Research abstract:
The Role of Autonomic Function in Exercise-induced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Healthy People by Jo Nijs, Lieven Danneels, Luc Lambrecht, Greta Moorkens, Mira Meeus, Lorna Paul, Jessica Van Oosterwijck, Uros Marusic, and Inge De Wandele in Pain Physician 2017; 20:E389-E399
BACKGROUND: 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.
OBJECTIVES: 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.
STUDY DESIGN: A controlled experimental study.
SETTING: The study was conducted at the Human Physiology lab of a University.
METHODS: 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.
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/CHFS the change in headache severity was inversely correlated (r = -.480, P = .038) with the change in high frequency heart rate variability.
LIMITATIONS: Based on the cross-sectional design of the study, no firm conclusions can be drawn on the causality of the relations.
CONCLUSIONS: 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 arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients.
Comment by Dr Charles Shepherd:
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
