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Is there any evidence that deconditioning alone causes pain and fatigue?

Discussion in 'General ME/CFS News' started by oceanblue, Apr 29, 2012.

  1. oceanblue

    oceanblue Senior Member

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    Normally I find it refreshing to read stuff from another field, away from the suffocating biases of many CFS researchers (and maybe my own too). But just read a 2007 review paper Physiological Basis of Fatigue that manages to say a lot about how deconditioning can cause fatigue - without backing it up with a single reference, which is odd given that other types of fatigue are well-referenced (180+ in total, zero on deconditioning). E.gs
    It's almost as if it's a consensus view that is excepted as self-evident without the need for any validation. A bit weird really. And a bit like CFS research too.
  2. Don Quichotte

    Don Quichotte Don Quichotte

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  3. Don Quichotte

    Don Quichotte Don Quichotte

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    The Hippocratic message concerning the foundation on which rest the relations between physician and patient may be summed up in a famous maxim: "as to disease, make a habit of two things- to help, or at least do no harm." Here Hippocrates clearly asserts that the purpose of medicine is to protect the interests of the patient. But the physician's unique point of view serves to lend nuance to what was to become a more dogmatic position with the philosophers. Because the injunction to "do good" represents an ideal that the physician cannot always attain, he adds "or at least do no harm" failing to be useful, the physician must not worsen a patient's condition through an untimely intervention.

    to know how to question a patient was indispensable, but it was also necessary to know how to listen…the patient's response served as a guide for the physician in the course of treatment-but only on the condition that the physician knew how to interpret it. Where he did, an attentive dialogue came to be established that marked the beginning of authentic partnership between physician and patient in fighting illness. The art had three factors, the disease, the patient and the physician.

    ( From: Hippocrates, Jacques Jouanna)
  4. oceanblue

    oceanblue Senior Member

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    Thanks, that was interesting.

    Just to summarise the key points: a new study found that in rigorously done trials of exercise, for around 1 in 10 of participants at least one measure of 'success' e.g. lower blood pressure or choloesterol levesl, got worse, not better. The authors looked for lots of possible explanations of this such gender, age or fitness level at the start of the trial butcouldn't find anything that predicted the negative responses.

    Also, the article points out that claims for the efficacy of exercise are based on improvements in measurable factors eg blood pressure, not long term-follow up showing that unfit people who take up exercise are actually healthier as a result.

    The evidence still suggests that exercise is good for most people, but it appears this isn't a universal truth.
  5. oceanblue

    oceanblue Senior Member

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    I agree re PACE/GET, but I am interested in how deconditioned CFS patients are as a secondary consequence. That review reference [27] above is - in a big surprise - not necessarily robust. Amongst the 'evidence against deconditioning' studies it lists the monster (n>400) De Becker study which actually seems to provide evidence FOR deconditioning. Stil working my way through all this.
  6. oceanblue

    oceanblue Senior Member

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    I'm still looking at deconditioning research but this Fulcher & White study from 2000 deservesspecial mention as it claims to make the case for both deconditioning as a perpetuating factor in and GET as the answer to CFS.

    Strength and physiological response to exercise in patients with chronic fatigue syndrome
    Kathy Y Fulcher, Peter D White

    Abstract

    OBJECTIVE To measure strength, aerobic exercise capacity and efficiency, and functional incapacity in patients with chronic fatigue syndrome (CFS) who do not have a current psychiatric disorder.

    METHODS Sixty six patients with CFS without a current psychiatric disorder, 30 healthy but sedentary controls, and 15 patients with a current major depressive disorder were recruited into the study. Exercise capacity and efficiency were assessed by monitoring peak and submaximal oxygen uptake, heart rate, blood lactate, duration of exercise, and perceived exertion during a treadmill walking test. Strength was measured using twitch interpolated voluntary isometric quadriceps contractions. Symptomatic measures included physical and mental fatigue, mood, sleep, somatic amplification, and functional incapacity.

