The role of deconditioning and therapeutic exercise in chronic fatigue syndrome (CFS) (2005)

Dolphin

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I read this yesterday. It reminded me of some of the frustrating things about Peter White's views - useful to motivate me to challenge him and people who have adopted graded exercise therapy.
Special Section Review

The role of deconditioning and therapeutic exercise in chronic fatigue syndrome (CFS)

Journal of Mental Health
2005, Vol. 14, No. 3 , Pages 237-252 (doi:10.1080/09638230500136308)

Lucy V Clark1 and Peter D White2

1Guy's, King's and St Thomas' School of Medicine, London, UK
2Barts and the London, Queen Mary School of Medicine and Dentistry, St Bartholomew's Hospital, UK

Correspondence: Lucy, Clark, Department of General Practice and Primary Care, Guy's, King's and St Thomas' School of Medicine, 5 Lambeth Walk, London, SE11 6SP, UK lucy.clark@kcl.ac.uk


Background: Patients with chronic fatigue syndrome (CFS) complain of tiredness or exhaustion, which is made worse by physical exertion.

This results in their avoidance of exercise, which may lead to physical deconditioning.

We do not know whether this deconditioning maintains the illness or is a consequence.

Graded exercise therapy aims to reverse this cycle of inactivity and deconditioning, and to subsequently reduce the fatigue and disability associated with CFS.

Aims:

To review the literature relating to the role of deconditioning in perpetuating CFS and the literature relating to the role of graded exercise therapy as a treatment of CFS.

Method:

Non-systematic review of published papers concerning deconditioning and therapeutic exercise in patients with CFS.

Findings:

Patients with CFS are at least as deconditioned as sedentary but healthy controls. Supervised graded exercise therapy reduces fatigue and disability in ambulant patients with CFS; efficacy may be independent of reversing deconditioning.

Conclusions:

Graded exercise has an important role to play in the treatment of patients with CFS.

Further work is necessary to elucidate the risks, benefits, and mechanisms of such treatment, especially in children and the severely disabled.

Patient education is necessary to inform patients of the positive benefit/risk ratio in order to improve acceptance and adherence.

Keywords

CFS, graded exercise therapy, deconditioning




Read More: http://informahealthcare.com/doi/abs/10.1080/09638230500136308
 

Dolphin

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From the Introduction:

Therapeutic exercise programmes were first designed for patients with CFS on the basis of reversing physical deconditioning. However, they are also a behavioural graded exposure treatment thought to work by habituating the patient to the stimulus of exercise which has caused the conditioned response of fatigue and malaise.
So no biological reasons for it? Apart from vague phrases like interoception, biological reasons (apart from deconditioning) are ignored in this paper.
 

Dolphin

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Deconditioning is a complex physiological process in which the lack of use of the body’s cardiovascular, neuromuscular, biomechanical, and musculoskeletal systems leads to a decrease in their functional capacity, and the body’s efficiency (McArdle, Katch & Katch, 2001). These changes to the body reduce the capacity for exercise and increase the perception of effort required for a given level of activity (Kottke, 1966; Saltin et al., 1968). They also manifest themselves as impairments to posture and mobility, muscular performance, and cardiovascular endurance, and are thought to lead to the occurrence of fatigue symptoms at a lower level of exercise, as well as giving rise to further symptoms such as a change in sleep patterns (Kottke, 1966), orthostatic hypotension (Convertino, Bloomfield & Greenleaf, 1997; Haruna, Suzuki, Kawakubo & Gunji, 1994), autonomic nervous system dysfunction (Freeman, Komaroff, 1997) and hypocortisolaemia (Cleare, 2004; White, 2000). This may in turn lead to exercise intolerance, which is the inability or unwillingness to exercise as normal.
I am not familiar with a lot of these references. But from what I recall from the references about hypocortisolaemia

Cleare A. J. (2004). The HPA axis and the genesis of chronic fatigue syndrome. Trends in Endocrinolgy &
Metabolism, 15, 55 – 59.

White, P. D. (2000). The role of physical inactivity in the chronic fatigue syndrome. Journal of Psychosomatic Research, 49, 283 – 284.
these were simply speculative papers i.e. they didn't show deconditioning brought about hypocoritisolaemia.
 

Dolphin

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The role of effort perceptions in CFS

Restriction of physical activity and subsequent deconditioning in CFS patients may be the result of an abnormal perception of effort, with the fatigue of CFS being a consequence of an alteration in central drive (Gibson et al., 1993; Lloyd, Hales & Gandevia, 1988). Some have even argued that CFS is a ‘disease’ of increased effort sense (Edwards, Gibson, Clague & Helliwell, 1993; Lawrie, Machale, Power & Goodwin, 1997). Studies investigating aerobic exercise, rather than muscular strength/endurance, have more consistently found higher perceived exertion scores in patients with CFS compared to controls (Fulcher & White, 2000; Gibson et al., 1993; Meningshoel, Vollestad & Forre, 1995; Riley et al., 1990; Sisto et al., 1996; Wagenmakers, Coakley & Edwards, 1988).

