RESUMEN
Even in healthy populations, conditioned pain modulation (CPM) magnitude varies. This may be accounted for by (non-)modifiable factors, including physical activity (PA). Yet, little research has thoroughly examined PA and its relation with CPM magnitude in a representative sample. Therefore, the present study investigated the predictive effect of PA on CPM magnitude in 105 healthy adults. PA was assessed during 7 consecutive days by self-report using the International Physical Activity Questionnaire and by monitor-based accelerometry. CPM was examined using a heterotopic noxious-conditioning stimulation protocol during which the effect of a hot water-conditioning stimulus on pressure pain thresholds was evaluated. Comparative, correlation, and hierarchical linear regression analyses were performed. Report-based walking predicts 4.8% of variance in pain-modulatory capacity, moderate PA predicts 10.2% of variance in pain-modulatory capacity, and report-based time spent on total PA predicts 7.0% of variance in pain-modulatory capacity. More metabolic equivalent-minutes/week spent on total PA, including walking and moderate PA, is associated with greater pain-modulatory capacity. The findings of this study add to the limited evidence on the predictive effect of PA on CPM. It urges to consider PA a confounding factor when examining CPM. The current study provides evidence that a physically active lifestyle benefits endogenous pain modulation in healthy adults. Given its potential, walking and moderate-intensity PA might be achievable treatment strategies for pain patients known to have impaired CPM. PERSPECTIVE: The results of this article show that a physically active lifestyle, including larger amounts of walking and moderate activity, predicts greater pain-modulatory capacity. TRIAL REGISTRATION: This study has not been preregistered.
RESUMEN
OBJECTIVE: Although there has been increasing interest in the role of systemic cytokines in chronic spinal pain (CSP), the evidence on their potential contribution is still unclear. Therefore, the current study systematically reviewed the evidence on systemic cytokine level differences between people with CSP compared to healthy controls (HCs) and the potential associations with pain severity. METHODS: An electronic search was conducted on PubMed, Web of Science and Embase. All included studies were classified as observational studies, exploring the comparison between a CSP group and a HC group, and the association between systemic cytokine levels and pain severity. RESULTS: Nine articles were included with a total sample of 400 CSP patients suffering from chronic whiplash associated disorder (CWAD) or chronic low back pain (CLBP). In CLBP, moderate evidence was found for elevated tumor necrosis factor (TNF) α, interleukin (IL) 6, IL-1 receptor antagonist (IL-1RA), and soluble TNF receptor (sTNF-R) type 2, for normal interferon (IFN) γ and IL-2 levels, and for reduced IL-10 levels. No association was found between pain severity and these cytokines in CLBP. In CWAD, moderate evidence was found for elevated CRP and evidence for changes in TNF-α was inconclusive. Evidence for the association between pain severity and CRP was limited, and there is probably no association between pain severity and TNF-α with limited evidence in CWAD. CONCLUSIONS: Moderate evidence indicates the presence of systemic inflammation in CSP. Evidence regarding the association between pain severity and systemic cytokines is inconclusive and limited.