ME/CFS and deconditioning

A previous post examined the Wessely School hypothesis that ME/CFS is caused by unhelpful beliefs. This idea was exploded as a myth. Here I examine a second Wessely School hypothesis (H2) that states:

Deconditioning causes, or exacerbates the symptoms of, ME/CFS and MUS.

Deconditioning refers to multiple, potentially reversible changes in body systems brought about by physical inactivity and disuse. The theory proposes that patient’s claims of an inability to exercise or exert themselves is due to a reluctance to or fear of exercise. Psychological interventions in the form of CBT are indicated to help the patient overcome their dysfunctional beliefs and physical exercise such as GET is offered to help the patient to recondition their body. Without properly controlled trials and investigations it is impossible to determine which is cause and effect, the illness or the deconditioning. If deconditioning causes or contributes to ME/CFS, then signs of deconditioning should be more pronounced in the sicker patients and less pronounced in the less sick ones.  In this section, I review the evidence for and against the deconditioning hypothesis of ME/CFS and MUS. Relevant studies have been conducted over a period of 20+ years. An early uncontrolled study suggested an association between CFS and deconditioning (De Lorenzo et al. (1998). To take a study seriously it must meet the minimum criteria for a controlled study: groups matched at baseline, blinded testing, with objective measures.

Fulcher and White (2000)

measured strength, aerobic exercise capacity and efficiency, and functional incapacity in pwCFS who did not have a current psychiatric disorder. Compared with sedentary controls, pwCFS were found to be physically weaker, had a significantly reduced exercise capacity, and perceived greater effort during exercise, but were equally unfit. Fulcher and White concluded that pwCFS were weaker than sedentary and depressed controls and as unfit as sedentary controls. The data were consistent with the hypothesis that physical deconditioning helps to maintain physical disability in CFS and that a treatment designed to reverse deconditioning would help to improve physical function. However there was a problem with the procedures used to test the participants.  However, as the authors acknowledge, the lack of ‘blind’ testing and other issues could have biased the results: “ We would in any case advise caution in interpreting and generalising from these data because of the bias inherent in a case-control study, the need for replication of these data, the lack of blindness in some of the measures, and the few comparison patients with a major depressive illness.” (Fulcher & White, 2000, p. 307).

Timmers et al. (2002)

found that head-up tilt evokes postural tachycardia or (pre)syncope in a minority of CFS patients. The authors concluded that observations in head-up tilt-negative CFS patients of a higher heart rate at baseline together with a marked decrease in stroke volume in response to head-up tilt could point to deconditioning.

Not so fast! Please read on to the end…

A narrative review

by Clark and White (2005) concluded that: “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…Further work is necessary to elucidate the risks, benefits, and mechanisms of such treatment, especially in children and the severely disabled” (p. 237).

A subjective measure and high drop-out rate

Moss-Morris, Sharon, Tobin and Baldi (2005) investigated GET in a sample of 49 CFS patients who were randomized to a 12-week graded exercise programme or to standard medical care. After treatment the group who had received GET rated themselves as significantly more improved and less fatigued than the control group. A decrease in symptom focusing rather than an increase in fitness mediated the treatment effect. The authors concluded that GET “appears to be an effective treatment for CFS and it operates in part by reducing the degree to which patients focus on their symptoms” (p. 245). The main problem with this study was the use of subjective measures of illness improvement and the high drop-out rate of 47% (23/49) from the physiological tests and the non-significant physiological improvement with ten patients refusing to have a second test as they believed the initial test was harmful to them.

A skeptical Catalonian study

concluded that “the decrease in the peak workload achieved in arm or leg exercise by CFS patients would not be justified exclusively by their personal characteristics or deconditioning”  (Javierre et al., 2007).

A curiously Contrarian study

Harvey, Wadsworth, Wessely and Hotopf (2008) reviewed the aetiology of CFS and tested hypotheses relating to immune system dysfunction, physical deconditioning, exercise avoidance, and childhood illness experiences, using a large prospective birth cohort consisting of 4779 participants from the National Survey of Health and Development. Participants  were prospectively followed for the first 53 years of their lives with 20 separate data collections. The authors identified CFS through self-report during a semi-structured interview at age 53 years with an additional case notes review. Of 2983 participants assessed at age 53 years, 34 percent reported a diagnosis of CFS and were no more likely to have suffered from childhood illness or atopy. Interestingly, the authors found that “increased levels of exercise throughout childhood and early adult life and a lower body mass index were associated with an increased risk of later CFS. Participants who later reported CFS continued to exercise more frequently even after they began to experience early symptoms of fatigue…Continuing to be active despite increasing fatigue may be a crucial step in the development of CFS” (p. 488). Based on Harvey et al.’s prospective evidence, which can give a valid interpretation of causality, exercising rather than its lack appears as a possible cause of later ME/CFS.


