One of the most consistent neurological abnormalities to be reported in ME/CFS involves what is called the autonomic nervous system (ANS).
This is a part of the nervous system that has its control centres in the brain. The regulatory centres then send messages, which are not under conscious control, via the sympathetic and parasympathetic nerves, to regulate the heart rate and blood pressure, the bowels and bladder, and blood flow to muscle and other key parts of the body – including the brain.
The ANS can either speed up or slow down activities in the heart, bowels and bladder – so overactivity will speed up the pulse rate and can also cause irritable bowel and irritable bladder type symptoms.
It also appears that the ANS has a role in pain production and post-exertional symptomatology.
This is why the MEA Ramsay Research Fund is keen to fund more research into the role of the ANS – including a large study that researchers in Brussels and Glasgow have been carrying out for us.
The results in this paper relate to a study that examined the role of the ANS in exercise induced-analgesia (more information on this normal physiological response below) in people with ME/CFS, and in healthy controls, following an exercise challenge and in relation to self-reporting of pain severity.
Measurements of ANS activity (i.e. pulse rate, blood pressure, respiratory rate) were carried out before and after exercise along with self reporting of pain levels.
The study concluded that there is dysfunctional exercise-induced analgesia in people with ME/CFS.
This is an important new finding that helps to increase our understanding of why pain occurs in ME/CFS and something that could lead to more effective methods of both prevention and treatment of pain in ME/CFS
Dr Charles Shepherd
Hon Medical Adviser, ME Association
29 March 2017
PUBLICATION OF PAPER IN ‘PAIN PHYSICIAN’
From Pain Physician (open access). March/April 2017.
The Role of Autonomic Function in Exercise-induced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis⁄Chronic Fatigue Syndrome and Healthy People
Oosterwijck JV, Marusic U(1), De Wandele I(2), Paul L(3), Meeus M(4), Moorkens G(5), Lambrecht L(6), Danneels L(2), Nijs J(7).
1) Science and Research Centre, Institute for Kinesiology Research, University of Primorska, Koper, Slovenia.
2) Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium.
3) Nursing and Health Care, School of Medicine, University of Glasgow, Glasgow, United Kingdom.
4) Pain in Motion Research Group (www.paininmotion.be); Rehabilitation Sciences and Physiotherapy, Faculty of Medicine & Health Sciences, Ghent University, Ghent, Belgium; Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine & Health Sciences, University of Antwerp, Antwerp, Belgium.
5) Department of Internal Medicine, University Hospital Antwerp (UZA), Antwerp, Belgium.
6) Private practice for internal medicine, Ghent, Belgium.
7) Pain in Motion Research Group (www.paininmotion.be); Department of Human Physiology and Physiotherapy, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Brussels, Belgium; Department of Physical Medicine and Physiotherapy, University Hospital Brussels, Brussels, Belgium.
Address Correspondence: Jo Nijs, PhD, MSc Universiteit Brussel, Building F-Kine, Laarbeeklaan 103, BE- 1090 Brussels, Belgium Email: Jo.Nijs@vub.ac.be
Patients with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are unable to activate 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. Autonomic dysfunction is also a feature of ME/CFS.
This study aims 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.
A controlled experimental study.
The study was conducted at the Human Physiology lab of the Vrije Universiteit Brussel.
Twenty women with ME/CFS and 20 healthy, sedentary controls 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.
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/CHFS the change in headache severity was inversely correlated (r = -.480, P = .038) with the change in high frequency heart rate variability.
Based on the cross-sectional design of the study, no firm conclusions can be drawn on the causality of the relations.
Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional 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, suggesting a role for the the arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients.
This study was funded by the Ramsay Research Fund of the ME Association (United Kingdom). Jessica Van Oosterwijck is a post-doctoral research fellow funded by the Special Research Fund of Ghent University and the ME Association’s Ramsay Research Fund. Jo Nijs is holder of a Chair entitled “Exercise immunology and chronic fatigue in health and disease” funded by the European College for Decongestive Lymphatic Therapy, The Netherlands.
MORE INFORMATION ON THE MEA RAMSAY RESEARCH FUND
ADDITIONAL INFORMATION ON ANALGESIA FOLLOWING EXERCISE
Over the past 20 years, a number of studies have examined whether analgesia occurs following exercise. Exercise involving running and cycling have been examined most often in human research, with swimming examined most often in animal research. Pain thresholds and pain tolerances have been found to increase following exercise. In addition, the intensity of a given pain stimulus has been rated lower following exercise.
There have been a number of different noxious stimuli used in the laboratory to produce pain, and it appears that analgesia following exercise is found more consistently for studies that used electrical or pressure stimuli to produce pain, and less consistently in studies that used temperature to produce pain. There is also limited research indicating that analgesia can occur following resistance exercise and isometric exercise.
Currently, the mechanism(s) responsible for exercise-induced analgesia are poorly understood. Although involvement of the endogenous opioid system has received mixed support in human research, results from animal research seem to indicate that there are multiple analgesia systems, including opioid and non-opioid systems. It appears from animal research that properties of the exercise stressor are important in determining which analgesic system is activated during exercise.
Analgesia Following Exercise (PDF Download Available). Available from: www.researchgate.net/publication/12613422_Analgesia_Following_Exercise [accessed Mar 29, 2017].