii) whether there are any differences when OSA endotypes are measured using the CPAP dial‐down or clinical polysomnographic (PSG) methods.MethodsWe prospectively studied 23 OSA patients before and ≥3 months after multilevel upper airway surgery. Participants underwent clinical and research PSG to measure OSA severity (apnoea–hypopnoea index [AHI]) and endotypes (measured in supine non‐rapid eye movement [NREM]). Values are presented as mean ± SD or median (interquartile range).ResultsSurgery reduced the AHI_Total (38.7 [23.4 to 79.2] vs. 22.0 [13.3 to 53.5] events/h; p = 0.009). There were no significant changes in OSA endotypes, however, large but variable improvements in collapsibility were observed (CPAP dial‐down method: ∆1.9 ± 4.9 L/min, p = 0.09, n = 21; PSG method: ∆3.4 [−2.8 to 49.0]%V_eupnoea, p = 0.06, n = 20). Improvement in collapsibility strongly correlated with improvement in AHI (%∆AHI_SupineNREM vs. ∆collapsibility: p < 0.005; R² = 0.46–0.48). None of the baseline OSA endotypes predicted response to surgery.ConclusionSurgery unpredictably alters upper airway collapsibility but does not alter the non‐anatomical endotypes. There are no baseline predictors of response to surgery.