Exercise-induced Hypoalgesia Research Articles

Acute Effects of a Brief Physical Exercise Intervention on Somatosensory Perception, Lumbar Strength, and Flexibility in Patients with Nonspecific Chronic Low-Back Pain.

BackgroundEvidence-based clinical guidelines consider physical exercise one of the best nonpharmacological interventions for low-back pain (LBP), but it is necessary to clarify the exercise-induced hypoalgesia effect of different modalities of exercise in chronic pain populations.PurposeThis study focused on exploring acute changes in tactile and pressure-pain perception and lumbar strength and flexibility in patients with nonspecific chronic LBP (NSCLBP) after performing one of three 20-minute physical exercise modalities.MethodsA total of 81 patients with NSCLBP were pseudorandomly distributed into three groups of 20-minute physical exercise — 1) aerobic (n=21, mean age 42±9.72 years, nine men), 2) stretching (n=21, mean age 40±11.37 years, ten men), and 3) strengthening (n=20, mean age 35.80±11.56 years, ten men) — and 4) a control group (n=19, mean age 38.64±10.24 years, eight men), and completed self-reported questionnaires during the same period. Tactile and pressure-pain thresholds and isometric lumbar muscle endurance and flexibility were assessed before and after this brief exercise-based intervention.ResultsAll groups were comparable in terms of sociodemographic and clinical data, cardiovascular capacity, and self-reported data onphysical disability, mood, motivation, psychological response to stimulus properties of physical exercise, and physical activity enjoyment. Our analyses revealed higher tactile sensitivity (p<0.001) and pressure-pain thresholds (p<0.001) at the forefinger than other body locations. We also found lower pain sensitivity (p=0.010) and pressure pain–intensity ratings (p=0.001) and higher lumbar flexibility (p<0.001) after intervention. After calculation of absolute pre–post differences, higher tactile sensitivity was observed at the gluteus medius muscle than the erector spinal muscle only after aerobic intervention (p=0.046).ConclusionThese results add some evidence about different modalities of exercise-induced hypoalgesia in NSCLBP. However, the fact that we also found improvements in the control group limits our conclusions.

Impaired exercise-induced hypoalgesia in individuals reporting an increase in low back pain during acute exercise.

Exercise therapy is recommended for low back pain (LBP) although the immediate effects on pain are highly variable. In 96 individuals with LBP this cross-sectional study explored (a) the magnitude of exercise-induced hypoalgesia (EIH) and (b) measures of pain sensitivity and clinical pain manifestations in individuals reporting a clinical relevant increase in back pain during physical activity compared with individuals reporting low or no increase in back pain during physical activity. Cuff algometry was performed at baseline on the leg to assess pressure pain threshold (cPPT), tolerance (cPTT) and temporal summation of pain (cTSP). Manual PPTs were assessed on the back and leg before and after a 6-min walk test (6MWT). Back pain was scored on a numerical rating scale (NRS) after each minute of walking. The EIH-effect was estimated as the increase in PPTs after the walk exercise. Twenty-seven individuals reported an increase of ≥2/10 in pain NRS scores during walking and compared with the individuals with <2/10 NRS scores: cPPT and EIH-effects were lower whereas cTSP, pain intensity and disability were increased (p<0.03). Baseline NRS scores, EIH and pain thresholds were associated with the likelihood of an increase of ≥2/10 in back pain intensity during walking (p<0.05). Pain flares in response to physical activity in individuals with LBP seem to be linked with baseline pain sensitivity and pain intensity, and impair the beneficial EIH. Such information may better inform when individuals with LBP will have a beneficial effect of physical activity. Pain flares in response to physical activity in individuals with LBP seem to be linked with baseline pain sensitivity and pain intensity, and impair the beneficial exercise-induced hypoalgesia. Such information may better inform when individuals with LBP will have a beneficial effect of physical activity.

