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Exercising non-painful muscles can induce hypoalgesia in individuals with chronic pain

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Published/Copyright: April 1, 2017
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Scandinavian Journal of Pain
From the journal Scandinavian Journal of Pain Volume 15 Issue 1

1 What is exercise-induced hypoalgesia (EIH)?

Almost 40 years ago, Black et al. [1] published the first article on the effect of physical exercise on pain sensitivity in humans illustrating that a period of running significantly reduced the pain sensitivity. This phenomenon also known as ‘exercise-induced hypoalgesia (EIH)’ is now well established in pain-free subjects, and it is typically demonstrated as reduced pain sensitivity in response to exercise [2]. Recently, the influence of different types of exercises [3] as well as the mechanisms underlying EIH [4] has been investigated. However, the effect of acute exercise on the pain sensitivity in subjects with different chronic pain conditions is still controversial, since both hypoalgesia, as well as no change in pain sensitivity, or even hyperalgesia (i.e. impaired EIH) has been reported following exercise.

2 Isometric exercise differs from aerobic exercise in effect on pain sensitivity

In this issue of the Scandinavian Journal of Pain, Smith et al. [5] investigated the effect of two different types of exercises on pressure pain thresholds (PPTs) in 21 subjects with chronic whiplash-associated disorder (WAD) and in 19 pain-free controls. PPT at the neck and leg were recorded before and after isometric (3 min wall squat; leg muscle contraction without joint movement) and aerobic (30 min bicycling) exercises. In addition, conditioned pain modulation (CPM), heat and cold pain threshold, and psychological distress were assessed. The study showed increases in PPT at exercising (leg) and non-exercising (neck) body parts in subjects with WAD and pain-free controls after the isometric exercise condition, but not after the aerobic bicycling exercise. Surprisingly, no significant difference in EIH was found between subjects with WAD and pain-free controls. The magnitude of EIH was not associated with CPM, thermal pain sensitivity, or measures of psychological distress (pain catastrophization, fear of movement, and symptoms of posttraumatic stress).

3 Isometric exercises of pain-free muscles can induce EIH in chronic pain conditions

One interesting aspect of this study is certainly the hypoalgesic effect of just 3 min of isometric exercise. The induction of multi-segmental hypoalgesia after isometric exercise in subjects with WAD is consistent with previous studies on subjects with chronic pain [6], and EIH after isometric exercises appear to be less dependent on exercise intensity [3] than aerobic exercises which may increase its applicability in subjects with chronic pain. In addition, isometric exercise may reduce temporal summation of pain [7,8], which is often facilitated in subjects with chronic pain [9,10], illustrating the potential for isometric exercise as a rehabilitation procedure also targeting the central mechanisms of pain. A limitation to the interpretation of the current results is that aerobic exercise did not induce hypoalgesia in the pain-free controls questioning whether the exercise protocol used to induce hypoalgesia was sufficient. It should be mentioned that aerobic exercise at similar intensity as used in the current study did not significantly affect temporal summation of pain in pain-free subjects [7] and further facilitated temporal summation of pain in subjects with chronic musculoskeletal pain and high pain sensitivity [11]. Temporal summation was not evaluated by Smith et al. [5] and this is obviously an area requiring further investigations.

4 Exercising pain-full muscles may increase central pain-facilitatory mechanisms

In Smith et al. [5], PPTs were investigated before and after exercises performed at extra-segmental sites to the clinical pain region. EIH after exercises performed at non-painful body parts has previously been observed in subjects with different chronic pain conditions [6,12,13,14]. One question that the current study cannot answer is how exercises performed at sites within the clinical pain region would have affected the pain sensitivity. There is a hint of comparative effects from another study investigating EIH in 20 subjects with trapezius myalgia showing increased PPTs at painful and non-painful body parts only during contractions of non-painful muscles but not during contractions of painful muscles [6]. Similar results were reported in subjects with chronic knee osteoarthritis where only upper body exercise, and not lower body exercises, significantly increased PPTs at upper and lower body parts. Impaired EIH is often demonstrated in subjects with fibromyalgia [15,16] and chronic fatigue syndrome [13,17], which are pain conditions characterized by more widespread pain distributions reducing the likelihood of exercising non-painful body parts. Exercising painful body areas may activate local, spinal or supraspinal pain facilitatory mechanisms [18] and over-ride the pain inhibitory effects of exercise.