Gibson et al. (1993) found not only a disproportionate increase in the perception of effort throughout an incremental exercise test, but that this heightened effort sensation was recorded immediately exercise was started. Effort ratings during incremental exercise in healthy subjects show a linear increase with increasing exercise intensity (Noble & Robertson, 1996), but perceived effort increases only above a threshold of 20 – 30% of maximum power (Jones, 1988). Thus it would appear that CFS patients have a lower threshold for the sensation of effort during exercise compared to normal subjects, or that CFS patients have an additional burden of fatigue at rest over and above that experienced due to the exertion of exercise. These finding also give some credence to the hypothesis that submaximal perceived exertion is related to a central process involving a reduced threshold for afferent body sensations (Stokes, Cooper & Edwards, 1988). This hypothesis is also supported by the differences in somatic amplification scores, whereby the patients with CFS showed greater sensitivity to bodily sensations than the sedentary group (Gibson et al., 1993). This concept is called interoception, and enhanced interoception has recently been suggested as a potential causal mechanism of CFS (White, 2004).
This is about as biological as it gets.

However, it ignores all sorts of other biological evidence.

It then starts talking about "effort syndromes"

There are reports of improvements in the perception of effort at submaximal exercise intensities after GET programmes in sedentary healthy subjects (Ekblom & Goldberg, 1971), patients with ‘effort syndromes’ (see Lewis, 1918) (a syndrome very similar to CFS described during the period before CFS had been operationally defined) (Newham & Edwards, 1979) and patients with CFS (Fulcher & White, 1997; Wallman, Morton, Goodman, Grove & Guilfoyle, 2004). This suggests that GET reverses the enhanced perception of effort during exercise, brought on by inactivity and/or physical deconditioning.
"improvements in the perception of effort"
is not the same as
"reversing the enhanced perception of effort"

It is plausible that some people with CFS are not as fit as they could be and that could partly explain different perceptions of effort between healthy people and people with CFS. It is quite another to claim this fully explains this.
 

Dolphin

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Model underlying GET:

In summary, patients with CFS reduce their participation in physical activity, which could exacerbate or perpetuate their fatigue. The possible mechanisms are: directly through reduced physical strength and cardiovascular deconditioning, or indirectly through the physiological consequences of inactivity such as autonomic nervous system changes, hypothalamic-pituitary – adrenal (HPA) axis down-regulation (leading to low cortisol concentrations), or through changes in central nervous system interoception. Such impairments lead to symptoms at a lower level of physical activity. The inability to function at previous levels may lead to frustration, low mood and a lack of motivation and lethargy. A vicious circle of increased exercise avoidance and symptoms occurs, which serves to perpetuate fatigue, and therefore CFS. Edwards (1986) was the first to illustrate how inactivity, brought about by fatigue, can itself exacerbate and perpetuate fatigue; his model is shown in Figure 2.
-->--Depression and/or Anxiety ---> Debility lethargy ---> Inactivity ---> Reduced exercise capacity ---> Symptoms --------------> -----------------------------------------------------------------------------

Figurre 2. Based on an early model showing the relationship between physical inactivity and fatigue
This ignores the fact that all the symptoms can't be explained by deconditioning e.g. alcohol intolerance (otherwise there would be far fewer problem drinkers around).

It also ignores how people can suddenly be experiencing extra symptoms after relapses, without being more deconditioned, etc.
 

Dolphin

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The role of graded exercise therapy in CFS

The theoretical basis of therapeutic exercise for CFS is the premise that, irrespective of its causes, patients experience fatigue after minimal exertion; and it is their subsequent prolonged avoidance of physical activity and exercise, due to either fear or belief that it will exacerbate their condition, that eventually leads them to experience decreased physical fitness, muscular strength and endurance.
Lots of people went around undiagnosed for many years, unaware that they had CFS, so not convinced of this model.

In my own case, I was ill over five years before being diagnosed. When I initially became ill, I was 16 and in full-time education. Notes from the time suggest I missed two days of school. After that I was always on my feet. The bus stop was nearly a mile from our school (and in college it was further). People in our house never went to bed if ill and neither did I. About the longest I was relatively inactive was around two days within the house.


