Epidemiological literature on the relationship between physical activity and chronic pain is scarce and inconsistent. Hence, our aim was to assess the relationship applying comprehensive methodology, including self-reported and accelerometer measures of physical activity and different severity levels of chronic pain. We used data from the Tromsø Study (2015Study ( -2016. All residents in the municipality, aged 40 years and older were invited to participate (n 5 32,591, 51% women). A total of 21,083 (53%) women reported on questionnaires. Additionally, 6778 participants (54% women) were invited to wear accelerometers (6125 with complete measurements). Our exposure measures were self-reported leisure time physical activity, exercise frequency, duration, and intensity and 2 accelerometer measures (steps per day and minutes of moderate to vigorous physical activity per day). Outcome measurements were chronic pain and moderateto-severe chronic pain. We used Poisson regression to estimate chronic pain prevalence and prevalence ratios for each physical activity measure, with adjustments for sex, age, education level, smoking history, and occupational physical activity. Our main analyses showed an inverse dose-response relationship between all physical activity measures and both severity measures of chronic pain, except that the dose-response relationship with exercise duration was only found for moderate-to-severe pain. All findings were stronger for the moderate-to-severe pain outcomes than for chronic pain. Robustness analyses gave similar results as the main analyses. We conclude that an inverse dose-response association between physical activity and chronic pain is consistent across measures. To summarize, higher levels of physical activity is associated with less chronic pain and moderate-to-severe chronic pain.
Physical activity (PA) might influence the risk or progression of chronic pain through pain tolerance. Hence, we aimed to assess whether habitual leisure-time PA level and PA change affects pain tolerance longitudinally in the population. Our sample (n = 10,732; 51% women) was gathered from the sixth (Tromsø6, 2007–08) and seventh (Tromsø7, 2015–16) waves of the prospective population-based Tromsø Study, Norway. Level of leisure-time PA (sedentary, light, moderate, or vigorous) was derived from questionnaires; experimental pain tolerance was measured by the cold-pressor test (CPT). We used ordinary, and multiple-adjusted mixed, Tobit regression to assess 1) the effect of longitudinal PA change on CPT tolerance at follow-up, and 2) whether a change in pain tolerance over time varied with level of LTPA. We found that participants with high consistent PA levels over the two surveys (Tromsø6 and Tromsø7) had significantly higher tolerance than those staying sedentary (20.4 s. (95% CI: 13.7, 27.1)). Repeated measurements show that light (6.7 s. (CI 3.4, 10.0)), moderate (CI 14.1 s. (9.9, 18.3)), and vigorous (16.3 s. (CI 6.0, 26.5)) PA groups had higher pain tolerance than sedentary, with non-significant interaction showed slightly falling effects of PA over time. In conclusion, being physically active at either of two time points measured 7–8 years apart was associated with higher pain tolerance compared to being sedentary at both time-points. Pain tolerance increased with higher total activity levels, and more for those who increased their activity level during follow-up. This indicates that not only total PA amount matters but also the direction of change. PA did not significantly moderate pain tolerance change over time, though estimates suggested a slightly falling effect possibly due to ageing. These results support increased PA levels as a possible non-pharmacological pathway towards reducing or preventing chronic pain.
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