5 Activated central descending inhibitory mechanisms facilitate exercise-induced hypoalgesia

Can the results be generalized to other subjects with chronic pain? Similar to other subjects with chronic pain conditions [19], the subjects with WAD investigated by Smith et al. [5] demonstrated reduced pain threshold for pressure and cold at painful and non-painful assessment sites indicating generalized hyperalgesia. However, the included subjects were also characterized by relatively low levels of clinical pain intensity and disability, and showed no sign of dysfunctional CPM compared with pain-free controls. Although no association between EIH and CPM was found in this study, impaired EIH has been demonstrated in subjects with impaired CPM [11,20] indicating that subjects who demonstrate a greater ability to activate the descending inhibitory systems, report greater hypoalgesia following exercise.

6 Exercise may activate endogenous opioid and cannabinoid systems

How does exercise reduce the pain sensitivity? To date, the mechanisms underlying EIH is not clear but based on previous findings, hypoalgesia after exercise is related to activation of systemic pain inhibitory mechanisms with widespread anti-nociceptive effects in concert with local or segmental pain inhibitory mechanisms [3]. Previous findings have implicated that several mechanisms are involved in the widespread anti-nociceptive effects of exercise including activation of the endogenous opioid system [21], the endocannabinoid system [4], and the cardiovascular system [22], but further research into the underlying mechanisms is warranted to optimize the clinical utility of exercise as a method of pain management.

7 Conclusion and implications for research and management of chronic pain

Hypoalgesia after exercise in subjects with chronic pain seems to be influenced by type of exercise and whether the muscles performing the exercises are painful or not. This study by Smith et al. [5] adds to the current literature regarding the effect of exercise on pain sensitivity in subjects with chronic pain, and the results have implications for research and clinical management in this important area.

DOI of refers to article: http://dx.doi.org/10.1016/j.sjpain.2016.11.007.

Pain Research Group, Pain Center South, University Hospital Odense, Heden 7-9, Indgang 200, DK-5000 Odense C, Denmark.

  1. Conflict of interest: The author has no conflict of interest to declare.

References

[1] Black J, Chesher GB, Starmer GA, Egger G. The painlessness of the long distance runner. Med J Aust 1979;1:522–3.Search in Google Scholar

[2] Naugle KM, Fillingim RB, Riley 3rd JL. A meta-analytic review of the hypoalgesic effects of exercise. J Pain 2012;13:1139–50.Search in Google Scholar

[3] Vaegter HB, Handberg G, Graven-Nielsen T. Similarities between exercise-induced hypoalgesia and conditioned pain modulation in humans. Pain 2014;155:158–67.Search in Google Scholar

[4] Koltyn KF, Brellenthin AG, Cook DB, Sehgal N, Hillard C. Mechanisms of exercise-induced hypoalgesia. J Pain 2014;15:1294–304.Search in Google Scholar

[5] Smith A, Ritchie C, Pedler A, McCamley K, Roberts K, Sterling M. Exercise induced hypoalgesia is elicited by isometric, but not aerobic exercise in individuals with chronic whiplash associated disorders. Scand J Pain 2017;15:14–21.Search in Google Scholar

[6] Lannersten L, Kosek E. Dysfunction of endogenous pain inhibition during exercise with painful muscles in patients with shoulder myalgia and fibromyalgia. Pain 2010;151:77–86.Search in Google Scholar

