Loss of capacity to recover from acidosis on repeat exercise in Chronic Fatigue Syndrome: A case control study. European Journal of Clinical Investigation, 30 June 2011.
Loss of capacity to recover from acidosis on repeat exercise in Chronic Fatigue Syndrome: A case control study.
The conclusion to the paper contains important practical information regarding exercise therapy.
This study was partly funded by The MEA Ramsay Research Fund – which is paying for research into muscle function in ME/CFS being carried out by Professor Julia Newton and colleagues at the University of Newcastle.
More information can be found in the section on research in the summary of the June 2011 meeting of the MEA Board of Trustees.
1. David EJ Jones MD PhD1,†,
2. Kieren G Hollingsworth PhD1,2,†,
3. Djordje G Jakovljevic PhD3,4,5,
4. Gulnar Fattakhova MD3,4,
5. Jessie Pairman3,4,
6. Andrew M Blamire PhD1,2,
7. Michael I Trenell PhD1,4,5,‡,
8. Julia L Newton MD PhD3,4,‡
DOI: 10.1111/j.1365-2362.2011.02567.x
European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation
Author Information
1 Institute of Cellular Medicine
2 Newcastle Magnetic Resonance Centre
3 Institute for Ageing and Health
4 the UK NIHR Biomedical Research Centre in Ageing and Age Related Diseases
5 Newcastle Centre for Brain Ageing and Vitality. Newcastle University, UK
*Correspondence: Professor Julia L Newton Institute for Ageing and Health Medical School Framlington Place Newcastle-upon-Tyne NE2 4HH, UK Email: j.l.newton@ncl.ac.uk
Publication History
1. Accepted manuscript online: 10 JUN 2011 11:17AM EST
2. Received Date: 16-Mar-2011, Accepted Date: 05-Jun-2011
Abstract
Background: Chronic fatigue syndrome (CFS) patients frequently describe difficulties with repeat exercise. Here we explore muscle bioenergetic function in response to 3 bouts of exercise.
Methods: 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.
Results: CFS patients undertaking MVC fell into 2 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, VO2, VO2 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 intra-muscular acidosis compared to controls after similar work after each of the 3 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.
The conclusion to this paper is confusing. Is anyone able to find out what they intended to say?
Ok. I am taking this as ‘good’ news. About time we started going back to basics.
Proving our symptoms are not ‘imagined’ or what have you.
Enough with the ‘viral’ causes and chasing ghosts – let’s look for what is actually happening and prove our points.
Then we can see why it is happening. Never know might even get more funding this way.
Nice one RRF [Thumbs Up]! 🙂
It is not clear what they are thinking.
Can someone please interpret this in non scientific terms… whats acidosis? i googled it but the small bits i was able to read on wiki etc didnt seem to have any connection with exercise.
Also I dont understand
“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.”
what does ‘initiate’ mean in this context? sounds like “people who dont want to take the initiative on their own to do exercise”… but surely that cant be what they’re meaning???
They say that the solution for our 50x normal acidosis is GET!
As in many of these ridiculous papers, they find actual physical pathology and then in the conclusion warp it some way to suggest GET and/or psychogenesis.
The last two sentences are very troubling to me. It says that ME should be treated with ‘exercise intervention’ (GET) because this is the proper treatment for acidosis. Also says that pw”CFS” who do not normally exercise should be excluded from any study because they may not comply with the GET instructions and thus artificially lower the measured effectiveness of GET in trials like PACE. Obviously, if pw-Oxford defined “CFS” who normally exercise are studied, all of the people in the study will have Idiopathic Chronic Fatigue not ME.
Here’s a nice/interesting quote:
“Using this approach, *****total post-exercise acid exposure is of the order of 50-fold higher in CFS patients exercising to the same degree as normal controls*****, with no reduction in this pattern of sustained high level acidosis with repeat exercise. We believe that the local and systemic sequelae of this sustained acid exposure contribute significantly to the expression of fatigue in CFS.”
From this paragraph:
“There are aspects of the abnormality in acid homeostasis in CFS which differ to those seen in PBC and which may significantly contribute to the severity of fatigue in CFS. We have previously reported that when PBC patients undergo repeat exercise the degree of acidosis seen within muscle reduces with each exercise episode, suggesting the retention of some compensatory capacity for excess muscle acidosis in PBC (28). One mechanism for this is increase in proton flux, and the speed of onset of maximum proton excretion, with repeat exercise. This phenomenon, which is also a feature of mitochondrial disease where increased proton efflux after exercise helps compensate for reduced aerobic capacity [35], was absent from the CFS patients. These findings suggest that CFS patients are unable to compensate for the increased reliance upon anaerobic energy sources during muscle contraction in comparison to other conditions with reduced aerobic capacity.
The net effect of these combined effects can be seen in terms of cumulative acid exposure determined from the area under the curve for pH. Using this approach total post-exercise acid exposure is of the order of 50-fold higher in CFS patients exercising to the same degree as normal controls, with no reduction in this pattern of sustained high level acidosis with repeat exercise. We believe that the local and systemic sequelae of this sustained acid exposure contribute significantly to the expression of fatigue in CFS.”
Well here is a very short vid from BBC Look North Programme a while back where Prof Julia Newton speaks about what i can only assume is this same research (since she is cited above, & it’s the same topic (acid) and clearly done by her dept)
http://www.youtube.com/watch?v=UoxlyhOLCSA
Explanation:
In very simple terms, skeletal muscle produces acid as a result of various biochemical reactions that occur when someone exercises.
So one of the components of this study looked at acid production (the ph levels) in muscle during exercise.
This is an aspect of ME/CFS research that I have personally been involved with and back in 1984 a similar piece of research published in The Lancet, using my own muscle, produced similar results.
The research demonstrates that a sub-group of people with ME/CFS produce more acid than normal during exercise and that it then takes longer to return to normal baseline levels after the exercise is over. The results help to confirm a complex biological basis for ME/CFS. They also explain why activity management programmes need to be prescribed with great care. In addition the findings might lead to forms of treatment that are directed at this interesting metabolic abnormality within muscle.
This study was partly funded by the MEA Ramsay Research Fund.
Exercise is dangerous for people with ME. Why would anyone then prescribe such a program to a patient?
thks for taking the time to give us that explanation Dr Shepherd, it sounds really promising.
I do hope something comes of it though and it doesnt just get swallowed into the void and make zero impact where it matters, like all the other promising small scale studies over the years.
and i still dont understand what they are meaning with the “initiate exercise comment”? I’m sure it cant mean what it sounds like, so it’d be helpful to know what they are *actually* driving at with that comment & prevent any misunderstanding.