    RESULTS Compared with sedentary controls, patients with CFS were physically weaker, had a significantly reduced exercise capacity, and perceived greater effort during exercise, but were equally unfit. Compared with depressed controls, patients with CFS had significantly higher submaximal oxygen uptakes during exercise, were weaker, and perceived greater physical fatigue and incapacity. Multiple regression models suggested that exercise incapacity in CFS was related to quadriceps muscle weakness, increased cardiovascular response to exercise, and body mass index. The best model of the increased exercise capacity found after graded exercise therapy consisted of a reduction in submaximal heart rate response to exercise.

    CONCLUSIONS Patients with CFS were weaker than sedentary and depressed controls and as unfit as sedentary controls. Low exercise capacity in patients with CFS was related to quadriceps muscle weakness, low physical fitness, and a high body mass ratio. Improved physical fitness after treatment was associated with increased exercise capacity. These data imply that physical deconditioning helps to maintain physical disability in CFS and that a treatment designed to reverse deconditioning helps to improve physical function.
  7. oceanblue

    oceanblue Senior Member

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    Commentary on Fulcher & White deconditioning paper

    First, full credit to the authors for using objective measures of improvment alongside the self-reported ones. That said, there's some sleight of hand in this study, particularly when it comes to the interpretation and I'll pick out some key points:

    1. The sedentary controls may not be very sedentary

    2. In any case the patients in this sample don't appear particularly deconditioned

    3. GET improvements in fitness don't relate correlate with self-rated overall improvements

    4. The authors themselves caution against generalising from the study findings

    Other than that, this study is definitive.

    True levels of deconditioning in patients
    As I said before, the overall evidence isn't clear cut, but this particular study suggests low levels of patient deconditioning, so it is unlikely to be clinically important.

    Controls may not have beenthat sedentary: "Only those subjects who took part in no strenuous activity and exercised moderately less than once a week were accepted for entry into the study". Other studies specified that controls must have jobs where they are sitting down most of the time. As controls were recurited via Bart's hospital (in central London), it's likely they included staff who will spend a lot of time walking given the size of hospitals. And many commuters have to walk quite a way as part of their daily journey to and from work, and if this was the case the controls would be even further from sedentary.

    The treadmill results also suggest that controls were in decent physical shape with a VO2 max of 34.1 ml/kg/min, higher, but not statistically different from the patients figure of 30.6 ml/kg/min. Compared with population norms (see next post) the Control mean would count as average (making the 'sendentary' claim uncertain) while the mean for CFS patients would be the top-end of 'Fair', ahead of a good chunk of the population - and therefore unlikely to be the cause of CFS.

    Questionable model assumptions & interpretation
    The authors used multiple regression modelling to 'explain' their findings among CFS patients. Unsurprisingly, BMI, quadriceps muscle strength and submaximal heart rate were predictors of exercise tolerance, as you would expect in any population. Anything specific to CFS patients? Not if you ignore it:
    Now a lot of people with CFS/ME, and probably even quite a few researchers studying it might not be surprised to see a strong association between RPE and exercise intorlerance. They and might even think it was a hallmark of the illness and that unusually high levels of fatigue characteristic of the illness explained the exercise intolerance.

    So deliberately excluding this factor from their model is a little 'careless' and might explain why the modelcould only explain around 50% of the variance - it would be interesting to know what %age of variance would be explained with RPE included.

    Er, I think that might rather contradict the deconditioning model.

    Even the authors urge caution in interpreting and generalising their results
    :aghhh: If this study were a used car, would you buy it?

    Those author caveats hardly squares with the Peter White's subsequent citing of this study as evidence for the importance of GET and treating 'deconditioning'.
    biophile and Valentijn like this.
  8. oceanblue

    oceanblue Senior Member

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    VO2 max as a measure of fitness
    They most widely used measure of fitness is VO2 max, the amount of oxygen consumed at peak exertion, which is usually measured using an incremental treadmill or cycle ergometer test. It's standardised by expressing as millilitres of O2 conumed per minute, per Kg of body mass. VO2 max decreases with age and is generally a bit higher for men, but should be comparable in age and sex matched samples.

