## 4 Discussion
### Interpretation and Implications  
Previous research has already reported increased pain sensitivity in persons with CNSLBP at rest when compared to HC [61; 62]. Additionally, several studies have demonstrated a potential EIH effect in HCs [13]. There is still a debate regarding whether this effect is present in patients with CNSLBP [62]. The current study did find a higher pain sensitivity in persons with CNSLPB compared to HCs and corroborated the EIH effect in HCs. But, this effect was not present in persons with CNSLBP. This suggests that a single HIIT session may not be sufficient to elicit measurable improvements in pain sensitivity in this chronic pain population. These findings are supported by a recent clinical trial by [PERSON] et al. [63]. However, in the latter, only PPTs were analyzed, and dynamic QST outcomes such as TS or CPM were not included. Hence, the current study provided a more comprehensive analysis of pain modulation processes that might show EIH. The limited impact of HIIT in persons with CNSLBP contrasts the impact in HCs, where HIIT did lead to improvements, corroborating that this training modality enhances acute pain tolerance and pain modulation in non-clinical individuals. Indeed, similar results with higher-intensity protocols in HCs have been shown previously [16]. The findings regarding the comparison between HIIT and MICT indicate that both protocols had similar minimal effects on pain sensitivity within persons with CNSLBP, suggesting that the intensity of exercise may not be a critical determinant for this outcome in this disorder. Nonetheless, it remains unclear if applying different modalities (especially at specific intensities) would alter these findings. Previous trials have reported inconsistent results, with some showing unchanged pain sensitivity following strength training [58], while others have demonstrated increased EIH after aerobic [64] and stabilization training [65]. Notably, these studies had to differentiate between local and remote site effects, suggesting the involvement of distinct underlying mechanisms. Beyond the relationship with inflammation discussed in the present study, other neurophysiological (e.g., increased local blood flow [65] and activation of the endogenous opioid system [13]) and psychological (heightened anxiety and pain catastrophizing [66]) factors have been proposed. However, these theoretical models require validation in future trials. Additionally, many studies lack clear intensity definitions, limiting comparability across trials. Implementing standardized reporting templates, such as the CERT [67], could help address this issue and improve cross-study comparisons. Altogether, these inconclusive findings in CNSLBP remain in clear contrast with the positive outcomes on EIH found through performing several exercise modalities, including aerobic, stabilization, and strength training, in other chronic musculoskeletal disorders such as osteoarthritis, shoulder pain, and patella femoralpain [20] and the overview literature showing a stronger impact through high-intensity protocols [16]. This variability highlights the need for further research into the underlying mechanisms governing disorder-specific responses to exercise. Likewise, these results contrast the outcomes after repeated-exposure and structured training programs, where an added value of exercise intensity on pain sensitivity in both persons with CNSLBP [68] and HCs [69] has been displayed. Hence, it remains unclear if (absent) acute EIH effects have any predictive value on long-term pain sensitivity [70]. Such an evaluation has only been performed in persons with knee osteoarthritis, where a high EIH before a standardized ET program was associated with a larger pain improvement after treatment [15], suggesting that EIH might be an early \"precursor\" for a positive response to long-term exercise therapy.