Within-session test-retest reliability of pressure pain threshold and mechanical temporal summation in healthy subjects

To determine the absolute and relative intra-rater within-session test-retest reliability of pressure pain threshold (PPT) and mechanical temporal summation of pain (TSP) at the low back and the forearm in healthy participants and to test the influence of the number and sequence of measurements on reliability metrics. In 24 participants, three PPT and TSP measures were assessed at four sites (2 at the low back, 2 at the forearm) in two blocks of measurements separated by 20 minutes. The standard error of measurement, the minimal detectable change (MDC) and the intraclass correlation coefficient (ICC) were investigated for five different sequences of measurements (e.g. measurement 1, 1-2, 1-2-3). The MDC for the group (MDCgr) for PPT ranged from 28.71 to 50.56 kPa across the sites tested, whereas MDCgr for TSP varied from 0.33 to 0.57 out of 10 (numeric scale). Almost all ICC showed an excellent relative reliability (between 0.80 and 0.97), except when only the first measurement was considered (moderate). Although minimal differences in absolute PPT reliability were present between the different sequences, in general, using only the first measurement increase measurement error. Three TSP measures reduced the measurement error. We established that two measurements of PPT and three of TSP reduced the measurement error and demonstrated an excellent relative reliability. Our results could be used in future pain research to confirm the presence of true hypo/hyperalgesia for paradigms such as conditioned pain modulation or exercise-induced hypoalgesia, indicated by a change exceeding the measurement variability.

The tolerance to stretch is linked with endogenous modulation of pain.

The effect of stretching on joint range of motion is well documented, and although sensory perception has significance for changes in the tolerance to stretch following stretching the underlining mechanisms responsible for these changes is insufficiently understood. The aim of this study was to examine the influence of endogenous pain inhibitory mechanisms on stretch tolerance and to investigate the relationship between range of motion and changes in pain sensitivity. Nineteen healthy males participated in this randomized, repeated-measures crossover study, conducted on 2 separate days. Knee extension range of motion, passive resistive torque, and pressure pain thresholds wererecorded before, after, and 10min after each of fourexperimental conditions; (i) Exercise-induced hypoalgesia, (ii) two bouts of static stretching, (iii) resting, and (iv) a remote, painful stimulus induced by the cold pressor test. Exercise-induced hypoalgesia and cold pressor test caused an increase in range of motion (p<0.034) and pressure pain thresholds (p<0.027). Moderate correlations in pressure pain thresholds were found between exercise-induced hypoalgesia and static stretch (Rho>0.507, p=0.01) and exercise-induced hypoalgesia and the cold pressor test (Rho=0.562, p=0.01). A weak correlation in pressure pain thresholds and changes in range of motion were found following the cold pressor test (Rho=0.460, p=0.047). However, a potential carryover hypoalgesic effect may have affected the results of the static stretch. These results suggest that stretch tolerance may be linked with endogenous modulation of pain. Present results suggest, that stretch tolerance may merely be a marker for pain sensitivity which may have clinical significance given that stretching is often prescribed in the rehabilitation of different musculoskeletal pain conditions where reduced endogenous pain inhibition is frequently seen.

Modulation of Exercise-Induced Hypoalgesia Following an Exercise Intervention in Healthy Subjects.

Exercise is recommended to promote and maintain health and as treatment for more than 25 diseases and pain conditions. Exercise-induced hypoalgesia (EIH), a measure of descending pain inhibitory control, has been found to be impaired in some chronic pain conditions, but it is currently unclear if EIH is modifiable. This study investigated whether a long-term exercise intervention could modulate EIH in healthy subjects. In 38 healthy subjects, EIH was assessed as change in pressure pain threshold (PPT) after a three-minute isometric wall squat within the first week and after approximately seven weeks of military training (MT). Further, temporal summation of pain (TSP) and Knee injury and Osteoarthritis Outcome Score (KOOS) were assessed. Physical performance capacity was assessed using the Endurance 20-m shuttle run fitness test (20MSR). Hypoalgesic (EIH > 0.0 kPa) and hyperalgesic (EIH ≤ 0.0 kPa) subgroups were defined based on baseline EIH. Change in EIH following MT was used as the primary outcome. Increased EIH (P = 0.008), PPT (P < 0.003), and 20MSR (P < 0.001) were found following MT, with no changes in TSP and KOOS (P > 0.05). Subjects with a hyperalgesic EIH response at baseline (26% of the participants) presented significantly improved EIH following MT (P = 0.010). Finally, an association between 20MRS change and EIH change was found (r = 0.369, P = 0.023). MT increased EIH, especially in subjects who demonstrated a hyperalgesic response at baseline. Improvement in physical performance capacity was associated with an improvement in EIH, indicating that improvement in physical performance capacity may improve central pain mechanisms.