    VO2 max norms (ml O2/min/kg)
    There are also published population norms, e.g: for age 30-39
    Women: Good: 34-38; Average=30-33; Fair=26-29; Poor=22-25;
    Men:Good: 41-46; Average=36-40; Fair=31-35; Poor=27-30;

    For a 75% female sample (ml O2/min/kg):
    most CFS samples are 70%-80% female, so for a 75% female sample aged 30-39 (as for the Fulcher & White study), the weighted norm ranges would be:
    Average 32- 35
    Fair 27- 31
    Poor 23- 26

    Population distribution of VO2 max fitness levels:
    Above average: 33%
    Average: 34%
    Fair: 22%
    Poor: 8%
    Very Poor: 3%
  9. Sean

    Sean Senior Member

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    Torture data enough, and it will imply almost anything you want it to.
  10. WillowJ

    WillowJ Senior Member

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    @OB "@!# another paper to read! I mean, thanks, that looks highly relevant."
    lol
  11. oceanblue

    oceanblue Senior Member

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    While the data from most VO2 max studies strongly supports a lack of deconditioning in CFS patients, the largest study of all (n=427) provides strong evidence for deconditioning. I'm puzzled by the difference in results and would appreciate any comments. Here's the monster study:
    To put this into context, most studies find aVO2 max around 28-30 ml/kg/min (not much below average) while this study finds a VO2 max of 20.5, rising for 22.7 ml/kg/minfor the 40% of patients who were deemed to have reached maximal exertion - which is poor or very poor.

    I'm not entirely sure why the results from this large study are so different from the other studies. The fact that all the subjects are female rather than 75% would only account for a 1 point difference. This study used a cycle ergometer rather than a treadmill, but the consensus seems to be that this makes very little difference in VO2max levels, at least in healthy individuals.

    The authors say:
    This may well be a factor, but subjects still had to make it to the hospital and be willing to attempt the VO2max test and I don't if it it's enough to account for all the difference on its own.

    Unfortunately they give no other data (e.g. SF36 PF scores) to help assess the functional impairment of their patients. For comparison, the Fulcher paper that found a CFS VO2 max of around 30 reported a meanSF36 PF score of 48 (PACE was around 39 at baseline). Perhaps this De Becker study might have had a meanSF36 PF score as low as 30, but I suspect that it would be hard to make it to hospital for assessment withanything under 25 - andthey would need a lot of patients with a score of 25 to bring the mean down to 30.

    Comments very welcome

    Edit: one final observation - higher resting heart rates might be a factor in the lower VO2max of CFS patients relative to controls. Looking only at those who achieved "Maximal" effort, mean heart rates were:

    CFS: At rest=93 bpm, Maximal=167, difference=74bpm
    Controls: Rest=83.5 bpm, Maximal=174, difference=92bpm

    So controls' heart rates increased by an average of 92 bpm while controls only managed 74 bpm. Fewer bpm means less blood pumped and less O2 consumed. Though it's possible the higher resting heart rate is a general feature of deconditioning.
  12. biophile

    biophile Places I'd rather be.

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    Some quick comments from a brief glance of the De Becker et al 2000 paper.

    Fulcher study = Oxford criteria. De Becker study = CDC 1988 and/or CDC 1994 criteria.

    As you already pointed out, the CFS patients in this study may be more severely affected. The study can only, at most, support the (unsurprising) existence of deconditioning in more severely affected patients when compared to asymptomatic healthy sedentary controls "who did sitting work and performed a maximum of 1 hour of sports per week". This is different than supporting the claims for a major role for deconditioning in perpetuating CFS symptoms and disability.

    Also, the problem seems more complex than simple deconditioning anyway, the authors themselves seem to suspect (additional) autonomic nervous system disturbance judging from other data they collected.

    Similarly, VO2 scores may be misleading because these could be significantly affected by pathophysiology, for example, haven't some CFS studies shown VO2 can drop as much as 20-50% on serial testing? People don't just become 20-50% "deconditioned" in 24 hours due to inactivity, something else is going on. In my own experience, post-exertional relapse can make me feel suddenly much less fit than compared to 24 hours before.
    oceanblue and SOC like this.
  13. oceanblue

    oceanblue Senior Member

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    Thanks for all the comments, Biophile, that's really helpful. Good point about Oxford vs CDC criteria, don't know how I forgot about that (having made notes on the paper!)
    Completely agree with you that this only relates to the existence of deconditioing, not it playing a causal role. I hope to address this in future posts.

