ABSTRACT Background Aerobic exercise leads to transient hypoalgesia, but little is known about these effects over extended periods. This study aimed to investigate exercise‐induced hypoalgesia (EIH) responses in healthy individuals during long‐distance running on a treadmill. Methods Thirty healthy participants (18–50 years) completed a 15 km treadmill run. Pain sensitivity was assessed using pain pressure threshold (PPT) before and during the run. Additionally, cuff‐PPT (cPPT), cuff‐pressure pain tolerance threshold (cPTT), temporal summation of pain (TSP) and conditioned pain modulation (CPM) were assessed with pressure cuff algometry before and during the run. Data were analysed using repeated measures ANOVA. Exploratory subgroups, based on changes in PPT, were identified using latent growth mixture models, and logistic regression was used to predict subgroup membership. Results No significant changes were observed over time for PPT, PTT, cPPT or CPM at the group level. TSP decreased significantly after 10 and 15 km ( p ≤ 0.004) when compared to baseline. Exploratory analysis identified two distinct subgroups: ‘increasing PPT’ and ‘decreasing PPT’. Subgroup membership was predicted using baseline CPM and EIH ( p < 0.045). Conclusion This study found no significant changes in PPT, cPPT, or CPM following aerobic exercise. A significant change was observed in TSP. CPM and EIH predicted changes in PPT during the 15 km run (increasing vs. decreasing) in an explorative analysis. Further research should test if baseline tests can predict pro‐ or anti‐nociceptive responses to long‐distance running. Significance Statement These findings highlight the importance of individual variability in endogenous pain modulation during endurance exercise. The lack of group‐level effects underscores the need to move beyond average responses and consider subgroups when studying exercise‐induced hypoalgesia. Identifying distinct modulatory profiles may offer insight into personalized exercise interventions and reveal stable traits related to pain regulation. This has potential clinical implications for tailoring exercise as a pain management strategy and for identifying individuals at risk of negative or absent hypoalgesic responses.
Dixen et al. (Thu,) studied this question.