Well, in fairness, some people did try to replicate those initial positive findings and, as so often happens in science, were unable to do so in the majority of patients diagnosed with the construct of chronic fatigue syndrome. It would appear that your case is atypical.
Reply:
Yes, the numbers are small in all these muscle studies - so it's difficult to know what percentage of the ME/CFS population have this abnormality
My gut feeling remains that there is a sub-group with significant muscle abnormalities relating to acid handling - and in this respect we may be dealing with a type of post infectious mitochondrial myopathy
Did you see this more recent research from Julia Newton et al, which was funded by the MEA:
http://www.ncbi.nlm.nih.gov/pubmed/21749371
Eur J Clin Invest. 2012 Feb;42(2):186-94. doi: 10.1111/j.1365-2362.2011.02567.x. Epub 2011 Jul 12.
Loss of capacity to recover from acidosis on repeat exercise in chronic fatigue syndrome: a case-control study.
Jones DE1,
Hollingsworth KG,
Jakovljevic DG,
Fattakhova G,
Pairman J,
Blamire AM,
Trenell MI,
Newton JL.
Author information
Abstract
BACKGROUND:
Chronic fatigue syndrome (CFS) patients frequently describe difficulties with repeat exercise. Here, we explore muscle bioenergetic function in response to three bouts of exercise.
METHODS:
A total of 18 CFS (CDC 1994) patients and 12 sedentary controls underwent assessment of maximal voluntary contraction (MVC), repeat exercise with magnetic resonance spectroscopy and cardio-respiratory fitness test to determine anaerobic threshold.
RESULT:
Chronic fatigue syndrome patients undertaking MVC fell into two distinct groups: 8 (45%) showed normal PCr depletion in response to exercise at 35% of MVC (PCr depletion >33%; lower 95% CI for controls); 10 CFS patients had low PCr depletion (generating abnormally low MVC values). The CFS whole group exhibited significantly reduced anaerobic threshold, heart rate, VO(2) , VO(2) peak and peak work compared to controls. Resting muscle pH was similar in controls and both CFS patient groups. However, the CFS group achieving normal PCr depletion values showed increased intramuscular acidosis compared to controls after similar work after each of the three exercise periods with no apparent reduction in acidosis with repeat exercise of the type reported in normal subjects. This CFS group also exhibited significant prolongation (almost 4-fold) of the time taken for pH to recover to baseline.
CONCLUSION:
When exercising to comparable levels to normal controls, CFS patients exhibit profound abnormality in bioenergetic function and response to it. Although exercise intervention is the logical treatment for patients showing acidosis, any trial must exclude subjects who do not initiate exercise as they will not benefit. This potentially explains previous mixed results in CFS exercise trials.