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Van Oosterwijck J.1,2,3,4, Marusic U.5, De Wandele I.3, Paul L.6, Meeus M.1,3,4, Moorkens G.7, Lambrecht L.8, Danneels L.3, Nijs J.1,2,9
1Pain in Motion International Research Group, Brussels, Belgium, 2Vrije Universiteit Brussel, Department of Physiotherapy, Human Physiology and Anatomy, Brussels, Belgium, 3Ghent University, Department of Rehabiliation Sciences and Physiotherapy, Ghent, Belgium, 4University of Antwerp, Department of Rehabilitation Sciences and Physiotherapy, Antwerp, Belgium, 5University of Primorska, Institute for Kinesiology Research, Koper, Slovenia, 6University of Glasgow, Nursing and Health Care, Glasgow, United Kingdom, 7University Hospital Antwerp (UZA), Department of Internal Medicine, Antwerp, Belgium, 8Private Practice for Internal Medicine, Ghent, Belgium, 9University Hospital Brussels, Department of Physical Medicine and Physiotherapy, Brussels, Belgium
Background: Aerobic exercise causes an acute analgesic effect in healthy people. Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) are unable to activate this brain-orchestrated endogenous analgesia (or descending inhibition) in response to exercise. This physiological impairment is currently regarded as one factor explaining post-exertional malaise in these patients. At present, the precise mechanisms of exercise-induced analgesia (EIA) are unknown. Although autonomic dysfunction is a feature of ME/CFS, no studies have examined whether there is a relation between exercise-induced changes in pain and autonomic function.
Purpose: To examine the role of the autonomic nervous system in exercise-induced analgesia in healthy people and those with ME/CFS, by studying the recovery of autonomic parameters following aerobic exercise and the relation to changes in self-reported pain intensity.
Methods: Twenty female ME/CFS-patients and 20 healthy, sedentary subjects performed a submaximal bicycle exercise test known as the Aerobic Power Index with continuous cardiorespiratory monitoring. Before and after the exercise, measures of autonomic function (i.e. heart rate variability, blood pressure, and respiration rate) were performed continuously for 10 minutes and self-reported pain levels were registered. The relation between autonomous parameters and self-reported pain parameters was examined using correlation analysis.
Results: Some relationships of moderate strength between autonomic and pain measures were found. The change (post-exercise minus pre-exercise score) in pain severity was correlated (r=.580, p=.007) with the change in diastolic blood pressure in the healthy group. In the ME/CFS group, positive correlations between the changes in pain severity and low frequency (r=.552, p=.014), and between the changes in bodily pain and diastolic blood pressure (r=.472, p=.036), were seen. In addition, in ME/CFS the change in headache severity was inversely correlated (r=-.480, p=.038) with the change in high frequency heart rate variability.
Conclusion(s): Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional exercise-induced analgesia in ME/CFS, which indicates that the efficacy of autonomic recovery can possibly mediate the degree of impaired exercise-induced analgesia in ME/CFS. Poor recovery of diastolic blood pressure in response to exercise, with blood pressure remaining elevated, is associated with reductions of pain following exercise in ME/CFS as well as in healthy people. When blood pressure remains elevated this means that there is also an enhanced stretch on the coronary arteries, which leads to activation of the baroreceptors. Furthermore, poor recovery of low frequency heart rate variability in ME/CFS was related to poor exercise-induced analgesia, and it is known that the baroreflex is responsible for a part of this low frequency component. Hence these finding suggest a role for the arterial baroreceptors in the mechanisms of exercise-induced analgesia in healthy people, and the dysfunction of it in ME/CFS patients.
Implications: Understanding the mechanisms of exercise-induced analgesia will help us to develop strategies to improve the function of this phenomenon in those in which it is impaired. This of particular interest for patients with ME/CFS, as this could in part prevent the post-exertional malaise they experience. Preventing these exercise related symptom exacerbations is key in order to successfully increase exercise levels and levels of daily activities during rehabilitation.
Funding acknowledgements: This study was funded by the Ramsay Research Fund of the ME Association (United Kingdom).
Topic: Pain & pain management
Ethics approval: The study was approved by the Ethics Committee of the University Hospital Brussels/Vrije Universiteit Brussel.
All authors, affiliations and abstracts have been published as submitted.
