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Oosterwijck et al: The Role of Autonomic Function in Exercise-induced Endogenous Analgesia

Discussion in 'Latest ME/CFS Research' started by mango, Mar 26, 2017.

  1. mango

    mango Senior Member

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    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 U1, De Wandele I2, Paul L3, Meeus M4, Moorkens G5, Lambrecht L6, Danneels L2, Nijs J7.

    Author information
    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.
    Pain Physician. 2017 Mar;20(3):E389-E399.

    Abstract
    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.

    Key words: Aerobic exercise, aerobic power index, autonomic nervous system, exercise-induced analgesia, exercise-induced hypoalgesia, fibromyalgia, heart rate variability, stress-induced analgesia, pain.

    https://www.ncbi.nlm.nih.gov/pubmed/28339438
     
  2. Effi

    Effi Senior Member

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    This crew has written nothing but BPS articles in the last decade or so, and were involved in carrying out the CBT/GET approach in Belgium for many years. This research article seems different (unless I'm missing something?). They still don't understand that not every ME patient experiences pain, or think that PEM equals pain. But apart from that this seems interesting? I wonder if they have finally seen the light... Unless they want to 'solve' these problems through more exercise and meditation practice (which is what their line of reasoning has been for a long time).

    Right now I don't have the brain capacity to analyse this, so I'd be interested to hear other people's views on this.
     
  3. RogerBlack

    RogerBlack Senior Member

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    Only having read the abstract - I'm unconvinced. There are clearly issues with blood-flow, but they seem to be claiming that the pain is just normal pain, which in the healthy controls is alleviated by exercise induced analgesia.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578581/ is a review in exercise induced analgesia.
    I have not fully digested the study design.

    The additional problem then becomes if it's lack of exercise induced analgesia, why am I still sore after exercise often in non-exercised muscles, in a manner very different from delayed onset muscle soreness. Sometimes even in the case of pure cognitive exercise.
    I am also unsure if they're in fact picking up sicker patients with worse exercise response and pain, and picking up a meaningless correlation in bloodflow.

    This study might in principle be interesting, but it needs at a minimum nonsubjective measures of pain other than exercise caused pain. Hot/cold, ...
     
  4. Snow Leopard

    Snow Leopard Hibernating

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    Yes, I think the altered blood pressure is a consequence, not a cause of the underlying dysfunction. I'm not convinced it's the baroreceptors that are dysfunctional.
     
  5. RogerBlack

    RogerBlack Senior Member

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    Not to say it's not - I don't think anyones come up with a convincing explanation for POTS in ME/CFS.
     
  6. charles shepherd

    charles shepherd Senior Member

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    Cheesus and Invisible Woman like this.
  7. Webdog

    Webdog Senior Member

    I'm fairly newly diagnosed, so this is an honest question. Do most with ME/CFS experience muscle pain/soreness following exercise?

    I ask because I've never experienced pain beyond what I would consider normal. Brain fog, cognitive issues, memory issues, fatigue, and occasionally headaches. But never body or muscle pain.
     
  8. RogerBlack

    RogerBlack Senior Member

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    It varies.
    For me, I used to in the first few years of the disease.
    This then went away largely from perhaps age 16-20, when I was moderately in remission.
    At the moment, pain is uncommon, and very much a secondary symptom of severe overexertion which typically hits the next day.
    This is really unfortunate, as I have no immediate signal to stop.

    I do wonder if any of the reports of pain are not in fact pain, but the people responding to questionnaires for reason to stopping. What do you do if the questionaire doesn't list 'wanting to be able to get to the toilet tomorrow'.
    Pain for me occurs during particularly severe post-exertional episodes, all muscles, not the exercised ones.
     
    Webdog likes this.
  9. Webdog

    Webdog Senior Member

    Thanks for the reply. I too have no pain giving me a signal when to stop. If only we could monitor our exertion like diabetics monitor their blood sugars.

    I also have no (abnormal) pain the next day, even after I've overexerted. I do have flu-like symptoms, cognitive issues and am bedridden, however.

    My long term ME/CFS experiences leave me unsure as to the relevance of this or any pain study. But clearly others experience pain. So many questions.

    ETA: I seem to have fewer "aches and pains" than most of my "healthy" friends of similar age. What a strange disease.
     
    Last edited: Mar 29, 2017
  10. trishrhymes

    trishrhymes Senior Member

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    I've had pain in all my muscles from the start, and the more i use a muscle, the worse the pain. I wake up with a moderate level of pain, and it increases with activity. Since my ME has become more severe in the last few years, the daily variation is less because I'm less active, but the pain is always there.
     
