Characteristics, Mechanisms, and Health Implications of Exercise-Induced Hypoalgesia

2019 ◽  
Author(s):  
Laura D. Ellingson ◽  
Christopher D. Black
Keyword(s):  
Chronic Pain ◽  
Isometric Exercise ◽  
Exercise Adherence ◽  
Exercise Bout ◽  
Pain Modulation ◽  
Dynamic Resistance ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Exercise Induced ◽  
Sensitivity To Pain

Exercise is known to exert an influence on pain. Specifically, sensitivity to pain decreases both during and following a single bout of exercise—a phenomenon that has been termed exercise-induced hypoalgesia (EIH). EIH has been shown to occur following a variety of types of exercise including aerobic, dynamic resistance, as well as intermittent and continuous isometric exercise, and with a variety of types of pain stimuli including pressure, thermal, and electrical, among others. Depending upon the type of exercise, the intensity and duration of the exercise bout may affect the magnitude of EIH observed. EIH also may be influenced by presence of chronic pain. In individuals with chronic pain conditions, exercise can have both hypo- and hyperalgesic effects, again depending on the specifics of the exercise stimulus itself. The mechanisms underlying EIH have not been definitively established. However, a number of potentially viable mechanisms have been examined including: release of stress mediators such as adrenocorticotrophic hormone and growth hormone (GH), stimulation of the endogenous opioid system, interactions between the pain modulatory system and the cardiovascular system resulting from shared neurological pathways, activation of the endocannabinoid (eCB) system, and engagement of supraspinal pain inhibitory mechanisms via conditioned pain modulation (CPM). There is also some evidence that psychosocial factors, including pain-related beliefs like catastrophizing and expectation, may influence EIH. Research in EIH has several important implications for research and practice. In healthy adults, reduced sensitivity to pain is a salient benefit of exercise and EIH responses may play a role in exercise adherence. For chronic pain patients, research on EIH has the potential to uncover mechanisms related to maintenance of chronic pain. Improving our understanding of how and why hyperalgesia occurs following exercise in these patients can aid in understanding central nervous system mechanisms of disease maintenance and ultimately may help to avoid symptom exacerbation with exercise. However, there remain practical and mechanistic questions to be examined. Translating reductions in pain sensitivity that occur with exercise under controlled laboratory conditions to situations that are more naturalistic will be an important next step for promoting physical activity as a treatment for pain.

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

2020 ◽  
Vol 52 (7S) ◽  
pp. 630-630
Author(s):  
Robert E. Hight ◽  
Jessica A. Peterson ◽  
Cameron Lohman ◽  
Michael G. Bemben ◽  
Rebecca D. Larson ◽  
...  
Keyword(s):  
Sex Differences ◽  
Isometric Exercise ◽  
Pain Modulation ◽  
Conditioned Pain Modulation ◽  
Lower Body ◽  
Exercise Induced

The influence of isometric exercise on endogenous pain modulation: comparing exercise-induced hypoalgesia and offset analgesia in young, active adults

2018 ◽  
Vol 18 (3) ◽  
pp. 513-523 ◽  
Author(s):  
Samuel Harris ◽  
Michele Sterling ◽  
Scott F. Farrell ◽  
Ashley Pedler ◽  
Ashley D. Smith
Keyword(s):  
Cervical Spine ◽  
Tibialis Anterior ◽  
Isometric Exercise ◽  
Pain Modulation ◽  
Exercise Interventions ◽  
Pressure Pain Thresholds ◽  
Pain Ratings ◽  
Exercise Induced ◽  
Active Adults ◽  
Endogenous Analgesia

