Systemic Exercise-Induced Hypoalgesia Following Isometric Exercise Reduces Conditioned Pain Modulation

Objective Physically active individuals show greater conditioned pain modulation (CPM) compared with less active individuals. Understanding the effects of acute exercise on CPM may allow for a more targeted use of exercise in the management of pain. This study investigated the effects of acute isometric exercise on CPM. In addition, the between-session and within-session reliability of CPM was investigated. Design Experimental, randomized crossover study. Setting Laboratory at Marquette University. Subjects Thirty healthy adults (19.3±1.5 years, 15 males). Methods Subjects underwent CPM testing before and after isometric exercise (knee extension, 30% maximum voluntary contraction for three minutes) and quiet rest in two separate experimental sessions. Pressure pain thresholds (PPTs) at the quadriceps and upper trapezius muscles were assessed before, during, and after ice water immersions. Results PPTs increased during ice water immersion (i.e., CPM), and quadriceps PPT increased after exercise (P \u3c 0.05). CPM decreased similarly following exercise and quiet rest (P \u3e 0.05). CPM within-session reliability was fair to good (intraclass correlation coefficient [ICC] = 0.43–0.70), and the between-session reliability was poor (ICC = 0.20–0.35). Due to the variability in the systemic exercise-induced hypoalgesia (EIH) response, participants were divided into systemic EIH responders (N = 9) and nonresponders (N = 21). EIH responders experienced attenuated CPM following exercise (P = 0.03), whereas the nonresponders showed no significant change (P \u3e 0.05). Conclusions Isometric exercise decreased CPM in individuals who reported systemic EIH, suggesting activation of shared mechanisms between CPM and systemic EIH responses. These results may improve the understanding of increased pain after exercise in patients with chronic pain and potentially attenuated CPM

Exercise Increases Pressure Pain Tolerance but Not Pressure and Heat Pain Thresholds in Healthy Young Men

Background: Exercise causes an acute decrease in the pain sensitivity known as exercise-induced hypoalgesia (EIH), but the specificity to certain pain modalities remains unknown. This study aimed to compare the effect of isometric exercise on the heat and pressure pain sensitivity. Methods: On three different days, 20 healthy young men performed two submaximal isometric knee extensions (30% maximal voluntary contraction in 3 min) and a control condition (quiet rest). Before and immediately after exercise and rest, the sensitivity to heat pain and pressure pain was assessed in randomized and counterbalanced order. Cuff pressure pain threshold (cPPT) and pain tolerance (cPTT) were assessed on the ipsilateral lower leg by computer-controlled cuff algometry. Heat pain threshold (HPT) was recorded on the ipsilateral foot by a computer-controlled thermal stimulator. Results: Cuff pressure pain tolerance was significantly increased after exercise compared with baseline and rest (p \u3c 0.05). Compared with rest, cPPT and HPT were not significantly increased by exercise. No significant correlation between exercise-induced changes in HPT and cPPT was found. Test–retest reliability before and after the rest condition was better for cPPT and CPTT (intraclass correlation \u3e 0.77) compared with HPT (intraclass correlation = 0.54). Conclusions: The results indicate that hypoalgesia after submaximal isometric exercise is primarily affecting tolerance of pressure pain compared with the pain threshold. These data contribute to the understanding of how isometric exercise influences pain perception, which is necessary to optimize the clinical utility of exercise in management of chronic pain. Significance: The effect of isometric exercise on pain tolerance may be relevant for patients in chronic musculoskeletal pain as a pain-coping strategy. What does this study add? The results indicate that hypoalgesia after submaximal isometric exercise is primarily affecting tolerance of pressure pain compared with the heat and pressure pain threshold. These data contribute to the understanding of how isometric exercise influences pain perception, which is necessary to optimize the clinical utility of exercise in management of chronic pain

Prognostic factors for disability and sick leave in patients with subacute non-malignant pain:a systematic review of cohort studies

OBJECTIVE: This systematic review aims to identify generic prognostic factors for disability and sick leave in subacute pain patients. SETTING: General practice and other primary care facilities. PARTICIPANTS: Adults (>18 years) with a subacute (≤3-month) non-malignant pain condition. Eligibility criteria were cohort studies investigating the prediction of disability or long-term sick leave in adults with a subacute pain condition in a primary care setting. 19 studies were included, referring to a total of 6266 patients suffering from pain in the head, neck, back and shoulders. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was long-term disability (>3 months) due to a pain condition. The secondary outcome was sick leave, defined as ‘absence from work’ or ‘return-to-work’. RESULTS: PubMed, EMBASE, CINAHL and PEDro databases were searched from 16 January 2003 to 16 January 2014. The quality of evidence was presented according to the GRADE WG recommendations. Several factors were found to be associated with disability at follow-up for at least two different pain symptoms. However, owing to insufficient studies, no generic risk factors for sick leave were identified. CONCLUSIONS: Multiple site pain, high pain severity, older age, baseline disability and longer pain duration were identified as potential prognostic factors for disability across pain sites. There was limited evidence that anxiety and depression were associated with disability in patients with subacute pain, indicating that these factors may not play as large a role as expected in developing disability due to a pain condition. Quality of evidence was moderate, low or very low, implying that confidence in the results is limited. Large prospective prognostic factor studies are needed with sufficient study populations and transparent reporting of all factors examined. TRIAL REGISTRATION NUMBER: CRD42014008914

