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

Andy

Andy

Retired committee member
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
 
Creekside said:
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."
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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 —

Factors associated with increased concentrations of blood lactate have been explained elsewhere2 but include oxygen delivery, mitochondrial capacity, and the ability to clear and utilize lactate by other cells throughout the body. Lactate (C3 H6 O3) originates from accumulating pyruvate (C3 H4 O3), an important substrate in metabolic pathways during both anaerobic (metabolic activity that occurs in the absence of oxygen) and aerobic (in the presence of oxygen) exercise3. The development and validation of portable blood lactate monitors4 , that use small amounts of blood (>0.7 microliters), have made monitoring blood lactate an accessible and popular tool for athletes and coaches to monitor the responses to exercise and/or training.
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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 PostCOVID 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 (mostly) and/or weeks (rarely) 5. Whilst a dearth of understanding remains in the pathophysiologic mechanisms in these conditions 6 , PEM/PESE is associated with an abnormal response and worsening of symptoms that includes loss of physical and mental stamina, rapid muscular, and cognitive fatigability following physical, cognitive, emotional, and orthostatic exertion7.
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Detail pertaining to the mechanisms is outside the scope here, but relates to the transport, delivery, and utilisation of oxygen within skeletal muscles, thus affecting aerobic and anaerobic contributions to the provision of energy at a cellular level. It is postulated that anaerobic thresholds are reduced in athletic populations with Long COVID which the authors attribute to virally mediated mitochondrial dysfunction that extends beyond expected post-viral infection deconditioning and could be caused by impaired tissue oxygenation and substrate oxidation8.
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It is plausible that patients with ME/CFS and Long COVID could be working anaerobically at markedly lower intensities compared to healthy controls (Figure 1). Whilst lactate is not responsible for reduced muscular function9, and can be elevated in numerous clinical situations 10,11 , in the context of mild exertion in patients with ME/CSF and Long COVID accumulating lactate levels are a biomarker of abnormally increased anaerobic activity which is used to supplement metabolic activity/energy production. Therefore, monitoring blood lactate levels could be used effectively to monitor metabolic disturbance and regulate pacing strategies in patients with chronic diseases that are compounded by PESE and PEM.
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A secondary impact of PEM/PESE is to withdraw from social and economic activities that form an important part of each person’s identity 13,14 . In the absence of detailed mechanistic understanding and effective therapeutic approaches, there is a need to develop effective management strategies that allow patients to plan, monitor and adjust their activities of daily life. In time, blood lactate monitoring could be used alongside pharmacological treatments for Long COVID & ME/CSF to safely and effectively increase functional capacity through the design and implementation of informed and objective interdisciplinary rehabilitation programs 15,16 . However, we are aware that more detailed rehabilitation recommendations are needed which should be informed by a greater understanding of the complex, multi-system nature of ME/CFS and Long COVID.
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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. Approaches that are widely used in the exercise sciences 17,18 , should be considered and tested for use in chronic disease settings whilst research into therapeutics for Long COVID and ME/CSF is ongoing.
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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.
 
The article is now open access. I think it looks like an interesting idea, though before recommending it for individuals to assist with pacing, research needs to be done on patterns of lactate levels in ME/CFS and how they relate to activity when compared to healthy sedentary controls. If it does indeed show a clear pattern of difference, it might be useful both for self monitoring and as an objective outcome measure in treatment trials. But it seems like there's a lot more research needed before that happens.
 
Trish said:
The article is now open access. I think it looks like an interesting idea, though before recommending it for individuals to assist with pacing, research needs to be done on patterns of lactate levels in ME/CFS and how they relate to activity when compared to healthy sedentary controls. If it does indeed show a clear pattern of difference, it might be useful both for self monitoring and as an objective outcome measure in treatment trials. But it seems like there's a lot more research needed before that happens.
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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.
 
poetinsf said:
If lactate level in MECFS is any different, it would've been known long time ago, I would think.
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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.
 
Lactate might not be a useful measure for revealing pathology in ME, but there are likely to be a range of relatively simple measures that could be useful for helping to guide activity levels (pace) and avoid getting too deep into PEM.

Whether lactate is one of those, in principle and practically, is another story.
 
Sean said:
Lactate might not be a useful measure for revealing pathology in ME, but there are likely to be a range of relatively simple measures that could be useful for helping to guide activity levels (pace) and avoid getting too deep into PEM.

Whether lactate is one of those, in principle and practically, is another story.
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Do we know if lactate is only correlated with or actually causes PEM?
 
RobH said:
Do we know if lactate is only correlated with or actually causes PEM?
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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 bought a peripheral blood lactate monitor some years ago and experimented. I couldn't find anything noteworthy going on, both with levels and patterns of response to brief aerobic exercise. That's not to rule out the possibility that lactate levels in tissue are doing something interesting. I can't remember if I tested when I was actually in PEM.

I reported my results on one of the forums.

I could probably dig out the monitor if a member in New Zealand wants to play with it. You would have to buy some consumables I think, as I expect the ones I had would be outdated.
 
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?
 
Jonathan Edwards said:
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?
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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]!
 
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