Does isometric exercise result in exercise induced hypoalgesia in people with local musculoskeletal pain? A systematic review

ObjectiveThe aim of this review was to investigate if exercise induced hypoalgesia (EIH) occurs following isometric muscle contraction in people with local musculoskeletal symptoms. DesignSystematic review. Data sourcesMEDLINE, EMBASE, CINAHL & SportDiscus electronic databases were searched (inception to April 2020). Eligibility criteriaTwo authors independently evaluated eligibility. Randomised controlled and crossover (repeated measures) trials that measured the effects of isometric exercise in participants with localised musculoskeletal pain during, and up to 2 hours after isometric exercise were included. Other inclusion criteria included comparison to another intervention, or comparison to healthy controls. Primary outcomes were experimentally induced pain thresholds and secondary outcomes included measures of pain sensitivity from clinical testing. Results13 studies with data from 346 participants were included for narrative synthesis. EIH was reported in some upper and lower limb studies but there were no consistent data to show isometric exercises were superior to comparison interventions. ConclusionThere was no consistent evidence for EIH following isometric exercise in people with musculoskeletal pain. These findings are different to those reported in asymptomatic populations (where EIH is consistently demonstrated) as well as conditions associated with widespread symptoms such as fibromyalgia (where isometric exercise may induce hyperalgesia). Although well tolerated when prescribed, isometric exercise did not induce EIH consistently for people seeking care for local musculoskeletal symptoms. The variance in the dose, location of contraction and intensity of protocols included in this review may explain the inconsistent findings. Further work is required to better understand endogenous analgesia in musculoskeletal pain conditions.

Exercise-induced pain threshold modulation in healthy subjects: a systematic review and meta-analysis.

The use of exercise is a potential treatment option to modulate pain (exercise-induced hypoalgesia). The pain threshold (PT) response is a measure of pain sensitivity that may be a useful marker to assess the effect of physical exercise on pain modulation. The aim of this systematic review and meta-analysis is to evaluate the PT response to exercise in healthy subjects. We searched in MEDLINE, EMBASE, Web of Science, Lilacs, and Scopus using a search strategy with the following search terms: "exercise" OR "physical activity" AND "Pain Threshold" from inception to December 2nd, 2019. As criteria for inclusion of appropriate studies: randomized controlled trials or quasi-experimental studies that enrolled healthy subjects; performed an exercise intervention; assessed PT. Hedge's effect sizes of PT response and their 95% confidence intervals were calculated, and random-effects meta-analyses were performed. For the final analysis, thirty-six studies were included (n=1326). From this we found a significant and homogenous increase in PT in healthy subjects (ES=0.19, 95% CI= 0.11 to 0.27, I2=7.5%). According to subgroup analysis the effect was higher in studies: with women (ES=0.36); performing strength exercise (ES=0.34), and with moderate intensity (ES=0.27), and no differences by age were found. Confirmed by the meta-regression analysis. This meta-analysis provides evidence of small to moderate effects of exercise on PT in healthy subjects, being even higher for moderate strength exercise and in women. These results support the idea of modulation of the endogenous pain system due to exercise and highlight the need of clinical translation to chronic pain population.

Transcranial Direct Current Stimulation Accelerates The Onset of Exercise-Induced Hypoalgesia: A Randomized Controlled Study

Exercise-induced hypoalgesia (EIH) describes acute reductions in pain that occur following exercise. Current evidence suggests that the magnitude of EIH is small-to-moderate at best, warranting exploration of novel avenues to bolster these effects. Transcranial direct current stimulation (tDCS) has been shown to relieve pain and represents a promising intervention that may enhance EIH. This study aimed to determine whether anodal tDCS of the primary motor cortex (M1) can augment EIH in healthy individuals experiencing experimentally-induced musculoskeletal pain. Twenty-four healthy subjects attended 2 experimental sessions (“Day 0” and “Day 2”). On Day 0, subjects were injected with nerve growth factor into their right extensor carpi radialis brevis to induce persistent elbow pain. On Day 2, each subject received active or sham tDCS over M1 followed by an isometric grip exercise. Pain intensity, muscle soreness, sensitivity (pressure pain thresholds), and conditioned pain modulation were assessed prior to the nerve growth factor injection, on Day 2 before tDCS, immediately post-exercise, and 15 minutes post-exercise. Active tDCS expedited the onset of EIH, inducing immediate reductions in pain intensity that were not present until 15 minutes post-exercise in the sham group. However, active tDCS did not reduce muscle soreness or sensitivity when compared to sham tDCS. PerspectiveThese findings suggest that active tDCS accelerates the onset of EIH in healthy individuals experiencing experimentally-induced pain. This may represent a promising means of enhancing adherence to exercise protocols. However, larger randomised controlled trials in persistent pain populations are required to confirm the clinical impact of these findings.