    The authors did suggest there could be ANS disturbance, but I found their speculation pretty unconvincing. They also speculated, equally unconvincingly, that CFS patients might have a primary cardiac defect.

    Sure, it could in some, that's why the VO2 max data is interesting for patients who achieved >85% of age-predicted heart rate and with a respiratory quotient > 1 (ie well into anaerobic activity) - which is widely used to determine if patients have been able to achieve a 'true' maximum. The data for the 40% of patients deemed to reach a true max (vs 80% of controls) also showed very low VO2max; in other CFS studies that wasn't the case.
    Agreed, but I think this is a separate issue, since the first test would still show deconditioning (and there was just the one test in this study). Also, Pacific labs seemed to have failed to replicate that intriguing result, and in any case had a dodgy sample where 1 in 4 "CFS" patients reported no ill-effects from 2 maximal work outs in 24 hours. I've posted on this somewhere if you are interested.
  14. Esther12

    Esther12 Senior Member

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    This is the sort of research I know little about but...

    Is it possible that one group of researchers were less willing to push their patients than another? Or that one group of patients were less willing to be pushed?

    I've no idea how these sorts of tests are run though, so this could be a silly point.
    barbc56 likes this.
  15. oceanblue

    oceanblue Senior Member

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    Good point. Because it isn't easy to reach maximal exertion, it's normal practice to verbally encourage participants during the final stages of the test. This happened in the Fulcher study but the De Becker study doesn't say either way.

    However, the issue of 'truly' achieving maximal exertion is always an issue to some extent, which is why the De Becker study looked separately at those who reached the more objective measures of an RQ>1 and >85% of age-predicted heart rate (other studies have used a slightly higher threshold of RQ>1.1 and HR>90% predicted).

    Fulcher used blood lactate rather than RQ to measure levels of anaerobic activity (ie measure of how hard patients pushed) so they can't be compared. However, both gave peak Heart Rates and it looks like the 'maximum' De Becker patients were pushing almost as hard as the Fulcher patients:

    De Becker ('max'): 91.5% age-predicted heart rate,VO2max=22.7
    Fulcher (all): 93.4% age-predicted heart rate, VO2 max=30.6

    So the Fulcher patients may have been pushing fractionally more than the De Becker 'max' ones, but it wouldn't account for the large difference in VO2max.
  16. Esther12

    Esther12 Senior Member

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    I have no idea what most of that means, and now is not the time to learn!

    Thanks for your notes on this OB, I've been keeping up with this thread and found it interesting, even if I can't contribute much.
  17. oceanblue

    oceanblue Senior Member

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    You're not the first person to respond like that to one of my posts. Glad you are interestedin the thread.
  18. floydguy

    floydguy Senior Member

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    FWIW...I don't think "de-conditioning" causes fatigue and pain. Despite the fact that my ability to exercise is severely limited I don't consider myself "deconditioned" (until proven otherwise anyway). I am able to walk, ride a bike casually, etc. However, I do have significant issues with breathing, heart rate, etc. My personal experience suggests an ANS issue with exercise. And despite being somewhat active I am in complete physical misery, which doesn't seem to change with activity - unless I really "push" it, then I'll crash.
  19. PhoenixDown

    PhoenixDown Senior Member

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    Just to add my 2 cents, I was still looking relatively muscular (for my body mass) when my "fibromyalgia" pain stopped me from getting on with my already fatigue riddled life. It was that pain that put an end to years of accomplishment in the gym, talk about circular argument.

    So it was rather insulting to read what doctors really thought of fibromyalgia after I'd put in so much dedication. Just like doctors ignoring consequent PEM in other patients, they ignored the consequent pain/injury worsening I reported, and basically told me to exercise even if it made me worse. Disrespectful would be an understatement.

    So how are they objectively defining deconditioning?
  20. oceanblue

    oceanblue Senior Member

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    There are no absolute definitions Usually the controls in CFS studies on not appropriate, but there are VO2max norms which are useful.

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