A significant driver of pain in low back pain (LBP) is alteration to endogenous pain modulation (EPM). EPM can be measured using quantitative sensory tests (QST), which provides important information on nociceptive pathways. Exercise therapy is recommended as the first line of care for LBP; however, there is limited information on the mechanisms of action that lead to symptom improvements. The first manuscript was a scoping review that summarized protocols used to assess EPM using QST such as pain pressure threshold (PPT), temporal summation (TS), conditioned pain modulation (CPM) or exercise-induced hypoalgesia (EIH) in LBP. Scientific databases were searched for articles that used QST or EIH protocols in LBP. In total, 193 studies were included in this review: 172 used PPT, 54 used TS and 53 used CPM and 5 investigated EIH. There was high variability in the type of equipment, timing, trials, and testing location with many studies not reporting this information. The results demonstrate a need for standardized protocols and reporting guidelines as well as further research to aid in selecting the most appropriate QST parameters for different clinical presentations. The second manuscript was a pilot study that assessed the feasibility of a protocol investigating if changes in EPM occur after exercise therapy. Participants were recruited through a larger trial (WELBack) and were randomized to receive one of two exercise therapies. Participants attended two testing sessions (before and after an 8-week treatment) consisting of PPT, TS, CPM and EIH. Thirty-six participants were recruited and completed baseline assessments. In total, 32 (88.9%) participants completed the follow-up assessment. The results demonstrated that the protocol was feasible. Improvements to patient reported outcomes were seen, but not to all EPM measures. Future work should consider changes to the CPM protocol, and a fully powered study to investigate EPM changes after exercise therapy. / Thesis / Master of Health Sciences (MSc) / Low back pain (LBP) may occur because of changes in our nervous system, rather than a physical injury. However, there is no previous research on if exercise can improve these changes. The purpose of this thesis was to develop and test a protocol to assess how the body processes pain, and if this can change after exercise. We summarized past research on how four tests to assess pain processing have been performed. The results showed many differences in how these tests were performed and reported. More consistency and guidelines are needed to improve how these tests are conducted. Next, we conducted a study aimed to assess the feasibility of a protocol to see if changes occur in how the body processes pain after an exercise therapy program. The results of this study showed the protocol was feasible, and trends in improvement on some but not all measures.

Syfte: Syftet med denna studie var att undersöka hur statisk muskelkontraktion och cold pressor test påverkar kroppsegna smärtreglerande system (”Exercise induced analgesia” (EIA) och ”Conditioned pain modulation” (CPM)) hos patienter med kronisk ländryggssmärta kännetecknad av lumbal myalgi (LM) jämfört med friska kontroller. Försökspersoner och metod: Tjugosex friska köns- och åldersmatchade personer och tjugosex LM-patienter deltog. De utförde standardiserad statisk muskelkontraktion med m. Erector spinae (ME) i form av rygglyft och kontraktion av m. Quadriceps femoris (MQ) i form av knäledsextension. För att bedöma CPM användes sk cold pressor test. Smärttrösklar för tryck (PPTs) mättes över m. Deltoideus (MD), m. Erector spinae (ME) samt över m. Quadriceps (MQ) i vila och under resp. efter kontraktionen/cold pressor test. Under kontraktion mättes PPTs över den arbetande muskeln respektive över de två vilande musklerna. Dessutom undersöktes PPTs och känsligheten för övertrösklig trycksmärta (P7) i vila på 8 olika punkter på kroppen. Resultat: Kvinnliga LM-patienter hade ökad känslighet för trycksmärta (PPT) och övertrösklig trycksmärta (P7) jämfört med köns- och åldermatchade friska kontroller, medan manliga LM-patienter paradoxalt nog hade minskad känslighet för övertrösklig trycksmärta. Beträffande EIA fann vi att LM-patienter och kontroller kunde aktivera lokal EIA under kontraktion med ME. Vi fann dessutom en minskad förmåga hos LM-patienter att rekrytera generaliserad EIA under kontraktion med MQ. Slutligen hade LM-patienterna en normal funktion av CPM. Slutsats: LM-patienter kunde aktivera lokal EIA under kontraktion av ME, men hade mindre effektiv generaliserad EIA jämfört med kontrollerna, trots normal funktion av CPM. Våra resultat tyder på att muskelarbete med smärtande ryggmuskler skulle kunna användas för att minska smärtkänslighet i det drabbade området.