Exercise-induced hypoalgesia after acute and regular exercise: experimental and clinical manifestations and possible mechanisms in individuals with and without pain.

Exercise and physical activity is recommended treatment for a wide range of chronic pain conditions. In addition to several well-documented effects on physical and mental health, 8 to 12 weeks of exercise therapy can induce clinically relevant reductions in pain. However, exercise can also induce hypoalgesia after as little as 1 session, which is commonly referred to as exercise-induced hypoalgesia (EIH). In this review, we give a brief introduction to the methodology used in the assessment of EIH in humans followed by an overview of the findings from previous experimental studies investigating the pain response after acute and regular exercise in pain-free individuals and in individuals with different chronic pain conditions. Finally, we discuss potential mechanisms underlying the change in pain after exercise in pain-free individuals and in individuals with different chronic pain conditions, and how this may have implications for clinical exercise prescription as well as for future studies on EIH.

Exercise-induced Hypoalgesia Differ At Sites Local And Remote To The Exercising Muscle Group

Dysfunction of endogenous pain-inhibitory function such as exercise-induced hypoalgesia (EIH) may predict development of chronic pain conditions. While EIH has been shown to occur in both the exercised muscle group and in remote unexercised muscle group, few studies have compared the magnitude of EIH in an exercised muscle and remote muscle groups in the same individuals following the same exercise bout. PURPOSE: The purpose of the study was to examine the EIH response at four different sites following a bout of single legged isometric exercise. METHODS: Pressure pain thresholds (PPT) of 102 participants (50 females; 52 males) were assessed bilaterally in the vastus lateralis (VL) and brachioradialis (BR) using a pressure algometer before and after isometric knee extension at 25% of maximal voluntary contraction held until task failure using their dominant leg. The percent difference between post and pre measures was defined the EIH response. RESULTS: PPT’s increased in the left BR (18.1% ± 24.7; p<0.001, d=0.275), right BR (14.4% ± 26.1; p<0.001, d=0.233), non-dominant VL (17.4% ± 24.0; p<0.001, d=0.318) and the dominant VL (34.5% ± 28.3; p<0.001, d=0.643). There were no differences between the left and right BR and the non-dominant VL with regards to the EIH response (p>0.05), however the exercised leg demonstrated a greater EIH response compared to the remote, unexercised limbs (p<0.001). CONCLUSION: EIH occurred in all sites. However the EIH response in the exercised leg was significantly more robust than the remote, unexercised sites. This findings suggests the magnitude of EIH is determined by both local and systemic factors and this should be taken into consideration when comparing EIH among studies.

No Sex Differences In Conditioned Pain Modulation Or Exercise-induced Hypoalgesia Following Lower Body Isometric Exercise

Women are more at risk than men for developing chronic pain conditions. Differences in endogenous pain-modulatory function could be a contributing factor. PURPOSE: The aim of this study was to compare conditioned pain modulation (CPM) and exercise-induced hypoalgesia (EIH) responses between adult men and women. METHODS: In a cross-sectional, non-randomized study with two independent groups of college aged males (n = 52) and females (n = 45), pressure pain thresholds (PPT) were assessed bilaterally in the vastus lateralis (VL) and brachioradialis (BR) muscles using a pressure algometer prior to and immediately following a conditioning stimulus (placing their foot in an ice bath) and performing isometric knee extension exercise to failure at 25% of maximal strength. RESULTS: Men had higher baseline PPTs than females (LBR: 372 ± 217 vs. 303 ± 119; RBR : 396 ± 236 vs. 315 ± 143; NDVL: 552 ± 281 vs. 434 ± 157 DVL: 572 ± 253 vs. 454 ± 147; P < 0.01). PPTs increased significantly (P < 0.05) following the conditioning stimulus in both males and females (LBR: 387 ± 264 to 453 ± 318 kPa, and 315 ± 126 to 359 ± 145 kPa; RBR: 400 ± 225 to 450 ± 280 kPa; and 325 ± 135 to 372 ± 161 kPa; DVL; 579 ± 289 to 658 ± 349 kPa;, and 470 ± 200 to 541 ± 201 kPa; NDVL 542 ± 263 to 623 ± 326 kPa; and 433 ± 174 to 503 ± 185 kPa in the in the males and females, respectively) indicating a CPM response in all limbs tested. PPTs increased significantly (P < 0.05) following isometric knee extension exercise to a similar extent in both males and females in all limbs tested (LBR: 387 ± 177 to 466 ± 245 kPa; and 305 ± 140 to 353 ± 162 kPa; RBR: 409 ± 172 to 462 ± 228 kPa; and 312 ± 147 to 355 ± 173 kPa. DVL: 572 ± 253 to 763 ± 366 kPa; and 454 ± 147 to 611 ± 252 kPa; NDVL: 552 ± 281 to 633 ± 353 kPa and 434 ± 157 to 526 ± 210 kPa) There was no interaction between the group x testing site for either the CPM response (P = 0.314) or the EIH response (P = 0.242). CONCLUSIONS: Men had a higher resting pain threshold than women. However, men and women exhibited similar endogenous pain inhibitory function both locally and systemically following a conditioning stimulus and isometric lower body exercise.