[7] Vaegter HB, Handberg G, Graven-Nielsen T. Isometric exercises reduce temporal summation of pressure pain in humans. Eur J Pain 2015;19:973–83.Search in Google Scholar

[8] Koltyn KF, Knauf MT, Brellenthin AG. Temporal summation of heat pain modulated by isometric exercise. Eur J Pain 2013;17:1005–11.Search in Google Scholar

[9] Vaegter HB, Graven-Nielsen T. Pain modulatory phenotypes differentiate subgroups with different clinical and experimental pain sensitivity. Pain 2016;157:1480–8.Search in Google Scholar

[10] Jespersen A, Amris K, Graven-Nielsen T, Arendt-Nielsen L, Bartels EM, Torp-Pedersen S, Bliddal H, Danneskiold-Samsoe B. Assessment of pressure-pain thresholds and central sensitization of pain in lateral epicondylalgia. Pain Med 2013;14:297–304.Search in Google Scholar

[11] Vaegter HB, Handberg G, Graven-Nielsen T. Hypoalgesia after exercise and the cold pressor test is reduced in chronic musculoskeletal pain patients with high pain sensitivity. Clin J Pain 2016;32:58–69.Search in Google Scholar

[12] Hoffman MD, Shepanski MA, Mackenzie SP, Clifford PS. Experimentally induced pain perception is acutely reduced by aerobic exercise in people with chronic low back pain. J Rehabil Res Dev 2005;42:183–90.Search in Google Scholar

[13] Meeus M, Roussel NA, Truijen S, Nijs J. Reduced pressure pain thresholds in response to exercise in chronic fatigue syndrome but not in chronic low back pain: an experimental study. J Rehabil Med 2010;42:884–90.Search in Google Scholar

[14] Burrows NJ, Booth J, Sturnieks DL, Barry BK. Acute resistance exercise and pressure pain sensitivity in knee osteoarthritis: a randomised crossover trial. Osteoarthr Cartil 2014;22:407–14.Search in Google Scholar

[15] Kosek E, Ekholm J, Hansson P. Modulation of pressure pain thresholds during and following isometric contraction in patients with fibromyalgia and in healthy controls. Pain 1996;64:415–23.Search in Google Scholar

[16] Staud R, Robinson ME, Price DD. Isometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain 2005;118:176–84.Search in Google Scholar

[17] Whiteside A, Hansen S, Chaudhuri A. Exercise lowers pain threshold in chronic fatigue syndrome. Pain 2004;109:497–9.Search in Google Scholar

[18] Voscopoulos C, Lema M. When does acute pain become chronic? Br J Anaesth 2010;105:i69–85.Search in Google Scholar

[19] O’Neill S, Manniche C, Graven-Nielsen T, Arendt-Nielsen L. Generalized deep-tissue hyperalgesia in patients with chronic low-back pain. Eur J Pain 2007;11:415–20.Search in Google Scholar

[20] Fingleton C, Smart K, Doody C. Exercise-induced hypoalgesia in people with knee osteoarthritis with normal and abnormal conditioned pain modulation. Clin J Pain 2016 [in Press]. https://www.ncbi.nlm.nih.gov/pubmed/?term=27518487.Search in Google Scholar

[21] Janal MN, Colt EW, Clark WC, Glusman M. Pain sensitivity, mood and plasma endocrine levels in man following long-distance running: effects of naloxone. Pain 1984;19:13–25.Search in Google Scholar

[22] Koltyn KF, Umeda M. Exercise, hypoalgesia and blood pressure. Sports Med 2006;36:207–14.Search in Google Scholar
Published Online: 2017-04-01
Published in Print: 2017-04-01

