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afwijkende effecten

van inspanning

bij ME (CVS)-patiŽnten








In een overzichtsartikel worden de afwijkende effecten van inspanning en orthostatische stress

in ME en CVS samengevat, die in samenhang post-exertionele 'malaise' plausibel kunnen verklaren.






Dangerous exercise.

The detrimental effects of exertion and orthostatic stress

in Myalgic Encephalomyelitis and chronic fatigue syndrome.

Phys Med Rehabil Res. 2017. 2(1):3-3. doi: 10.15761/PMRR.1000134.

Twisk FNM.




Exercise, especially regular exercise,

is known to have has various beneficial effects on the health status [1,2].


However, when immunological, stress and other responses to physical activity are dysregulated

exercise can become detrimental to health [3].


Looking at the evidence so far,

this latter observations seems also to be applicable to

Myalgic Encephalomyelitis (ME) and chronic fatigue syndrome (CFS).


Although ME and CFS are often declared to be synonyms [4],

the diagnostic criteria define two distinct clinical entities.


ME is primarily defined by

muscle weakness (and myalgia) after a minor exertion lasting for days and

characteristic neurological features,

while CFS is primarily defined by (unexplained, incapacitating) chronic fatigue [4].


Although ME and CFS are to be considered to be

two distinct, partially overlapping, diagnostic labels [4],

the Institute of Medicine [5] confirmed that

post-exertional 'malaise',

defined as a prolonged aggravation of typical symptoms

(e.g. 'brain fog'/cognitive deficits and muscle and joint pain)

is the hallmark feature of 'ME/CFS'.


Despite this methodologic hurdle,

i.e. research into mixed ME and/or CFS patient populations,

various characteristic aberrations have been found repetitively.


Exercise-related abnormalities [6] are associated with

  1. energetic abnormalities,
  2. which seem to be amplified by exertion,

    including mitochondrial dysfunction [7-10],

    (very) low oxygen uptake [11-13],

    reduced oxygen supply to muscles [14] and brain [15], and

    excessive acidosis and recovery from exercise-induced acid [13,16,17];

  3. muscular abnormalities related to exercise [18-20];
  4. increased pain sensitivity and lower pain threshold induced by exercise [21-23];
  5. long-lasting oxidative stress in response to exercise [19,21,24];
  6. cardiovascular abnormalities [25-27];
  7. deviant autonomic responses to exertion and orthostatic stress [28-30];
  8. neurological abnormalities in relation to exercise [31-33];
  9. immunologic abnormalities after exertion [32,34,35];
  10. exercise-induced gastro-intestinal abnormalities, including bacterial translocation [36-38];
  11. attenuated stress responses to exercise [39,40]; and
  12. ion channel dysfunction during rest and in response to exercise [41-43].

These abnormalities can plausibly explain post-exertional 'malaise' in ME/CFS [44].


Physical deconditioning is not a perpetuating factor in ME/CFS [45].


Deconditioning also cannot account for the aberrations observed,

especially since various studies have used sedentary controls, e.g. [11,13,46].


Deconditioning also cannot explain

the profound fall in exercise capacity

(maximum oxygen uptake/workload and/or

oxygen uptake/workload at the anaerobic threshold)

at a second exercise test and

the inability of ME/CFS patients to reproduce VO2peak 24 hours later [47-49].


Interestingly, recent studies observed a hypometabolic state [50,51],

which was characterized by one study as 'dauer' [52].


Although male and female patients seem to compensate differently,

these studies show 'inadequate ATP generation

by oxidative phosphorylation and

excessive lactate generation upon exertion' [53].


So, while the deconditioning hypothesis seems tempting,

graded exercise protocols seem to have detrimental effects on many patients [54].


In the case of ME/CFS

it is wise to acknowledge

the potential dangers of exercise to avoid iatrogenic harm.