The Effect Of Blood Flow Restriction Resistance Training On Exercise-induced Hypoalgesia

PURPOSE: Exercise-induced hypoalgesia (EIH) describes a reduction in pain sensitivity following exercise, characterised by an elevation in pain threshold or decrease pain intensity ratings following exercise. Recent research suggests that performing light-load resistance exercise with blood flow restriction (BFR-RE) may have a pain-modulation effect. Therefore, the aim of this study was to compare the magnitude of EIH with BFR-RE to resistance exercise at both low and high intensities. METHODS: Twelve recreationally active individuals were recruited to participate. In a randomised crossover design, participants completed 4 experimental trials of resistance exercise ((1) light load resistance exercise (LLRE); (2) BFR-RE with low pressure (BFR40); (3) BFR-RE with high pressure (BFR80) and (4) heavy load resistance exercise (HLRE)). Pressure pain threshold (PPT) was then assessed at multiple body sites (dominant and non-dominant quadriceps and non-dominant trapezius muscle) pre, 5 min, 10 min and 24 hr post exercise. RESULTS: There was a two-way interaction effect for the dominant quadriceps site. Post-hoc analysis showed that, compared to LLRE, PPT was higher following BFR40, BFR80 and HLRE. PPT was higher following BFR80 compared to BFR40 and HLRE. At 24h post-exercise, PPTs were 14.5 ± 6.7% and 23.9 ± 8.2% higher than pre-exercise values in the BFR40 and BFR80 trials, respectively, whereas PPTs had returned to baseline in the LLRE and HLRE trials. Compared to LLRE, the increase in PPT was greater following BFR40 (0.28 ± 0.13 AU), BFR80 (0.64 ± 0.42 AU) and HLRE (0.34 ± 0.20 AU) in the non-dominant quadriceps. At 24h PPTs had returned to baseline. Compared to LLRE, the increase in PPT was greater following BFR40 (0.31 ± 0.27 AU), BFR80 (0.30 ± 0.17 AU), and HLRE (0.26 ± 0.13 AU) for the trapezius. At 24h PPTs had returned to baseline. CONCLUSIONS: In conclusion BFR with higher pressure leads to EIH in both dominant and non-dominant limbs suggesting both central and peripheral mechanisms of action.

Exercise-induced Hypoalgesia Is Impaired in Chronic Whiplash-associated Disorders (WAD) With Both Aerobic and Isometric Exercise.

Exercise-induced hypoalgesia (EIH) can be impaired in patients with chronic pain and may be dependent on exercise type. Factors predictive of EIH are not known. This study aimed to: (1) compare EIH in participants with chronic whiplash-associated disorders (WAD) to asymptomatic controls, (2) determine if EIH differs between aerobic and isometric exercise, (3) determine predictors of EIH. A pre-post study investigated the effect of single sessions of submaximal aerobic treadmill walking and isometric knee extension on EIH in 40 participants with chronic WAD and 30 controls. Pressure pain thresholds were measured at the hand, cervical spine, and tibialis anterior. Pain intensity, reported previous week physical activity, temporal summation, and conditioned pain modulation (CPM) were measured at baseline. Participants with WAD demonstrated impaired EIH. Although, the WAD participants demonstrated a partial EIH response (EIH induced at the hand during exercise), no EIH response was found immediately after exercise. There was no difference in EIH between exercise types. In the WAD group, moderate physical activity levels predicted EIH at the hand and high physical activity levels predicted impaired EIH at the neck. More efficient CPM predicted EIH at the hand and less efficient CPM predicted impaired EIH at the neck. These associations were found for isometric exercise only. Individuals with chronic WAD have impaired EIH with both aerobic and isometric exercise. Higher levels of physical activity and less efficient CPM may be associated with impaired EIH. This may have implications for exercise prescription in this patient group.