Abstract Background and aims Impairment of endogenous analgesia has been associated with the development, maintenance and persistence of pain. Endogenous analgesia can be evaluated using exercise-induced hypoalgesia (EIH) and offset analgesia (OffA) paradigms, which measure temporal filtering of sensory information. It is not clear if these paradigms are underpinned by common mechanisms, as EIH and OffA have not previously been directly compared. A further understanding of the processes responsible for these clinically relevant phenomena may have future diagnostic and therapeutic utility in management of individuals with persistent pain conditions. The primary aim of this study was to investigate if there is a correlation between the magnitudes of EIH and OffA. The secondary aim of the study was to examine whether exercise influences OffA. Methods Thirty-six healthy, pain-free participants were recruited. EIH was evaluated using pressure pain thresholds (PPT) and pain ratings to suprathreshold pressure stimuli over tibialis anterior and the cervical spine. OffA evaluation utilised a three-step protocol, whereby individualised heat pain thermal stimuli [Numerical Rating Scale (NRS)=50/100] were applied (T1), before increasing 1 °C (T2), followed by 1 °C reduction (T3). The magnitude of OffA was calculated as the percentage reduction in the NRS from T2 to T3. PPT/suprathreshold pain ratings and OffA measures were recorded, before and after 5 min of isometric quadriceps exercise performed at 20–25% maximum voluntary contraction (MVC); and following a 15 min rest period. Data were analysed using repeated measures (RM) ANCOVA and correlational analyses. Results There was no correlation between EIH measures (PPTs or pain ratings to suprathreshold pressure stimuli over tibialis anterior or the cervical spine) and OffA (p>0.11 for all). OffA was induced and not modulated by exercise (p=0.28). Conclusions Five minutes of 20–25% MVC lower limb isometric exercise provided non-pharmacological pain modulation in young, active adults. Magnitude of EIH was not correlated with that of OffA, and exercise did not influence magnitude of OffA. Implications These results suggest that in young, pain-free individuals, separate testing of these two paradigms is required to comprehensively evaluate efficacy of endogenous analgesia. If these results are replicated in patient populations, alternative or complementary methods to exercise interventions may be required to modulate impaired OffA.

scholarly journals Identification of MOR-Positive B Cell as Possible Innovative Biomarker (Mu Lympho-Marker) for Chronic Pain Diagnosis in Patients with Fibromyalgia and Osteoarthritis Diseases

2020 ◽  
Vol 21 (4) ◽  
pp. 1499 ◽  
Author(s):  
William Raffaeli ◽  
Valentina Malafoglia ◽  
Antonello Bonci ◽  
Michael Tenti ◽  
Sara Ilari ◽  
...  
Keyword(s):  
Chronic Pain ◽  
B Cells ◽  
B Cell ◽  
Biological Marker ◽  
Analysis Data ◽  
Negative Control Group ◽  
Negative Control ◽  
Control Group ◽  
Endogenous Opioid System ◽  
Endogenous Opioid

Fibromyalgia (FM) diagnosis follows the American College of Rheumatology (ACR) criteria, based on clinical evaluation and written questionnaires without any objective diagnostic tool. The lack of specific biomarkers is a tragic aspect for FM and chronic pain diseases in general. Interestingly, the endogenous opioid system is close to the immune one because of the expression of opioid receptors on lymphocytes membrane. Here we analyzed the role of the Mu opioid receptor on B lymphocytes as a specific biomarker for FM and osteoarthritis (OA) patients. We enrolled three groups of females: FM patients, OA patients (chronic pain control group) and healthy subjects (pain-free negative control group). We collected blood samples to apply immunophenotyping analysis. Written tests were administrated for psychological analysis. Data were statistically analyzed. Final results showed that the percentage of Mu-positive B cells were statistically lower in FM and OA patients than in pain-free subjects. A low expression of Mu-positive B cell was not associated with the psychological characteristics investigated. In conclusion, here we propose the percentage of Mu-positive B cells as a biological marker for an objective diagnosis of chronic pain suffering patients, also contributing to the legitimacy of FM as a truly painful disease.