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 welldocumented 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

Pain modulatory phenotypes differentiate subgroups with different clinical and experimental pain sensitivity

Pain biomarkers are warranted for individualized pain management. Based on different pain modulatory phenotypes, the objectives of this study were to explore the existence of subgroups within patients with nonmalignant chronic pain and to investigate differences in clinical pain and pain hypersensitivity between subgroups. Cuff algometry was performed on lower legs in 400 patients with chronic pain to assess pressure pain threshold, pressure pain tolerance, temporal summation of pain (TSP: increase in pain scores to 10 repeated stimulations), and conditioned pain modulation (CPM: increase in cuff pressure pain threshold during cuff pain conditioning on the contralateral leg). Heat detection and heat pain thresholds at clinical painful and nonpainful body areas were assessed. Based on TSP and CPM, 4 distinct groups were formed: group 1 (n 85) had impaired CPM and facilitated TSP; group 2 (n 148) had impaired CPM and normal TSP; group 3 (n 45) had normal CPM and facilitated TSP; and group 4 (n 122) had normal CPM and normal TSP. Group 1 showed more pain regions than the other 3 groups (P &lt; 0.001), indicating that impaired CPM and facilitated TSP play an important role in widespread pain. Groups 1 and 2 compared with group 4 had lower heat pain threshold at nonpainful areas and lower cuff pressure pain tolerance (P &lt; 0.02), indicating that CPM plays a role for widespread hyperalgesia. Moreover, group 1 demonstrated higher clinical pain scores than group 4 (P &lt; 0.05). Although not different between subgroups, patients were profiled on demographics, disability, pain catastrophizing, and fear of movement. Future research should investigate interventions tailored towards these subgroups.</p

Differential pain response at local and remote muscle sites following aerobic cycling exercise at mild and moderate intensity

Physical exercise has been shown to inhibit experimental pain response in the post-exercise period. Modulation of the pain system may be differentiated between muscle sites engaging in contractile activity. The purpose of this study was to assess the pain response at remote and local muscle sites following aerobic exercise at different work intensities. Participants included 10 healthy and physically active males (mean age ± SD, 21.2 ± 3.4). Somatic pressure pain threshold (PPT) at the rectus femoris (local) and brachioradialis (remote) muscle site was measured at before (Pre), 5 min after (Post1), and 15 min after (Post2) aerobic cycling exercise at 70 and 30 % of peak oxygen uptake (VO(2peak)) performed on different occasions in a counterbalanced order, separated by minimum of 3 days interval. Repeated measures ANOVA for PPT reveals significant main effect for time (f = 3.581, p = 0.049, observed power = 0.588) and muscle site (f = 17.931, p = 0.002, observed power = 0.963). There was a significant interaction shown for exercise intensity by time (f = 11.390, p = 0.012, observed power = 0.790). PPT at rectus femoris following cycling exercise at 70 % of VO(2peak) reveals a significant increase between Pre-Post1 (p = 0.040). PPT for rectus femoris following cycling exercise at 30 % of VO(2peak) revealed a significant decrease between Pre-Post1 (p = 0.026) and Pre-Post2 (p = 0.008). The PPT for brachioradialis following cycling exercise at 30 % of VO(2peak) revealed a significant decrease between Pre-Post1 (p = 0.011) and Pre-Post2 (p = 0.005). These results show that aerobic exercise increases PPT locally at the exercise muscle site following exercise at 70 % of VO(2peak) but reduces PPT following exercise at 30 % of VO(2peak)

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.</p

Facilitated pronociceptive pain mechanisms in radiating back pain compared with localized back pain

Facilitated pain mechanisms and impaired pain inhibition are often found in chronic pain patients. This study compared clinical pain profiles, pain sensitivity, as well as pronociceptive and antinociceptive mechanisms in patients with localized low back pain (n = 18), localized neck pain (n = 17), low back and radiating leg pain (n = 18), or neck and radiating arm pain (n = 17). It was hypothesized that patients with radiating pain had facilitated pain mechanisms and impaired pain inhibition compared with localized pain patients. Cuff algometry was performed on the nonpainful lower leg to assess pressure pain threshold, tolerance, temporal summation of pain (increase in pain scores to 10 repeated stimulations at pressure pain tolerance intensity), and conditioning pain modulation (increase in pressure pain threshold during pain conditioning on the contralateral leg). Heat detection and heat pain threshold at the nonpainful hand were also assessed. Clinical pain intensity, psychological distress, and disability were assessed with questionnaires. Temporal summation of pain was increased in patients with radiating back pain compared with localized back pain (P &lt;.03). Patients with radiating arm pain or localized low back pain demonstrated hyperalgesia to heat and pressure in nonpainful body areas (P &lt;.05), as well as well as a facilitated clinical pain profile compared with patients with localized neck pain (P =.03). Patients with radiating pain patterns demonstrated facilitated temporal summation suggesting differences in the underlying pain mechanisms between patients with localized back pain and radiating pain. Perspective These findings have clinical implications because the underlying mechanisms in different back pain conditions may require different treatment strategies.</p

