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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.
Scand J Pain. 2019 01 28; 19(1):183-192.SJ

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.

Authors+Show Affiliations

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.Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium. Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium.Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium. Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Antwerp, Belgium.Private Practice for Internal Medicine, Ghent, Belgium.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.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.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30325737

Citation

Polli, Andrea, et al. "Exercise-induce Hyperalgesia, Complement System and Elastase Activation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - a Secondary Analysis of Experimental Comparative Studies." Scandinavian Journal of Pain, vol. 19, no. 1, 2019, pp. 183-192.
Polli A, Van Oosterwijck J, Meeus M, et al. Exercise-induce hyperalgesia, complement system and elastase activation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - a secondary analysis of experimental comparative studies. Scand J Pain. 2019;19(1):183-192.
Polli, A., Van Oosterwijck, J., Meeus, M., Lambrecht, L., Nijs, J., & Ickmans, K. (2019). Exercise-induce hyperalgesia, complement system and elastase activation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - a secondary analysis of experimental comparative studies. Scandinavian Journal of Pain, 19(1), 183-192. https://doi.org/10.1515/sjpain-2018-0075
Polli A, et al. Exercise-induce Hyperalgesia, Complement System and Elastase Activation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - a Secondary Analysis of Experimental Comparative Studies. Scand J Pain. 2019 01 28;19(1):183-192. PubMed PMID: 30325737.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exercise-induce hyperalgesia, complement system and elastase activation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - a secondary analysis of experimental comparative studies. AU - Polli,Andrea, AU - Van Oosterwijck,Jessica, AU - Meeus,Mira, AU - Lambrecht,Luc, AU - Nijs,Jo, AU - Ickmans,Kelly, PY - 2018/04/26/received PY - 2018/08/20/accepted PY - 2018/10/17/pubmed PY - 2019/7/20/medline PY - 2018/10/17/entrez KW - chronic fatigue syndrome KW - exercise KW - hyperalgesia KW - immune system KW - pain KW - pain threshold SP - 183 EP - 192 JF - Scandinavian journal of pain JO - Scand J Pain VL - 19 IS - 1 N2 - 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. SN - 1877-8879 UR - https://www.unboundmedicine.com/medline/citation/30325737/Exercise_induce_hyperalgesia_complement_system_and_elastase_activation_in_Myalgic_Encephalomyelitis/Chronic_Fatigue_Syndrome___a_secondary_analysis_of_experimental_comparative_studies_ L2 - https://www.degruyter.com/document/doi/10.1515/sjpain-2018-0075 DB - PRIME DP - Unbound Medicine ER -