Does Motor Cortex Engagement During Movement Preparation Differentially Inhibit Nociceptive Processing in Patients with Chronic Whiplash Associated Disorders, Chronic Fatigue Syndrome and Healthy Controls? An Experimental Study.

Background: Patients with chronic fatigue syndrome (CFS) and chronic whiplash associated disorders (cWAD) present a reduced ability to activate central descending nociceptive inhibition after exercise, compared to measurements before exercise. It was hypothesised that a dysfunctional motor-induced inhibition of nociception partly explains this dysfunctional exercise-induced hypoalgesia. This study investigates if engagement of the motor system during movement preparation inhibits nociception-evoked brain responses in these patients as compared to healthy controls (HC). Methods: The experiment used laser-evoked potentials (LEPs) during three conditions (no task, mental task, movement preparation) while recording brain activity with a 32-channel electroencephalogram in 21 patients with cWAD, 20 patients with CFS and 18 HC. Two-factor mixed design Analysis of variance were used to evaluate differences in LEP amplitudes and latencies. Results: No differences in N1, N2, N2P2, and P2 LEP amplitudes were found between the HC, CFS, and cWAD groups. After nociceptive stimulation, N1, N2 (only at hand location), N2P2, and P2 LEP amplitudes significantly decreased during movement preparation compared to no task (within group differences). Conclusion: Movement preparation induces a similar attenuation of LEPs in patients with CFS, patients with cWAD and HC. These findings do not support reduced motor-induced nociceptive inhibition in these patients.

The Association of Psychosocial Factors and Exercise-Induced Hypoalgesia in Healthy People and People With Musculoskeletal Pain: A Systematic Review.

Exercise, a cornerstone in current treatments for people with musculoskeletal pain, elicits a phenomenon called exercise-induced hypoalgesia (EIH), which may result in reduced pain intensity and/or increased pain thresholds. However, EIH can be impaired in patients with musculoskeletal pain, and psychosocial factors may play a mediating role in EIH. The aim of this study was to systematically review the scientific literature regarding the association between psychosocial factors and EIH in healthy people and people with musculoskeletal pain. An extensive search in databases including Medline Ovid, Embase, Web of Science, PsycINFO Ovid, and the Cumulative Index to Nursing and Allied Health Literature (CINAHL) EBSCOhost was carried out. Two reviewers independently carried out study selection, data extraction, and critical appraisal. Included studies analyzed the association or effect of psychosocial factors on EIH in adults with or without musculoskeletal pain. Nine cross-sectional studies were included, 6 involving healthy people and 4 involving people with musculoskeletal pain; 1 study included both. Overall risk of bias was high. Different types of exercise bouts, psychosocial factors, and/or outcome measures were used across studies. In healthy people and people with musculoskeletal pain, most studies did not find an association between psychosocial factors and EIH. However, 1 study involving musculoskeletal pain and 2 studies with healthy people did find a significant association. Due to poor quality and heterogeneity between studies, no conclusions can be drawn regarding whether psychosocial factors are associated with EIH or not. This review includes recommendations and directions for further research to investigate the role of psychosocial factors on EIH.

Power of Words: Influence of Preexercise Information on Hypoalgesia after Exercise—Randomized Controlled Trial

Exercise increases pressure pain thresholds (PPT) in pain-free individuals, known as exercise-induced hypoalgesia (EIH). Positive preexercise information can elicit higher EIH responses, but the effect of positive versus negative preexercise information on EIH is unknown. The primary aim of this randomized controlled trial was to compare EIH at the exercising thigh muscle after an isometric squat exercise between individuals receiving positive versus negative preexercise information about the effect of exercise on pain. Secondary aims were to compare EIH at nonexercising muscles between groups, and to investigate the relationship between participants' expectations and EIH. Eighty-three participants were randomly assigned to brief positive (n = 28), neutral (n = 28) or negative (n = 27) verbal information. The neutral information group was included in the study as a reference group. Pressure pain thresholds at the thigh and trapezius muscles were assessed before and after the intervention (i.e., preexercise information+squat exercise). Expectations of pain relief were assessed using a numerical rating scale (-10 [most negative] to 10 [most positive]). Change in quadriceps and trapezius PPT after the squat exercise showed a large difference between the positive and negative information groups (quadriceps, 102 kPa; 95% confidence interval, 55-150; effect size, 1.2; trapezius, 41 kPa; 95% confidence interval, 16-65; effect size:, 0.9). The positive information group had a 22% increase in quadriceps PPT whereas the negative information group had a 4% decrease. A positive correlation was found between expectations and increase in PPT. Negative preexercise information caused hyperalgesia after the wall squat exercise, whereas positive or neutral preexercise information caused hypoalgesia. Positive preexercise information did not change the magnitude of EIH compared with neutral information.

