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Exercise-induce hyperalgesia, complement system and elastase activation in ME/cfs - a secondary analysis (2018) Polli et al

Discussion in 'BioMedical ME/CFS Research' started by Milo, Oct 18, 2018.

  1. Milo

    Milo Senior Member (Voting Rights)

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    Exercise-induce hyperalgesia, complement system and elastase activation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - a secondary analysis of experimental comparative studies

    Polli A1, Van Oosterwijck J2,3, Meeus M3,4, Lambrecht L5, Nijs J6, Ickmans K6.
    Author information
    1
    Pain in Motion Research Group, Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussels, Laarbeeklaan 103, 1090 Jette, Brussels, Belgium, Phone/Fax: +32 (0) 2 477 45 29.
    2
    Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium.
    3
    Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.
    4
    Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Antwerp, Belgium.
    5
    Private Practice for Internal Medicine, Ghent, Belgium.
    6
    Pain in Motion Research Group, Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussels, Laarbeeklaan 103, 1090 Jette, Brussels, Belgium.


    Abstract

    Background and aims:

    The interaction between the immune system and pain has been thoroughly explored in the recent decades.

    The release of inflammatory mediators from immune cells has the capability of activating neurons and glial cells, in turn sensitizing the nervous system.

    Both immune system alterations and pain modulation dysfunctions have been shown in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) following exercise.

    However, no studies tried to explore whether these two phenomena are linked and can explain exercise-induced symptoms worsening in people with ME/CFS.

    We hypothesized that exercise-induced changes in descending pain modulation is associated to changes in immune system functions.

    We used complement system product C4a and elastase activity as indicators of immune system activity.

    Methods:

    The study design was a secondary analysis of controlled experimental studies.

    Twenty-two patients with ME/CFS and 22 healthy sedentary controls were enrolled.

    In experiment 1, subjects performed an aerobic submaximal exercise test; in experiment 2 they underwent a self-paced exercise test.

    One week of rest period were set between the two exercise tests.

    Before and after each experiment, subjects underwent clinical assessment, pain thresholds (PPTs) measurement, and blood sampling.

    Immune system function was assessed measuring complement system C4a products and elastase activity.

    Results:

    Changes in elastase activity were not associated to changes in PPTs.

    Associations were observed in the ME/CFS group between changes in PPTs and C4a products, following both types of exercise.

    After submaximal exercise, the change in C4a products was associated with the change in PPT at the thumb in patients (r=0.669, p=0.001).

    Similarly, after self-paced exercise the change in C4a products was associated witht the change in PPT at the calf in patients (r=0.429, p=0.047).

    No such correlations were found in healthy controls. Regression analysis showed that C4a changes after the submaximal exercise significantly predicted the change in PPTs (R2=0.236; p=0.02).

    Conclusions:

    Moderate associations between exercise-induced changes in PPTs and immune system activity were found only in ME/CFS.

    The change in the complement system following submaximal exercise might be able to explain part of the change in patient's pain thresholds, providing evidence for a potential link between immune system alteration and dysfunctional endogenous pain modulation.

    These results have to be taken with caution, as only one out of three measures of PPTs was found associated with C4a changes.

    We cannot reject the hypothesis that C4a might therefore be a confounding factor, and changes during exercise might be mediated by other mechanism.

    Implications:

    Immune system changes following exercise might contribute to exercise-induced symptoms worsening in patients with ME/CFS. However, the role of the complement system is questionable

    Link to abstract: https://www.degruyter.com/view/j/sjpain.ahead-of-print/sjpain-2018-0075/sjpain-2018-0075.xml
     
    Last edited: Oct 18, 2018
  2. Michiel Tack

    Michiel Tack Senior Member (Voting Rights)

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    Milo, MEMarge, Joh and 2 others like this.
  3. Andy

    Andy Committee Member & Outreach

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    https://www.facebook.com/MEResearchUK/posts/2260753547303223


    Their link in that post just goes to a copy of the abstract on their website, though it does note that "Polli et al, Scandinavian Journal of Pain, 2018 October 16; Epub ahead of print" so perhaps they are only addressing it now as it has been printed?
     
    andypants likes this.

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