© 2016 Scandinavian Association for the Study of Pain

Articles in the same Issue

  2. Scandinavian Journal of Pain
  3. Editorial comment
  4. Cardiovascular risk reduction as a population strategy for preventing pain?
  5. Observational study
  6. Diabetes mellitus and hyperlipidaemia as risk factors for frequent pain in the back, neck and/or shoulders/arms among adults in Stockholm 2006 to 2010 – Results from the Stockholm Public Health Cohort
  7. Editorial comment
  8. Exercising non-painful muscles can induce hypoalgesia in individuals with chronic pain
  9. Clinical pain research
  10. Exercise induced hypoalgesia is elicited by isometric, but not aerobic exercise in individuals with chronic whiplash associated disorders
  11. Editorial comment
  12. Education of nurses and medical doctors is a sine qua non for improving pain management of hospitalized patients, but not enough
  13. Observational study
  14. Acute pain in the emergency department: Effect of an educational intervention
  15. Editorial comment
  16. Home training in sensorimotor discrimination reduces pain in complex regional pain syndrome (CRPS)
  17. Original experimental
  18. Pain reduction due to novel sensory-motor training in Complex Regional Pain Syndrome I – A pilot study
  19. Editorial comment
  20. How can pain management be improved in hospitalized patients?
  21. Original experimental
  22. Pain and pain management in hospitalized patients before and after an intervention
  23. Editorial comment
  24. Is musculoskeletal pain associated with work engagement?
  25. Clinical pain research
  26. Relationship of musculoskeletal pain and well-being at work – Does pain matter?
  27. Editorial comment
  28. Preoperative quantitative sensory testing (QST) predicting postoperative pain: Image or mirage?
  29. Systematic review
  30. Are preoperative experimental pain assessments correlated with clinical pain outcomes after surgery? A systematic review
  31. Editorial comment
  32. A possible biomarker of low back pain: 18F-FDeoxyGlucose uptake in PETscan and CT of the spinal cord
  33. Observational study
  34. Detection of nociceptive-related metabolic activity in the spinal cord of low back pain patients using 18F-FDG PET/CT
  35. Editorial comment
  36. Patients’ subjective acute pain rating scales (VAS, NRS) are fine; more elaborate evaluations needed for chronic pain, especially in the elderly and demented patients
  37. Clinical pain research
  38. How do medical students use and understand pain rating scales?
  39. Editorial comment
  40. Opioids and the gut; not only constipation and laxatives
  41. Observational study
  42. Healthcare resource use and costs of opioid-induced constipation among non-cancer and cancer patients on opioid therapy: A nationwide register-based cohort study in Denmark
  43. Editorial comment
  44. Relief of phantom limb pain using mirror therapy: A bit more optimism from retrospective analysis of two studies
  45. Clinical pain research
  46. Trajectory of phantom limb pain relief using mirror therapy: Retrospective analysis of two studies
  47. Editorial comment
  48. Qualitative pain research emphasizes that patients need true information and physicians and nurses need more knowledge of complex regional pain syndrome (CRPS)
  49. Clinical pain research
  50. Adolescents’ experience of complex persistent pain
  51. Editorial comment
  52. New knowledge reduces risk of damage to spinal cord from spinal haematoma after epidural- or spinal-analgesia and from spinal cord stimulator leads
  53. Review
  54. Neuraxial blocks and spinal haematoma: Review of 166 case reports published 1994–2015. Part 1: Demographics and risk-factors
  55. Review
  56. Neuraxial blocks and spinal haematoma: Review of 166 cases published 1994 – 2015. Part 2: diagnosis, treatment, and outcome
  57. Editorial comment
  58. CNS–mechanisms contribute to chronification of pain
  59. Topical review
  60. A neurobiologist’s attempt to understand persistent pain
  61. Editorial Comment
  62. The triumvirate of co-morbid chronic pain, depression, and cognitive impairment: Attacking this “chicken-and-egg” in novel ways
  63. Observational study
  64. Pain and major depressive disorder: Associations with cognitive impairment as measured by the THINC-integrated tool (THINC-it)
https://doi.org/10.1016/j.sjpain.2016.12.005