Cognitive Inhibition Correlates with Exercise-Induced Hypoalgesia After Aerobic Bicycling in Pain-Free Participants.

PurposeExercise-induced hypoalgesia (EIH) is the short-term reduction of pain sensitivity after a single bout of exercise. Descending pain inhibition has been proposed to at least partly underlie EIH. Cognitive inhibition is the ability to inhibit a pre-potent response and has in turn been associated with descending pain inhibition, as indexed by conditioned pain modulation. Therefore, we hypothesized that cognitive inhibition is associated with higher EIH.MethodsIn this cross-sectional study, 37 pain-free participants (16 male, age 27.75 ± 9.91) completed a stop-signal task assessing cognitive inhibition ability and a control condition in the first session. In the second session, pre–post-test design EIH was assessed by means of aerobic bicycling (15 min., 75% VO2max) and isometric knee extension (90 sec, 30% MVC). EIH was assessed with pressure pain thresholds (PPT) and temporal summation of pain (TSP), each at the hand and at the leg. Correlational analyses quantified the associations between cognitive inhibition and EIH change scores.ResultsBetter cognitive inhibition correlated with EIH change scores in PPTs after aerobic bicycling at the hand (r = −0.35, 95% CI: −0.57; −0.08, p =0.021), but not at the leg (rho = −0.10, 95% CI: −0.36; 0.18, p = 0.277). No correlations between cognitive inhibition and change in PPTs after isometric knee extension at the hand (rho = −0.03, 95% CI: −0.30; 0.25, p = 0.857) nor at the leg (rho = −0.03, 95% CI: −0.25; 0.30, p = 0.857) were observed. There were no EIH effects after isometric exercise and, generally, no effects of exercise on TSP.ConclusionThis study provides preliminary evidence for the notion that cognitive inhibition might play a supportive role in EIH. Although these results are clearly in need of replication, they accord well with previously reported associations between cognitive inhibition, experimental pain and descending pain inhibition.

The effect of blood flow restriction exercise on exercise-induced hypoalgesia and endogenous opioid and endocannabinoid mechanisms of pain modulation.

This study aimed to investigate and compare the magnitude of exercise-induced hypoalgesia (EIH) with low-intensity blood flow restriction (BFR) resistance exercise (RE) at varying pressures to other intensities of resistance exercise and examine endogenous mechanisms of pain reduction. Twelve individuals performed four experimental trials involving unilateral leg press exercise in a randomized crossover design: low-load RE at 30% of one repetition maximum (1RM), high-load RE (70% 1RM), and BFR-RE (30% 1RM) at a low and high pressure. BFR pressure was prescribed relative to limb occlusion pressure at 40% and 80% for the low- and high-pressure trials. Pressure pain thresholds (PPT) were assessed before and 5 min and 24 h following exercise in exercising and nonexercising muscles. Venous blood samples were collected at the same timepoints to determine plasma concentrations of beta-endorphin and 2-arachidonoylglycerol. High-pressure BFR-RE increased PPTs in the exercising limb to a greater extent than all other trials. Comparable systemic EIH effects were observed with HLRE and both BFR-RE trials. PPTs in the exercising limb remained elevated above baseline at 24 h postexercise following both BFR-RE trials. Postexercise plasma beta-endorphin concentration was elevated during the BFR-RE trials. No changes to 2-arachidonoylglycerol concentration were observed. High pressure BFR-RE causes a greater EIH response in the exercising limb that persists for up to 24 h following exercise. The reduction in pain sensitivity with BFR-RE is partly driven by endogenous opioid production of beta-endorphin. BFR-RE should be investigated as a possible pain-modulation tool in individuals with acute and chronic pain.NEW & NOTEWORTHY High-pressure blood flow restriction (BFR) causes a greater hypoalgesia response in the exercising limb (48%) compared with light and heavy load resistance exercise (10-34%). Performing light load resistance exercise with BFR causes systemic hypoalgesia comparable with heavy load resistance exercise (10-18%). BFR resistance exercise prolonged the exercise-induced hypoalgesia response for 24 h in the exercising limb (15% and 24%, respectively). Activation of endogenous opioid production and a conditioned pain modulation effect partly mediate the relationship between exercise and hypoalgesia.