Gender Differences in Pain

2017 ◽  
Author(s):  
Gregory Carpenter ◽  
Meenal Patil
Keyword(s):  
Chronic Pain ◽  
Clinical Findings ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Women Studies ◽  
Pain Experience ◽  
Increased Risk ◽  
Sociocultural Differences ◽  
Opioid Medications ◽  
Pain Inhibition

Epidemiologic and clinical findings demonstrate that women are at increased risk for chronic pain, experience greater pain-related distress, and show heightened sensitivity for pain compared to men. There are differences in analgesic responses to pain and to both opioid and non-opioid medications as well as for endogenous analgesic processes. Many stress-related disorders, such as fibromyalgia and chronic pain, are more prevalent in women. Studies of experimentally induced pain show that women exhibit greater pain sensitivity, enhanced pain facilitation, and reduced pain inhibition compared to men. Mechanisms that implicated in the underlying sex differences include biological involvement of estrogen and progesterone versus testosterone. Sex-related differences in pain may also reflect differences in the endogenous opioid system. Other mechanisms include steroid action differences in adulthood, modulation of various biological systems such as the cardiovascular and inflammatory pathways, and sociocultural differences

Influence of endogenous opioids on the response of selected hormones to exercise in humans

1986 ◽  
Vol 61 (3) ◽  
pp. 1051-1057 ◽  
Author(s):  
P. A. Farrell ◽  
A. B. Gustafson ◽  
T. L. Garthwaite ◽  
R. K. Kalkhoff ◽  
A. W. Cowley ◽  
...  
Keyword(s):  
Venous Blood ◽  
Endogenous Opioids ◽  
Psychological State ◽  
Opioid Antagonist ◽  
Plasma Norepinephrine ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Naltrexone Treatment ◽  
The Difference ◽  
Exercise Induced

To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.

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

Pain Medicine ◽  
2018 ◽  
Vol 20 (1) ◽  
pp. 180-190 ◽  
Author(s):  
Ali Alsouhibani ◽  
Henrik Bjarke Vaegter ◽  
Marie Hoeger Bement
Keyword(s):  
Isometric Exercise ◽  
Pain Modulation ◽  
Conditioned Pain Modulation ◽  
Exercise Induced

scholarly journals Exercise- and Stress-Induced Hypoalgesia in Musicians with and without Shoulder Pain: A Randomized Controlled Crossover Study

2016 ◽  
Vol 19 (2;2) ◽  
pp. 59-68
Author(s):  
Dr. Nathalie Roussel
Keyword(s):  
Crossover Study ◽  
Shoulder Pain ◽  
Isometric Exercise ◽  
Testing Procedure ◽  
Pain Modulation ◽  
Pain Thresholds ◽  
Remote Areas ◽  
Stressful Task ◽  
Exercise Induced ◽  
Psychological Demands

Background: Professional and pre-professional musicians are characterized by physical and psychological demands inherent to their musical activity, and therefore at risk for developing performance related musculoskeletal pain. Physical and psychological demands are known to influence human pain modulation. Objectives: In this study we compared the influence of a physically and emotionally stressful task on pain thresholds in musicians with and without shoulder pain. Study Design: A single-blinded randomized and controlled crossover study design was used to compare the effects of a physical versus emotional testing procedure on pressure pain thresholds (PPTs) in musicians with and without shoulder pain. Setting: All data were obtained in the field (e.g., at the physiotherapy accommodation in the Royal Conservatory). Methods: During the physical testing procedure, the subjects performed an isometric exercise of the glenohumeral external rotators. The emotional task comprised watching “unpleasant” images selected from the International Affective Picture System. The outcome was the assessment of change in PPTs before and after the physical and emotional task. Results: Our results indicate similar effects of both protocols in either group, i.e., musicians with and without shoulder pain (P > 0.05). All musicians showed elevated PPTs at local and remote areas after isometric exercise (P < 0.05). The emotional stress task increased PPTs at remote areas only (P < 0.05). Limitations: Despite the small sample size of musicians without shoulder pain, a power of 78.5% was achieved to detect the necessary effect size of Cohen’s d = 1. Furthermore, comparing these results with those of non-musicians (both healthy subjects and patients with shoulder pain) might reveal information regarding the specific adaptations. Finally a high variability was observed in shoulder disability (i.e., SDQ-scores) as typically seen in a population with shoulder pain. Conclusions: In musicians with and without regional shoulder pain, no significant differences were found with respect to pain modulation during a physically and an emotionally stressful task. Both interventions adequately activated central and widespread pain inhibitory mechanisms in both groups. Key words: Pressure pain threshold, PPT, exercise induced hypoalgesia, exercise induced analgesia, stress induced hypoalgesia, shoulder pain, musicians, regional pain:

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

2020 ◽  
Vol 128 (4) ◽  
pp. 914-924 ◽  
Author(s):  
Luke Hughes ◽  
Stephen David Patterson
Keyword(s):  
High Pressure ◽  
Blood Flow ◽  
Resistance Exercise ◽  
Load Resistance ◽  
Pain Modulation ◽  
Blood Flow Restriction ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Flow Restriction ◽  
Exercise Induced

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.

scholarly journals Anxiety enhances pain in a model of osteoarthritis and is associated with altered endogenous opioid function and reduced opioid analgesia

2020 ◽  
Author(s):  
Amanda Lillywhite ◽  
Stephen G. Woodhams ◽  
David J. G. Watson ◽  
Li Li ◽  
James J. Burston ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Opioid Analgesic ◽  
Opioid Analgesics ◽  
Endogenous Opioid System ◽  
High Anxiety ◽  
Endogenous Opioid ◽  
Pain Behaviour ◽  
Chronic Pain Patients ◽  
Pain Patients ◽  
Analgesic Use

AbstractChronic pain states such as osteoarthritis (OA) are often associated with negative affect, including anxiety and depression. This is, in turn, associated with greater opioid analgesic use, potentially contributing to current and future opioid crises. We utilise an animal model to investigate the neurobiological mechanisms underlying increased opioid use associated with high anxiety and chronic pain.Combining a genetic model of negative affect, the Wistar Kyoto (WKY) rat, and intra-articular injection of monosodium iodoacetate (MIA; 1mg), our model of high anxiety and augmented OA-like pain behaviour mirrors the clinical problem. Effects of morphine (0.5-6mg.kg-1) on pain behaviour and spinal nociceptive neuronal activity were determined in WKY rats, and normo-anxiety Wistar rats, 3 weeks after MIA injection. WKY rats developed augmented OA-like pain, and had blunted inhibitory responses to morphine, when compared to Wistar rats. Potential alterations in endogenous opioid function were probed via systemic blockade of opioid receptors with naloxone (0.1-1mg.kg-1), quantification of circulating levels of β-endorphin, and determination of spinal expression of the mu-opioid receptor (MOR). These studies revealed increased opioidergic tone, and increased spinal desensitization of MORs via the master phosphorylation site at serine residue 375, in this model.We demonstrate attenuated MOR function in the absence of previous exogenous opioid ligand exposure in our model of high anxiety and OA-like pain, which may account for reduced analgesic effect of morphine and provide a potential explanation for increased opioid analgesic intake in high anxiety chronic pain patients.Significance StatementChronic pain affects large numbers of people, and pain management often relies on poorly effective opioid analgesics, the iatrogenic effects of which are increasingly recognised. The endogenous opioid system - the target for exogenous opioid analgesics - plays key roles in emotional affective states and pain control, but the complex interplay between anxiety, chronic pain, and endogenous opioid system function is challenging to study in people. Here, we have addressed this using a clinically-relevant experimental model. Anxiety-like behaviour was associated with increased chronic arthritis-like pain behaviour, altered opioid receptor function, and reduced efficacy of opioid analgesics. We provide new evidence, which may explain why chronic pain patients with comorbid high anxiety have higher opioid analgesic use.

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