NYT Article Long Covid Sufferers Are Struggling With Exercise

I have read through it. I agree that the article is generally helpful. I also agree that the first main point comes across clearly and is rightly the focus.

The problem comes with the second. From my perspective, Systrom's work tells us nothing about PEM. PEM is feeling ill after exertion. A problem with getting oxygen to tissues does not explain that - it would explain not being able to do so much. CPET studies on people with ME don't really show that, certainly not at day 1.

So my grouse here is the implication that PEM is something to do with circulation and that researchers understand it. In my book it is unlikely to have much to do with circulation and nobody has a clue - when we are talking about PEM as feeling ill after exertion.

Everything is still framed in terms of getting g up and exercising as soon as the pills have worked or you feel you might like to try it. The message from past experience with post-viral fatigue states is that you forget about doing exercise. You take things gently and wait until you find you are WELL. Not just a bit better, but WELL. For most of us, and certainly in my case it is not hard to sense that you are well.

I also see a downside in that people may get worried that oxygen is not getting to their tissues. They may genuinely get frightened unnecessarily. They may go and seek help from someone who prescribes goodness knows what.

The other downside is that the BPS crowd and the general sceptics in the Royal Colleges et al will be rolling eyes at the quotes from Systrom - and not unreasonably if there aren't yet any firm data and the studies don't actually explain the symptom anyway. Most pulmonologists and cardiologists are also going to think - uh oh!

It would be so much better if people said that exertion intolerance can be a serious long term problem and that as yet we have no understanding of it and no means to treat it - other than doing what was recommended fifty years ago - takes things gently and for the first year or two, at least, there is a good chance it will resolve.

 

There are two elements here - what is going on in the tissues and the response of the brain. We know that muscle afferents feed back into the brain, by inhibiting the excitability of the motor cortex (central fatigue). The primary purpose of this central fatigue is not to cease activity, increasing the level of ventliatory drive for a given level of motor drive. (Central fatigue is thus necessarily coupled to peripheral factors - the sensations associated with central fatigue are to signal to the conscious part of the mind that this process is taking place)

We know from Larun et al (2 day CPET study) that lactate levels remain elevated in patients so something inefficient is going on metabolically.

This could suggest the alterations in circulation (shunting) as hypothesised by Systrom and colleagues.

Stimulation of other afferents could also lead to those other symptoms you allude to, as hypothesised by others (eg the Vagus nerve).

Does it matter? Pulmonologists and Cardiologists don't understand ME or fatigue at all.

I do however agree that we are still quite a long way away from effective pharmacological treatments.

 

Would Trimetazidine be a drug helpful for people with ME and Long COVID?

 

Yes, in the world of grant-assessing advisory boards.

There is also a high risk of loss of faith between patients and doctors if patient go to clinic primed with unreliable information.