Walking increases pain tolerance in humans an experimental cross-over study

Background and aims: Exercise is commonly used as treatment for chronic pain with positive long-term effects on pain and pain-related disability. In pain-free subjects, hypoalgesia following an acute bout of exercise compared with a control condition has consistently been demonstrated also known as exercise-induced hypoalgesia (EIH). Walking exercise, a low intensity aerobic exercise, is frequently used in clinical practice as an easily applicable intervention for patients with chronic pain. Walking exercise is furthermore recommended as an effective treatment for patients with chronic musculoskeletal pain conditions to alleviate pain and reduce disability, however, the effect of walking on pain sensitivity is currently unknown. The aims of the present study were to investigate (1) the acute effect of walking on pain sensitivity, and (2) the relative (between-subjects) and absolute (within-subject) test-retest reliability of the hypoalgesic response across two sessions separated by 1 week. Methods: In this randomised experimental cross-over study including two identical sessions, 35 pain-free subjects performed a standardized 6 min walking test and a duration-matched quiet rest condition in a randomized and counterbalanced order in each session. Before and after both conditions, handheld pressure pain thresholds (PPTs) were assessed at the thigh and shoulder, and pressure pain thresholds (cPPT) and pain tolerance (cPTT) were assessed with computer-controlled cuff algometry at the lower leg. Change in the pain sensitivity measures were analysed with repeated-measures ANOVAs, and test-retest reliability with intraclass correlation coefficients (ICC) and agreements in classification of EIH responders/ non-responders between the two sessions. Results: All subjects completed the walking conditions in both session 1 and session 2. The perceived intensity of walking assessed with rating of perceived exertion (RPE) and walking distance did not differ significantly between session 1 (distance: 632.5 ± 75.2 meters, RPE: 10.9 ± 1.9) and session 2 (distance: 642.1 ± 80.2 meters, RPE: 11.0 ± 2.4) (p &gt; 0.11). Moreover, RPE showed excellent relative reliability with an ICC value of 0.95 [95%CI: 0.90–0.97]. Walking increased pain tolerance (mean difference: 2.6 kPa [95%CI: 0.5–4.9 kPa; p = 0.02]), but not pain thresholds compared with rest in both sessions. Hypoalgesia after walking demonstrated fair to good relative reliability (ICC = 0.61), however the agreement in classification of EIH responders/non-responders (absolute reliability) across sessions was low and not significant (κ = 0.19, p = 0.30). Conclusions: Walking consistently increased pain tolerance but not pain thresholds compared with a duration-matched control condition with fair to good relative reliability between sessions. Based on classification of EIH responders/non-responders the absolute reliability between the two sessions was low indicating individual variance in the EIH response. Future studies should investigate the hypoalgesic effect of a walking exercise in a clinical pain population.</p

Alterations in pro-nociceptive and anti-nociceptive mechanisms in patients with low back pain:a systematic review with meta-analysis

Altered pronociceptive and antinociceptive mechanisms are often implicated in painful conditions and have been increasingly studied over the past decade. For some painful conditions, alterations are well-established, but in populations with low back pain (LBP), there remains considerable debate whether these mechanisms are altered. The present systematic review aimed to address this issue by identifying studies assessing conditioned pain modulation (CPM) and/or temporal summation of pain (TSP) in patients with LBP, comparing with either a healthy control group or using a method with reference data available. Qualitative synthesis and quantitative meta-analysis of group differences were performed. For CPM and TSP, 20 and 29 original articles were eligible, with data for meta-analysis obtainable from 18 (1500 patients and 505 controls) and 27 (1507 patients and 1127 controls) studies, respectively. Most studies were of poor-to-fair quality with significant heterogeneity in study size, population, assessment methodology, and outcome. Nonetheless, CPM was impaired in patients with LBP compared with controls (standardized mean difference = -0.44 [-0.64 to -0.23], P &lt; 0.001), and the magnitude of this impairment was related to pain chronicity (acute/recurrent vs chronic, P = 0.003), duration (RS = -0.62, P = 0.006), and severity (RS = -0.54, P = 0.02). Temporal summation of pain was facilitated in patients with LBP compared with controls (standardized mean difference = 0.50 [0.29-0.72], P &lt; 0.001), and the magnitude of this facilitation was weakly related to pain severity (RS= 0.41, P = 0.04) and appeared to be influenced by test modality (P &lt; 0.001). Impaired CPM and facilitated TSP were present in patients with LBP compared with controls, although the magnitude of differences was small which may direct future research on the clinical utility.</p