This temporal, dose–response relationship suggests that psychiatric disorders, or shared risk factors for psychiatric disorders, are likely to have an aetiological role in some cases of CFS/ME.

An inconclusive update

of an earlier review (Larun et al., 2014) observed that: “Exercise therapy did not worsen symptoms for people with CFS. Serious side effects were rare in all groups, but limited information makes it difficult to draw firm conclusions about the safety of exercise therapy” (Larun, Brurberg, Odgaard-Jensen & Price, 2019). The authors arrived at a set of appropriately modest conclusions. In comparing exercise therapy with a ‘passive’ control, they state:

“Exercise therapy probably reduces fatigue at end of treatment… We are uncertain if fatigue is reduced in the long term because the certainty of the evidence is very low…We are uncertain about the risk of serious adverse reactions because the certainty of the evidence is very low…Exercise therapy may moderately improve physical functioning at end of treatment, but the long‐term effect is uncertain because the certainty of the evidence is very low. Exercise therapy may also slightly improve sleep at end of treatment and at long term. The effect of exercise therapy on pain, quality of life and depression is uncertain because evidence is missing or of very low certainty.” In sum, no definite conclusions about exercise and CFS patients could be reached.

The literature’s a mess

Nijs et al. (2011) conducted a systematic review to examine whether pwCFS differ from healthy sedentary controls in physiological exercise capacity, physical activity level and muscle strength. They refer to the conflicting data concerning physiological exercise capacity of pwCFS but suggest that the “weighted available evidence points towards a reduced physiological exercise capacity in CFS. Future studies should use a wash-out period for medication use, blinded assessments, a priori power calculation and a sedentary control group comparable for age, gender, body weight, body length and current physical activity level” (p. 1493).

A deleterious immunological effect of GET predicted

Another review by Pierce, Pierce and Campus (2008) discussed the deleterious immunological effect that is likely to follow the use of GET in pwME: “initial over-exertion (a period of metabolic stress) in conjunction with viral infection depletes concentrations of the metabolic regulator glutathione, initiating a cascade of physiological dysfunction…the exacerbation of symptoms for the majority is not subjective but has a physiological basis. Blanket recommendation of GET is not prudent for such a heterogeneous group of patients, most of which are likely to respond negatively to physical activity” (p. 55).

Finally, a properly controlled cardiological study

As noted, previous studies have established that effort intolerance along with a prolonged recovery from exercise and post-exertional exacerbation of symptoms are characteristic features of ME/CFS. Finally, Van Campen and Visser (2018), two cardiologists in the Netherlands, carried out a well-controlled investigation entitled: “The abnormal Cardiac Index and Stroke Volume Index changes during a normal Tilt Table Test in ME/CFS patients compared to healthy volunteers, are not related to deconditioning.” 

At last, a well-controlled cardiological study of the deconditioning hypothesis that leaves no doubt about its findings.

Figure 2: shows the percent change of the stroke volume and cardiac index in ME/CFS patients with mild, moderate and severe disease according to the ME criteria. Reproduced from van Campen and Visser (2018).

There were no significant differences between the three groups suggesting that deconditioning does not explain the larger decrease in stroke volumes and cardiac output in ME/CFS patients compared to healthy volunteers.

Over the 20-+ year period since research on ME/CFS and deconditioning first began, this is the first controlled investigation that looks at disease severity in a test of the conditioning hypothesis.  The study clearly indicates that deconditioning is NOT causally associated with ME/CFS severity, contrary to H2.


  1. After 20+ long years, a study by two cardiologists in the Netherlands, van Campen and Visser, have laid to rest the idea that ME/CFS symptoms are caused by deconditioning.
  2. It seems far more likely that ME/CFS causes deconditioning, not vice versa.
  3. This is the second of the Wessely School myths that has been exploded.
  4. The use of GET for ME/CFS patients should be banned immediately.
  5. ME/CFS patients must be listened to. At this stage, they are the only genuine experts, so it would appear.

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10 thoughts on “ME/CFS and deconditioning

  1. Whilst I can hardly be called one of the waxing/waning types of ME/CFS people, I I recently had a slightly better patch from being bedbpind to not quite bedbound and along with the ability to do that little bit more, but my maicles were strong er rgith at the beiging of this phase. As in as far as I could tell, they were back to normal after 2 years in bed. I can’t speak for all, but this reassured me that it was an issue somewhere of the right stuff getting to the right places causing weakness and not atrophy of the muscles themselves. There seems to be an on/off switch to this for me.

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