You state that:
“Graded Exercise Therapy (GET) appears to work for people not because it’s reversing deconditioning, but because it’s changing the perception of effort. The most scientifically convincing explanation is therefore not to do with any particular muscle abnormality, but rather an abnormality in the perception of the post-exertional fatigue, malaise or pain. This is a complex interplay that involves muscles, nerves, and the brain so can’t realistically be put down to one thing. I also wonder if the frustration (or downright stress) of not being able to do what one could before also amplifies the perception?”
You will be well aware that this explanation is held only by a small group of psychiatrists and like minded colleagues, whereas the great majority of researchers around the world consider post-exertional malaise to be physical in origin and do not recommend GET as a primary therapy.
I would be grateful if you would explain how all the following peer reviewed research evidence can be explained by this explanation of post-exertional fatigue.
These research papers invalidate the assertion that the problem is merely wrong perceptions and show that post-exertional fatigue is a verifiable physical phenomenon and that increasing exercise beyond what patients find tolerable is contraindicated by the objective evidence.
Also I would be grateful if you would provide me with references to papers showing MECFS patients do indeed have abnormal perceptions of fatigue and pain and that these wrong perceptions can cause the pathological findings referred to in the papers below, a necessary requisite for any theory.
Thank you for your time,
http://www.workwellfoundation.org/wp-co ... Final1.pdf
Workwell Foundation announces the publication of a new study supporting previous findings that a 2-day Cardiopulmonary Exercise Test (CPET) protocol objectively documents postexertional malaise (PEM), the most commonly recognized symptom in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).The study revealed a statistically significant performance decrease on Day 2 in workload at ventilatory threshold (VTWL), workload at peak exercise (WLpeak), volume of oxygen consumed at ventilatory threshold (VTO2) and volume of oxygen consumed at peak exercise (VO2peak). In short, individuals with CFS/ME were unable to reproduce their Day 1 performance on Day 2.The statistical classification analysis points to a diagnostic biomarker for CFS/ME with a 95.1% accuracy.
Here is the relevant paper:
http://ptjournal.apta.org/content/early ... 0368.short
“Discriminative Validity of Metabolic and Workload Measurements to Identify Individuals With Chronic Fatigue Syndrome”
Christopher R. Snell, Staci R. Stevens, Todd E. Davenport (firstname.lastname@example.org
J. Mark Van Ness
And the research evidence cited here:
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
Myalgic encephalomyelitis: International Consensus Criteria
“Malaise – a vague feeling of discomfort or fatigue”  is an inaccurate and inadequate word for the pathological low-threshold fatigability and post-exertional symptom flare. Pain and fatigue are crucial bioalarm signals that instruct patients to modify what they are doing in order to protect the body and prevent further damage. Post-exertional neuroimmune exhaustion is part of the body’s global protection response and is associated with dysfunction in the regulatory balance within and between the nervous, immune and endocrine systems, and cellular metabolism and ion transport [43-47]. The normal activity/rest cycle, which involves performing an activity, becoming fatigued, and taking a rest whereby energy is restored, becomes dysfunctional.
Numerous papers document abnormal biological responses to exertion, such as loss of the invigorating effects of exercise , decreased pain threshold [48-50], decreased cerebral oxygen and blood volume/flow [51-54], decreased maximum heart rate , impaired oxygen delivery to muscles , elevated levels of nitric oxide metabolites , and worsening of other symptoms . Patients reach the anaerobic threshold and maximal exercise at a much lower oxygen consumption level . Reported prolonged effects of exertion include elevated sensory signalling to the brain  that is interpreted as pain and fatigue , elevated cytokine activity , delay in symptom activation  and a recovery period of at least 48 hours . When an exercise test was given on two consecutive days, some patients experienced up to a 50% drop in their ability to produce energy on the second evaluation . Both submaximal and self-paced physiologically limited exercise resulted in post-exertional malaise .
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