Background & Aims
Poor quality of sleep and chronic pain are common comorbidities [9] and are associated with increased pain [2], increased psychological load [6], inflammation [1], and sensitization of pain mechanisms [3]. Experimental pain models mimic features of chronic pain and are useful in investigating changes after pain onset [7]. Delayed onset muscle soreness (DOMS) induces stiffness, mild-to-moderate pain, and restricted movement [4] but is mostly limited to provoking changes in the peripheral pain mechanisms [7]. Sleep provocations have previously been demonstrated to evoke changes in measurements of the central pain mechanisms [5,8]. Thus, the current study aimed to combine DOMS with sleep provocation to provide a unique model that affects both peripheral and central pain mechanisms and utilize this to investigate pain sensitivity, inflammation, and psychological state.
Methods
Thirty healthy, young participants attended two sessions separated by 24 hours of total sleep deprivation and a home rating distributed after 48 hours. Both experimental sessions were initi-ated with blood sampling to analyze plasma levels of interleukin 6 (IL-6) followed by validated questionnaires (Pittsburgh Sleep Quality Index, Pain Catastrophizing Scale, Positive and Negative Affective Schedule, and Four-Dimensional Symptom Questionnaire). Finally, pressure pain and tolerance thresholds, temporal summation of pain, and conditioned pain modulation were determined using cuff-pressure algometry. In the baseline session, the participants were instructed to complete 4 sets of 30 eccentric calf raises to induce DOMS and were instructed on a total sleep deprivation (TSD) protocol. The TSD was documented using wrist actigraphy and hourly mails to the research team. In each session information was collected about quality of sleep, level of rest, and DOMS pain during flexion.
Results
Mild DOMS pain was induced after 24 hours and further increased to moderate intensity after 48 hours (p<0.001). The mean pain tolerance threshold was significantly lowered comparing session 1 and session 2 (p=0.012), and the conditioned pain modulation effect was significantly impaired (p=0.036). Psychological changes after the intervention included lowered pain catastrophizing scale scores (p=0.027), lowered positive affect (p<0.001), lowered negative affect (p=0.003), and lowered anxiety (p=0.012). Using linear regression model to predict the extent of DOMS pain intensity, the first model predicted 58% of DOMS pain after 24 hours based on baseline BMI, IL-6, pressure pain detection thresholds, pain catastrophizing, positive and negative affect, and somatization (p=0.008), and 68% of DOMS pain after 48 hours based on baseline BMI, IL-6, pressure pain detection thresholds, temporal summation of pain, pain catastrophizing, positive affect, distress, and depression (p<0.001).
Conclusions
DOMS combined with one night of total sleep deprivation induced hypersensitivity to pain, impaired conditioned pain modulation, lowered positive and negative affective scores, lowered pain catastrophizing scores, and reduced symptoms of anxiety. Furthermore, a combination of baseline inflammation, psychological measures, and measures of pain sensitivity predicted 58% and 68% of DOMS pain after 24 and 48 hours, respectively.
References
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Presenting Author
Emma Hertel
Poster Authors
Emma Hertel
Msc
Aalborg University
Lead Author
Kristian Petersen
PhD
Aalborg University, Aalborg, Denmark
Lead Author
Elaxmi Sathiyalingam
Aalborg University
Lead Author
Linea Pilgaard
Aalborg University
Lead Author
Simone Juline Brommann
Aalborg University
Lead Author
Topics
- Models: Musculoskeletal