Insights from the Physiology of Post-Exertional Symptom Exacerbation by Dr. Todd Davenport

Sly Saint

Senior Member (Voting Rights)
About: Graded exercise is commonly prescribed after illness to improve symptoms and functional tolerance. Protracted and limited courses of recovery may be associated with post-exertional symptom exacerbation (PESE), which is common after many other forms of viral and bacterial infection including SARS-COV-2. PESE is a constellation of physical, cognitive, and constitutional symptoms that indicate a maladaptive recovery response from activity. Physiological characteristics of people with PESE differ from deconditioned people in clinically important ways, including differences in the volume of oxygen consumed, heart rate, and ventilation at peak exertion and ventilatory anaerobic threshold. These physiological differences make graded exercise harmful for people with PESE. This session will discuss the features of PESE compared to deconditioning, the physiology associated with PESE, and introduce the indications and basic principles of energy system first aid for people with PESE.

 
These physiological differences make graded exercise harmful for people with PESE.

This quote is SO important.

Is it in a published paper anywhere yet?

Many papers have stopped short of saying this. Here’s hoping they can back the statement with the type of evidence that means that caveats will be run alongside ALL advice to exercise.
 
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Good but no mention of LTSE which some members have claimed is accepted by researchers, I'm not seeing any evidence that researchers acknowledge it.
Then you will be delighted to know that DecodeME (sign up to the study at www.decodeme.org.uk) includes a question about course of illness in which an option is available to indicate progressive deterioration.
 
I watched this whole presentation. Nothing in it was totally new, but I liked it. It was a solid overview of PEM and useful for educating doctors and PTs. Dr. Davenport is insightful and empathetic. Repeatedly, he emphasized that PEM and deconditioning have both entirely different causes and effects. For example, exercise should not cause cognitive dysfunction.

He reviewed a graph of symptoms people experience at 6:31, emphasizing that the symptoms pwME experienced were vastly worse than the sedentary controls.

Around 14:51, he colors his explanation with quotes from pwME. "[Felt] like I was in a barrel and rolled down hill!" was the funniest.

At 16:30, he discusses LC symptoms and how PEM is very common.

Around 20:00, he uses a slide from Workwell to explain that he thinks the short-term PEM symptoms are more neurological, and the longer-term ones more physical.

At 23:27, he explains the criteria for evaluating maximum effort in the CPETs, emphasizing they use respiratory exchange ratio: "Probably the criteria we put the most stock in is this RER because you can't fake that. There's no faking it." Then describes how people with all sorts of other conditions can reproduce their performance, but pwME can't.

Around 27:40, he discusses the body's different energy sources, and how aerobic metabolism is impaired in ME. He goes into how the anaerobic threshold drops on the second day, and speculates acidosis could contribute to some ME symptoms. At 33:20, he says that exercise tests correctly classify 90% of controls and 95% of pwME. He sees the 2-day CPET as a biomarker:
And if we just looked at VO2 and workload at that breakpoint (that breakpoint between aerobic and anaerobic metabolism), we can correctly classify 95% of patients with CFS and 90% of matched sedentary control subjects. So here we talk about "no biomarkers," "we need a biomarker," acknowledging the significant challenges and issues associated with cardiopulmonary exercise testing, this seems like the closest biomarker we may have in order to characterize patients.
He summarizes all this at 33:58, and provides an analogy of a plug-in hybrid car.

Then he describes screening for PEM, and management. First, you pace. Once you're good at pacing, exercise may help, but he makes it amply clear that patients must stay within their energy envelope--"exercise to the exclusion of activities of daily living is not restorative." He later clarifies that what he calls "exercise" is very light.

At 43:44, he discusses "Moving beyond energy system first aid." Unfortunately, there's not much you can do, especially with direct treatments. He says POTS palpitations should be ignored for heart-rate based pacing, which seems fishy to me. (Maybe he means, only if they're brief?)

They conclude with Q&A at 44:47:
Could PEM be related to the cardiovascular risks of Covid? He seems to lean towards no.

A woman with fibromyalgia says the presentation may have given her some insights about her symptoms.

How does pacing allow you to tolerate exercise and how does it compare to reversing deconditioning? Deconditioned people don't need to pace. In ME or LC, the body's response is entirely different. Unfortunately, we don't know why. Mentions a pwME whose exercise test results improved after resting more (!) Maybe ME is vaguely similar to overtraining.

Could PEM in LC be related to viruses hijacking mitochondria? Maybe if viral persistance is true. Mentions upcoming metabolomics studies of ME/CFS.

Are you investigating NF-kB pathway in LC? It might be involved.

Do you do heart rate with monitors with exercise therapy? Yes. "Exercise doesn't look much like exercise. It looks very light. We're doing stretching and breathing...and that's enough exercise for people" The vast majority of his time is spent on pacing and energy conservation.

Someone is wondering why exercise helps her back pain. He says it's better for a group discussion.
 
Thank you @RedFox.

It is good to see that this presentation was delivered at a conference on pain since exercise is the go-to treatment for chronic pain (despite the evidence base being as flawed and as unconvincing as that for ME/CFS) and so few physiotherapists are aware of PEM.
 
My favorite quote from the video:
Todd Davenport said:
And the reason we do this [2-day CPETs] is because that first test kind of gets everyone more towards the same level. We're kicking them into their post-exertional state, so I'm always very respectful of this. That the data that I present is going to be based on people who chose to become symptomatic to understand this better. I'm just so deeply grateful for that. They knew they were gonna feel bad. They did feel bad, and we're just doing our best to learn from it.
He understands that people were willing to suffer for the important research he's doing. His empathy actually brought a tear to me eye.

I watch these videos to learn, but also to feel safe. Hearing biomedical doctors talk about ME makes me feel validated, that someone recognizes my suffering, and that they want to make me better.

Edit:formatting
 
He says POTS palpitations should be ignored for heart-rate based pacing, which seems fishy to me. (Maybe he means, only if they're brief?)

I have read articles about this on the Workwell website which might explain this better. There are various ways to work out a rough approximation of your anaerobic threshold if you are using a heart rate monitor. The goal is to keep your HR under your threshold rate especially for prolonged periods.

This is complicated for people who also have POTS because your HR will go up because of that even if you are not going over your anaerobic threshold. I think it means that there is not the same risk of getting PEM the next day.
 
I have read articles about this on the Workwell website which might explain this better. There are various ways to work out a rough approximation of your anaerobic threshold if you are using a heart rate monitor. The goal is to keep your HR under your threshold rate especially for prolonged periods.

This is complicated for people who also have POTS because your HR will go up because of that even if you are not going over your anaerobic threshold. I think it means that there is not the same risk of getting PEM the next day.

It's an interesting point, because is it not the same risk of getting PEM the next day - have they tested this way for POTS vs norms over longer term?
 
The increase in heart rate when you have done too much is because your heart is trying to overcome the fact you have used up your aerobic respiration output and are now relying on emergency anaerobic respiration for more ATP. In a healthy person this will be because of running for a bus or doling aerobic exercise.

For people with ME it means we have to exert less and be careful the next day because the same thing will happen with even less exertion.

In POTS your heart rate goes up to get more blood to the brain when you stand. The extra exertion in the heart and compensating for any consequences may add to your total energy needs for the say but it is a completely different system.

If you do less because of a high heart rate and it is actually POTS it won't do any harm to rest more than you need to because we usually do too much.
 
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