This occurrence of deconditioning is based on the ‘reversibility concept’ which holds that when exercise or physical activity is stopped or reduced, the body’s systems readjust in accordance with the decreased physiological stimuli (Bloomfield & Coyle, 1993). It is this reversibility concept that provides theoretical support for GET as a suitable treatment for patients with CFS, and empirical evidence supports this theory (Edmonds, McGuire & Price, 2004).

The primary aim of therapeutic exercise in patients with CFS and other fatiguing illnesses is therefore to gradually increase first the duration and then the intensity of physical exercise in a way that is less contingent on symptoms determining activity, so that physiological functioning, muscular strength, endurance, and interoception can be directly improved (Hall, 1998).
GET is not about listening to one's body.

Another example of this:
If a patient develops symptoms as a response to increased activity, they should keep exercising at that level, rather than either stop or increase the intensity/duration. As the body adapts and symptoms subside, they should then be encouraged to increase by an incremental point again, mutually agreed between therapist and patient.
No talk about the body not adapting.
 

Dolphin

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In summary, GET is not based upon any assumptions about the aetiology of CFS. Treatment is based upon the theory that exercise avoidance perpetuates symptoms through deconditioning, a reconditioned response, and changes in interoception. Modifying avoidant behaviour breaks the vicious circle of fatigue and disability; physiological consequences are reversed, promoting recovery.
Note that this is making a distinction between the aetiology (initial cause of the illness) and the pathophysiology (ongoing causes). As the subsequent sentence shows, it is based on some assumptions/it is based on a model of pathophysiology/what is perpetuating the condition.

Note the use of the term recovery - their model suggests GET should be able to bring about recovery.
 

Dolphin

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The paper goes on to review the GET studies that have been published:

On Wearden et al (1998) it says:
More patients allocated to GET withdrew before the end of the therapy compared with those receiving no exercise (37% vs 22%), and 66% of patients allocated to GET did not complete the full 6 months’ programme.
I'm not sure I noticed the latter statistic being mentioned before. The authors themselves don't in the text, just in a figure (which has other info too):

33 randomised to graded exercise and fluoxetine --> 9 complied fully with graded exercise

34 randomised to graded exercise and drug placebo --> 14 complied fully with graded exercise

So only 23 out of 67 (34%) were said to fully comply with graded exercise

Subjects adhered to the exercise programme if their charts showed that they had performed the required activity, at the required intensity, at least three times per week.
 

Dolphin

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Does therapeutic exercise cause harm?

There is a discrepancy between reports of self-help group members and published evidence from trials in this matter. Fifty per cent of 2,338 members of the largest self-help group in the UK, Action for M.E., reported that they felt worse after exercise therapy, whereas the trial evidence suggests minimal or no risk with these treatments (Action for ME, 2001). However, a further survey by Action for M.E. of their members in 2003 (Action for ME, 2003) suggests that reports of deterioration following therapy were related to either poorly administered treatment or lack of appropriate professional supervision, rather than GET itself. Properly administered GET requires an appropriately qualified and trained professional, such as a physiotherapist, mutually agreeing with the patient and adjusting the programme depending on their response. The recent systematic review by Edmonds et al. (2004) concludes that, on average, there is no evidence that GET may worsen outcomes in patients with CFS.
The Action for ME 2003 survey, which has a small sample size anyway, doesn't have quantitative data that shows that at all. The report was written by Chris Clark who was in some ways close to Peter White e.g. wrote a letter supporting the application for MRC fuding for the PACE Trial; it is possible he asked for PDW's input for the report or was conscious of PDW's views when writing it. It is frustrating when Peter White keeps claiming this when the evidence isn't there. I've attached the file to let people read for themselves.
I haven't looked at it in a while - I think this is the relevant table:


The recent systematic review by Edmonds et al. (2004) concludes that, on average, there is no evidence that GET may worsen outcomes in patients with CFS.
What the Edmonds et al. (2004) study showed that on average fatigue scores and the like were improved. That doesn't show that for some people, GET couldn't make them worse.

This paper discusses such issues in a lot more depth:
Kindlon T. Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Bulletin of the IACFS/ME. 2011;19(2):59-111
Free at: http://iacfsme.org/BULLETINFALL2011/Fall2011KindlonHarmsPaperABSTRACT/tabid/501/Default.aspx
Reminder: in the abstract they said:
Patient education is necessary to inform patients of the positive benefit/risk ratio in order to improve acceptance and adherence.
But the studies at that stage didn't give such information.

They also made a statement about harms in their summary:

There is little evidence of harm in published trials using GET that is properly supervised
by an appropriate professional and mutually agreed with the patient.
 

Attachments

Dolphin

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It's useful to have the data summarised like this.

What makes GET work?