Articles in the same Issue

  2. Scandinavian Journal of Pain
  3. Editorial comment
  4. Cardiovascular risk reduction as a population strategy for preventing pain?
  5. Observational study
  6. Diabetes mellitus and hyperlipidaemia as risk factors for frequent pain in the back, neck and/or shoulders/arms among adults in Stockholm 2006 to 2010 – Results from the Stockholm Public Health Cohort
  7. Editorial comment
  8. Exercising non-painful muscles can induce hypoalgesia in individuals with chronic pain
  9. Clinical pain research
  10. Exercise induced hypoalgesia is elicited by isometric, but not aerobic exercise in individuals with chronic whiplash associated disorders
  11. Editorial comment
  12. Education of nurses and medical doctors is a sine qua non for improving pain management of hospitalized patients, but not enough
  13. Observational study
  14. Acute pain in the emergency department: Effect of an educational intervention
  15. Editorial comment
  16. Home training in sensorimotor discrimination reduces pain in complex regional pain syndrome (CRPS)
  17. Original experimental
  18. Pain reduction due to novel sensory-motor training in Complex Regional Pain Syndrome I – A pilot study
  19. Editorial comment
  20. How can pain management be improved in hospitalized patients?
  21. Original experimental
  22. Pain and pain management in hospitalized patients before and after an intervention
  23. Editorial comment
  24. Is musculoskeletal pain associated with work engagement?
  25. Clinical pain research
  26. Relationship of musculoskeletal pain and well-being at work – Does pain matter?
  27. Editorial comment
  28. Preoperative quantitative sensory testing (QST) predicting postoperative pain: Image or mirage?
  29. Systematic review
  30. Are preoperative experimental pain assessments correlated with clinical pain outcomes after surgery? A systematic review
  31. Editorial comment
  32. A possible biomarker of low back pain: 18F-FDeoxyGlucose uptake in PETscan and CT of the spinal cord
  33. Observational study
  34. Detection of nociceptive-related metabolic activity in the spinal cord of low back pain patients using 18F-FDG PET/CT
  35. Editorial comment
  36. Patients’ subjective acute pain rating scales (VAS, NRS) are fine; more elaborate evaluations needed for chronic pain, especially in the elderly and demented patients
  37. Clinical pain research
  38. How do medical students use and understand pain rating scales?
  39. Editorial comment
  40. Opioids and the gut; not only constipation and laxatives
  41. Observational study
  42. Healthcare resource use and costs of opioid-induced constipation among non-cancer and cancer patients on opioid therapy: A nationwide register-based cohort study in Denmark
  43. Editorial comment
  44. Relief of phantom limb pain using mirror therapy: A bit more optimism from retrospective analysis of two studies
  45. Clinical pain research
  46. Trajectory of phantom limb pain relief using mirror therapy: Retrospective analysis of two studies
  47. Editorial comment
  48. Qualitative pain research emphasizes that patients need true information and physicians and nurses need more knowledge of complex regional pain syndrome (CRPS)
  49. Clinical pain research
  50. Adolescents’ experience of complex persistent pain
  51. Editorial comment
  52. New knowledge reduces risk of damage to spinal cord from spinal haematoma after epidural- or spinal-analgesia and from spinal cord stimulator leads
  53. Review
  54. Neuraxial blocks and spinal haematoma: Review of 166 case reports published 1994–2015. Part 1: Demographics and risk-factors
  55. Review
  56. Neuraxial blocks and spinal haematoma: Review of 166 cases published 1994 – 2015. Part 2: diagnosis, treatment, and outcome
  57. Editorial comment
  58. CNS–mechanisms contribute to chronification of pain
  59. Topical review
  60. A neurobiologist’s attempt to understand persistent pain
  61. Editorial Comment
  62. The triumvirate of co-morbid chronic pain, depression, and cognitive impairment: Attacking this “chicken-and-egg” in novel ways
  63. Observational study
  64. Pain and major depressive disorder: Associations with cognitive impairment as measured by the THINC-integrated tool (THINC-it)
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