Review Attenuating Post-exertional Malaise in [ME/CFS] and Long-COVID: Is Blood Lactate Monitoring the Answer? 2024 Faghy et al

Highlights

• Lactate monitoring has the potential to extend beyond applied sports settings and could be used to monitor the physiologic and pathophysiological responses to external and internal stimuli in chronic disease areas such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Post-Covid syndrome or Long Covid.
  
  
• It is applicable due to the recurrent, episodic and often disabling post-exertional symptom exacerbation (PESE) otherwise referred to as post-exertional malaise (PEM) which is a characteristic symptom of ME/CFS and Long Covid that can last for days and/or weeks.
  
  
• Lactate monitoring presents an opportunity to support those living with ME/CFS and Long COVID, by allowing patients and practitioners to determine the intensity and anaerobic contribution to everyday tasks which could aid the development of pacing strategies that prevent PEM/PESE.

No further abstract available.

Paywall, https://www.sciencedirect.com/science/article/abs/pii/S0146280624001932

 

That sounds like another "Here's an easy test that probably has nothing to do with the disease, but which we can get research funding for because it sounds good."

 

People can email for the full text:

Edited to add: Paper is being made open access:

 

Maybe, but he does seem to be looking at this from a good number of angles. I'm reticent to without a thorough dive through everything sign off someone as thumbs up but at least his lists of references aren't 'limited'.

He mentions that these portable monitors now being readily available has indeed made this possible and are used by athletes etc (he references a paper from 2010 that reviews some of these) so I guess as long as he is impartial when assessing whether it is a useful additional context then it is indeed something begging to be looked into. Interesting given his focus seems to have been coming from the covid, then long covid direction, that this is looked at ME/CFS directly here.

 

The pre-proof will need to correct any ME/CSF typos. It's a short opinion piece —

 

Is Blood Lactate Monitoring the Answer for any other health problems and do those have anything in common with ME/CFS?

Continous Blood Lactate Monitors are currently a big hype in sports, especially cycling, albeit these devices basically not even existing yet and their scientific accuracy currently being questionable.

 

I am also interested in learning about lactate levels in the brain and how they negatively interplay with cognitive and physical activities.

 

If lactate level in MECFS is any different, it would've been known long time ago, I would think. It should be just a matter of drawing blood every hour after the exertion and plot the time series, like they do in sports medicine with athletes.

 

It might be detectable by MRI too. Maybe not though. I recently read about a new MRI with 11.7 Tesla, which among other improvements, allows detection of molecules that don't show a strong enough signal in weaker fields. I also read about a new technique using a virus that produces a certain enzyme in astrocytes, making them glow in response to oxygen levels. A similar technique might be developed for detecting other molecules. Lots of new tools and techniques. I wish researchers would use them properly to study ME, rather than just repeat the same old experiments trying to get better-looking results.

 

Some threads discussing papers which showed abnormal brain lactate:
https://www.s4me.info/threads/multi...bidity-2017-natelson-et-al.37784/#post-522553
https://www.s4me.info/threads/ventr...disorder-2009-mathew-et-al.36734/#post-509955

 

ME Research UK:

Post exertional malaise is often referred to as the cardinal symptom of ME/CFS – & one also experienced by some with long COVID. A new paper looks at how monitoring lactate levels in the blood may provide a way to support pacing strategies for PEM
https://www.meresearch.org.uk/blood-lactate-monitoring-a-tool-to-support-the-management-of-post-exertional-malaise/

 

Do we know if lactate is only correlated with or actually causes PEM?

 

It is unlikely to correlate directly with PEM I think - it would go up with exertion and be down by the time of PEM. Of all the things that cause PEM during exertion it is only one of hundreds and I doubt a particularly likely candidate. It certainly wouldn't be causing it directly, having gone away.

From the way members talk it seems likely to me that all sorts of exertion that do not actually involve a great deal of metabolic activity, and so unlikely to change lactate, will cause PEM. If only bicycling as hard as you can were a problem ME/CFS would be a doddle. Just stop bicycling.

 

I did the same lactate monitoring, but also couldn't get a meaningful signal within the limitations of my exertion at the time. However, one datapoint that was interesting to me was with the first of two hospital admissions, following an initial crash although I didn't have much of a clue what was going on with me at the time except that it was not good. Lactate was 1.8 IIRC with the upper limit of normal being 1.9. For an otherwise healthy, fit, active person capable of substantial exertion a few weeks prior, who had been sitting or lying for a couple of hours, that result was very abnormal. @Kiwipom (a runner) had a similar observation.

I imagine lactate could contribute to symptoms, perhaps in ways similar to the provocation studies in people who suffer panic attacks. But the delay and duration for PEM implicates other things beyond those more immediate and presumably short-acting anaerobic effects. As Jo notes above, the exertion for me, as for others, is pretty damn trivial compared to what I was capable of. Perhaps it's not a great deal of metabolic activity but instead a relatively great deal of inefficient metabolic activity. ROS production might well take more time to accumulate above threshold-for-badness and take effect systemically; and then take time to get under control and retreat.

Maybe the generation of lactate in muscles generates metabolic debt that is paid back pretty quickly in other tissues, eg liver, but that that payback is with interest and also generates metabolic waste products that contribute to symptoms?

 

I have not taken the trouble to search through but do we know how lactate is being measured in these devices? Is it on optical spectrum or is blood actually sampled or what?

I wonder if venous pooling affects it? Someone lying in bed doing nothing might have a high reading simply because of slow perfusion rate?

 

EDIT --- Oops --- thread about blood lactate --- didn't pick that up! So comment below is off-topic!
Higher lactate in the brain is based on MRI but you do raise an interesting point - e.g. do you have comparable controls; even if the controls are comparable, is the experience of MRI comparable [stressed ME/CFS versus un-stressed control]!