Plastic changes in amygdala subregions by voluntary running contribute to exercise-induced hypoalgesia in neuropathic pain model mice.

Physical exercise has been established as a low-cost, safe, and effective way to manage chronic pain, but exact mechanisms underlying such exercise-induced hypoalgesia (EIH) are not fully understood. Since a growing body of evidence implicated the amygdala (Amyg) as a critical node in emotional affective aspects of chronic pain, we hypothesized that the Amyg may play important roles to produce EIH effects. Here, using partial sciatic nerve ligation (PSL) model mice, we investigated the effects of voluntary running (VR) on the basal amygdala (BA) and the central nuclei of amygdala (CeA). The present study indicated that VR significantly improved heat hyperalgesia which was exacerbated in PSL-Sedentary mice, and that a significant positive correlation was detected between total running distances after PSL-surgery and thermal withdrawal latency. The number of activated glutamate (Glu) neurons in the medal BA (medBA) was significantly increased in PSL-Runner mice, while those were increased in the lateral BA in sedentary mice. Furthermore, in all subdivisions of the CeA, the number of activated gamma-aminobutyric acid (GABA) neurons was dramatically increased in PSL-Sedentary mice, but these numbers were significantly decreased in PSL-Runner mice. In addition, a tracer experiment demonstrated a marked increase in activated Glu neurons in the medBA projecting into the nucleus accumbens lateral shell in runner mice. Thus, our results suggest that VR may not only produce suppression of the negative emotion such as fear and anxiety closely related with pain chronification, but also promote pleasant emotion and hypoalgesia. Therefore, we conclude that EIH effects may be produced, at least in part, via such plastic changes in the Amyg.

Effects of fitness level and exercise intensity on pain and mood responses.

The phenomenon of exercise-induced hypoalgesia and concomitant mood changes is well-established. How exercise-induced hypoalgesia and affective responses are shaped by the intensity of an acute exercise bout and individual fitness levels is as yet not well-understood. This study investigates whether heat pain threshold (PTh), pain tolerance (PTol) and affective parameters are modulated by the intensity of an acute exercise bout and/or individuals' fitness level. Stronger analgesic responses are hypothesized after high-intensity exercise in physically fitter subjects, possibly in sync with concomitant mood changes. Thirty-three healthy men were recruited (sedentary: N=17 or recreational: N=14; mean age: 25.3±4.4years). After a fitness assessment on a cycle ergometer, subjects underwent three experimental conditions on separate days: high (20min exercise 20% above lactate threshold), low (20min exercise 20% below lactate threshold) and control (seated rest). Before and after each intervention Positive and Negative Affect Schedule, PTh and PTol (cold water emersion test) were assessed. Results indicate an increase of the Positive Affect Scale (high: 26.7±9.0 vs. 32.9±7.1, p<.001; low: 26.3±7.2 vs. 32.0±7.0, p<.001) and PTh (high: 45.1±3.1°C vs. 46.0±2.6°C, p=.003; low: 45.4±2.7°C vs. 45.9±2.6°C, p=.012) after both exercise conditions. In an exploratory analysis, PTol significantly increased only after the high exercise condition (51.2±33.7s vs. 72.4±64.0s, p=.045). Fitness level was positively correlated with the increase in PTol from pre to post high-intensity exercise (r=.59, p (one-tailed)=.002). Exercise-induced hypoalgesia depends on exercise intensity and appears to be influenced by individual fitness status, independent of mood responses. Antinociceptive effects can be elicited by physical exercise and have been extensively investigated in the literature. However, the relation between exercise intensity, fitness status, and the degree of antinociception is not well-understood. This randomized intervention provides novel evidence that antinociceptive effects indeed depend on exercise intensity, but also on general fitness status. Data extend the existing literature by highlighting aspects of exercise behaviour that promote antinociception. Effects do not simply mirror positive affective responses induced by exercise, hence, indicating partially distinct underlying mechanisms.