Maximal oxygen uptake and lactate metabolism are normal in chronic fatigue syndrome, 2002, Charli Sargent et al

Abstract

Purpose: Previous studies in chronic fatigue syndrome (CFS) have reported reductions in maximal oxygen uptake (VO(2max)), yet often the testing procedures have not followed accepted guidelines, and gender data have been pooled. The present study was undertaken to reevaluate exercise capacity in CFS patients by using "gold standard" maximal exercise testing methodology and stratifying results on a gender basis.

Methods: Sixteen male and 17 female CFS patients and their gender-, age-, and mass-matched sedentary controls performed incremental exercise to volitional exhaustion on a stationary cycle ergometer while selected cardiorespiratory and metabolic variables were measured.

Results: VO(2max) in male CFS patients was not different from control values (CFS: 40.5 +/- 6.7; controls: 43.3 +/- 8.6; mL x kg(-1) x min(-1)) and was 96.3 +/- 17.9% of the age-predicted value, indicating no functional aerobic impairment (3.7 +/- 17.9%). In female CFS patients, VO(2max) was lower than control values (CFS: 30.0 +/- 4.7; controls: 34.2 +/- 5.6; mL x kg(-1) x min(-1), P = 0.002), but controls were higher than the age-predicted value (112.6 +/- 15.4%, P = 0.008) whereas the CFS patients were 101.2 +/- 20.4%, indicating no functional aerobic impairment (-1.2 +/- 20.4%). Maximal heart rate (HR(max)) in male CFS patients was lower than their matched controls (CFS: 184 +/- 10; controls: 192 +/- 12; beats x min(-1); P = 0.016) but was 99.1 +/- 5.5% of their age-predicted value. In female CFS patients, HR(max) was not different from controls (CFS: 183 +/- 11; controls: 186 +/- 10; beats x min(-1)) and was 98.9 +/- 5.1% of the age-predicted value. The VO(2) at the lactate threshold (LT) in each gender group, whether expressed in mL x kg(-1) x min(-1) or as a percentage of VO(2max), was not different between CFS patients and controls.

Conclusions: In contrast to most previous reports, the present study found that VO(2max), HR(max), and the LT in CFS patients of both genders were not different from the values expected in healthy sedentary individuals of a similar age.

https://pubmed.ncbi.nlm.nih.gov/11782647/

 

What patient criteria did they use for the study?

 

This obviously disproves the myth that deconditioning leads to ME/CFS symptoms.

 

It's a long time ago, but I recall two of the authors, Garry Scroop and Richard Burnet, were investigating lactate levels in ME/CFS after exercise. There was a lot of hype about this not long after I first became ill, but it disappeared without a trace not long after.

A friend who was a doctor and was a colleague of Dr Burnet prescribed Spironolactone for me on this experimental basis. It didn't do anything for me.

 

Lactate may not be a waste by-product of metabolism. For a newer view on the role of lactate as a universal fuel that can balance the energy needs across the entire body, see the thread on Lactate: the ugly duckling of energy metabolism.

 

Yes, lactic acid is a metabolic buffer and is less acidic than pyruvate.

While during intense exercise, it is flushed out of cells into circulation, it can later be turned back into glucose by the liver, so that the energy that remains isn't wasted.

We also know that the presence of lactate alone does not cause pain or the symptoms of fatigue. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3946674/

 

In 2002 I think it was Fuduka. So, participants may/may not have PEM unless specified.

 

I can't find anything about this that I can understand. When I overexert my muscles burn like acid runs through them. If this is now known not to be lactic acid are there any ideas what it is?

 

Mark VanNess describes CO2 and Lactic Acid. Time stamped here:

https://www.youtube.com/watch?v=q_cnva7zyKM

 

That is interesting. So it looks like the burning could be because we can't clear carbonic acid. That would make sense if we run our aerobic system until it can do no more so the acid builds up. It would explain why it is not always so bad, burning, yes but not agony.

 

It is not just carbonic acid though, the Light study also showed that stimulation of purinergic G protein coupled receptors was necessary for the sensation of fatigue - or to put it another way, there shouldn't be ATP (which is a high energy/reactive molecule) floating around outside of cells in significant quantities - it should not be leaking from cells.

That is a great talk, I wish more people would watch it.

 

This video has given me a basic understanding of energy production and ME more than anything else. It's easy to follow for a non-scientist. I used the information in it to get myself reasonably fit without crashing before some major surgery a few years ago. It's a keeper for me.