    Jan and Webdog like this.
  11. Jan

    Jan Senior Member

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    I honestly can't remember if I had pain from the start, though I don't remember it being a huge concern and it didn't appear in the report from my consultant. I had a lot of muscle twitching, I remember that clearly, watching my arms or legs twitching. Still have this, but to a lesser degree.

    Pain is something that has worsened considerably over time for me. It is now constant, though I'm pretty sure I also have FM as everywhere is tender to touch. My pain is exacerbated by PEM, but also increases during the day. Proper rest, which I'm not very good at, can decrease it a little, but it's still always present, most of my muscles feel very tight and tense and pain is present from the moment I wake up. I am taking a lot of pain meds, which I don't like having to take, but the alternative was lying on the sofa virtually all day, strapped to a Tens machine and crying in agony.
     
  12. Johnskip

    Johnskip Senior Member

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    what kind of meds are you on I don't like to take them either but I think I got no choice now
     
  13. charles shepherd

    charles shepherd Senior Member

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    Re: Cause of muscle pain in ME/CFS

    There are still many uncertainties surrounding the cause of pain in ME/CFS - which is why the MEA Ramsay Research Fund is funding research into pain causation and management

    Having seen or dealt with several thousand people with ME/CFS over the past 30+ years, my personal experience is that most people have pain

    However, a significant minority (myself included) experience little or no pain at all

    Pain can be mild, moderate of severe in intensity
    It can involve muscles, joints and sometimes nerves - neuopathic pain
    It can be continuous, intermittent, and in the case of muscle pain be exercise induced

    As far as exercise-induced muscle pain is concerned, it is often suggested that this is due to an excessive build up of lactic acid

    Having used my own skeletal muscles to investigate this with Professors George Radda (in Oxford) and Mina Behan (in Glasgow) back in the early 1980s, we discovered that in a sub-group of people there is an important metabolic abnormality involving an early and excessive production of lactic acid during exercise

    Our results from Oxford (which was a 31P neuroimaging study) were published in The Lancet back in 1984 - see below

    However, as I had no muscle pain at the time, and still do not have any muscle pain, the lactic acid hypothesis does to really fit in with exercise induced pain production

    So the explanation is clearly more complex

    Dr Charles ShepherdHon Medical Adviser, MEA

    Lancet. 1984 Jun 23;1(8391):1367-9.
    Excessive intracellular acidosis of skeletal muscle on exercise in a patient with a post-viral exhaustion/fatigue syndrome. A 31P nuclear magnetic resonance study.
    Abstract
    A patient (CS) with prolonged post-viral exhaustion and excessive fatigue was examined by 31P nuclear magnetic resonance. During exercise, muscles of the forearm demonstrated abnormally early intracellular acidosis for the exercise performed. This was out of proportion to the associated changes in high-energy phosphates.

    This may represent excessive lactic acid formation resulting from a disorder of metabolic regulation. The metabolic abnormality in this patient could not have been demonstrated by traditional diagnostic techniques.
     
  14. Jan

    Jan Senior Member

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    I have Tramadol (I usually need the max dose I'm allowed per day) and Lyrica on prescription and also take Ibuprofen I buy otc as not I've not got around to having an anti-inflammatory put back on my prescription list. I use a small dose of Diazepam when pain is keeping me awake or if it's so severe I am unable to relax. I also need Zopiclone in order to sleep.

    I also take Naratriptan for migraines/A Typical Trigeminal Neuralgia

    I wouldn't recommend these medications, If I wasn't already taking these I would probably try LDN or CBD before going down this route. I really want to get off of the Lyrica, it has many horrible side effects.
     
  15. lnester7

    lnester7 Seven

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    I have tried it all for pain and nothing like lglutamine ( baking soda also but I can't never be away from foods long enough)
     
  16. Jan

    Jan Senior Member

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    Can I ask what dose you take of these? I think I'll give them a try, I'm so desperate to get off the Lyrica. I've heard some good things about baking soda, but I keep forgetting to buy it.
     
  17. lnester7

    lnester7 Seven

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    Baking soda 1/4 teaspoon on a glass 8oz water.
    L-glutamine is for leaky gut so I do about 30mg a day please google for leaky gut( I have it set on my scoops so don't remember whT they add up to). I didn't expect to do anything other than fixing my gut, was a coincidence that was magic for my latic acid pain.
     

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