Fulcher and White (1997) examined the associations of improvement with GET. They found, to their surprise, that improved fitness and strength were not associated with selfrated global improvement. When they examined the correlations of improvement in physical disability, however, there were significant associations with a reduction in submaximal heart rate response to exercise and an increase in quadriceps strength (Fulcher & White, 2000). They concluded that feeling better was related to the graded exposure to the exercise programme, whereas it was necessary to be fitter in order to improve functioning.

Moss-Morris et al. (2005) also investigated potential mechanisms underlying the efficacy of GET. They found that a reduction in symptom-focusing was related to self-rated improvement and physical functioning. Moreover, patients in the exercise group were significantly less likely to focus on their symptoms after treatment than were patients in the control group. The authors suggest that the use of heart rate monitors (HRM) may have provided an important medium for distraction from symptom-focusing and therefore fatigue, as patients were instructed to use the HRM, rather than their symptoms, as an external cue to determine their exercise intensity. Moss-Morris et al. (2005) also found that if during GET treatment patients had an increased perception their fatigue could be controlled, they showed greater improvements in fatigue and disability. This finding suggests that a GET treatment which challenges patients’ negative beliefs about symptoms may maximize the treatment effect, and is supported by the findings of the previous trial by Powell et al. (2001) in which this was an element of the treatment. It is even possible that by challenging negative beliefs about physical activity GET will reduce disability via reductions in fear-related avoidance, although this possible mechanism of GET has not yet been demonstrated empirically.
All sorts of quack therapies could also get many of these results. (There were improvements in physical fitness in Fulcher and White (1997) but the level of improvements don't seem to have been replicated in White et al. (2011)).
 

Dolphin

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Work needs to be done to improve acceptance and adherence
There is no mention that increased adherence might increase chances of adverse reactions.
---

That's about it for me on this paper. I haven't tried to do an indepth critique with lots of counterexamples so I'm sure others can add more.
 

Esther12

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Thanks for those notes D.

It is frustrating when Peter White keeps claiming this when the evidence isn't there. I've attached the file to let people read for themselves.
I haven't looked at it in a while - I think this is the relevant table:
So it was when there was no professional guidance that patients were least likely to report harm?

As you say though, it's a very small sample.
 
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Model underlying GET:

This ignores the fact that all the symptoms can't be explained by deconditioning e.g. alcohol intolerance (otherwise there would be far fewer problem drinkers around).

It also ignores how people can suddenly be experiencing extra symptoms after relapses, without being more deconditioned, etc.
Yes, the sudden increase in symptoms after a relapse is a spectacular hole in the deconditioning theory, yet the proponents of it have never even addressed the 'relapse problem'.

Another problem is that when healthy people become severely deconditioned by space travel, or voluntarily in bed rest studies, they don't suffer with anything like the level of fatigue seen in CFS - even though they are more deconditioned than CFS (out)patients.
 
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Clark & White said:
In summary, GET is not based upon any assumptions about the aetiology of CFS. Treatment is based upon the theory that exercise avoidance perpetuates symptoms through deconditioning, a reconditioned response, and changes in interoception. Modifying avoidant behaviour breaks the vicious circle of fatigue and disability; physiological consequences are reversed, promoting recovery
Note that this is making a distinction between the aetiology (initial cause of the illness) and the pathophysiology (ongoing cuases). As the subsequent sentence shows, it is based on some assumptions/it is based on a model of pathophysiology/what is perpetuating the condition.
Agreed. Their point is wrong, and I think this is worth addressing as a similar line is used by Simon Wessely too when he talks about biologial 'causes' of the illness.

The key point is that CFS requires a minimum of 6 months of fatigue to be diagnosed. So the argument that people get sick or have some physical trauma and that is the cause of the illness is fallacious: most people recover in such situations. The 'cause' of CFS in such cases is what causes CFS to develop following on from those initial triggers shared by many.

The glandular fever model of CFS is a perfect example of this. Everyone gets fatigue as part of the illness and for some time afterwards - the question in this model is why do some people go on to develop CFS? According to Rona Moss-Morris, it's patients flawed beliefs and behaviours. The Dubbo study (which also looked at psychlogical factors) concluded that biological factors were central.

Note that people who get fatigue as part of the illness but don't develop CFS are in the majority - the 'trigger' for them did not trigger CFS. So whatever else is involved is a critical part of the aetiology of the illness. Therefore the perpetuating cycle of fatigue and disability that Clark and White hypothesise IS part of the aetiology of CFS, despite the hand-waving claims to the contrary.
 

Sean

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Non-systematic review of published papers concerning deconditioning and therapeutic exercise in patients with CFS.
Non-systematic reviews should simply be never be published. Shame on the journal editors for publishing it.