Open Cardiovascular Analysis of PEM, 2021, Natelson

This trial is not yet open for recruitment (Start date May 2021)

https://clinicaltrials.gov/ct2/show/NCT04740736

 

Will participants be in-patients? I was a bit worried about the group who have the sham infusion and take part in the exercise, i.e. possible hyponatraemia.

 

They could also induce PEM via cerebral exertion. Does anyone know whether socializing or other cerebral exertions are as likely to cause crashes as 'maximal exercise tests' are?

I was going to suggest this to the researchers, but I couldn't find a way to contact them.

 

Would there be a point in including people who are hypovolemic AFTER exercise?

 

@Creekside some of the people who are qualified to do a 2 day CPET for PwME will do cognitive assessments before and after testing to add to reports. This assesses (of course) both cognitive and physical impact of exertion.
I don't think there's been enough work on cognitive exertion and PEM. (Personal opinion.)

 

Eligibility criteria lists meeting SEID criteria as opposed to (for instance) having more focused criteria for this study.

 

That doesn't help with understanding the impact of cognitive exertion.

Experiments with cognitive exertion could lead to less-harmful methods of triggering PEM for research projects. That's assuming that cognitive-induced PEM actually is less harmful, which we don't know for sure, because no one's done research into that ... yet.

 

Are there any trials on PEM w/ heart variability, hr, blood pressure etc... just the bare fundamentals? Or possible more specific metrics?

Edit: I've looked through a bunch of papers but almost all are tested during or immediately after the stress test and the test isn't really designed to trigger PEM (might in some, but not in others) but as a stress test of one type or another. Generally PEM isn't defined as coming on immediately.

 

I was aware that being hypovolemic was a known symptom for some sufferers of ME, but something I wasn't aware of is that hypovolemia could be caused by exercise, so I've learned something new today.

 

I may have misunderstood what I was reading.

I'm assuming that the subjects are going to be doing exercises on 2 consecutive days, rather than 2 "subsequent" days.

If they are measuring total blood volume before each exercise test then it suggests to me that they think that some people may become hypovolemic as a result of the exercise on day 1 even if they weren't hypovolemic before the first exercise test.

 

Recruitment is open:
https://www.healthrising.org/blog/2...cise-long-covid-chronic-fatigue-metabolomics/

Interlude: Opportunity Knocks! The Natelson – Mancini ME/CFS Exercise Study Is Open
A fascinating exercise study led by longtime ME/CFS researcher Ben Natelson and long-COVID researcher Donna Mancini recently got underway. An NIH-funded 2-day exercise study – called “A Cardiovascular Analysis of Post-exertional Malaise” – aims to dig deeper into the exercise problems found in ME/CFS than has been done before.



The question they’re trying to answer is a central one: why do people with ME/CFS tend to blow through their aerobic energy production systems so quickly during exercise – leaving them trying to squeeze little bits of energy out of their anaerobic energy production system?



They believe reduced blood volume – which leads to reduced blood being pumped by the heart (stroke volume) – may have something to do with it. The deep, rapid breathing occurring in people with ME/CFS during exercise results in even greater losses of blood volume – and causes further drops in energy production during the second day.



It’s an intriguing idea given that Visser-Van Campen-Rowe found reduced blood flows to the brain in virtually every person with ME/CFS tested.

They’re going to determine blood volume levels before each exercise test and assess cardiac output, and then they’re going to replenish blood volume in a group of patients and see if their ability to exercise improves. That too is intriguing given that oral rehydration saline was recently found to be pretty darn effective at relieving orthostatic intolerance.

This several million-dollar, 120-person study is going to have severe and non-severe ME/CFS patients, and healthy controls. It’s taking place at the Icahn School of Medicine at Mount Sinai University In New York City. They have funds to help participants with travel expenses and time spent (but not airfare). To find out more, call the Pain & Fatigue Study Center research staff at 212-844-6665.

 

Can anyone tell me how blood volume is measured?

 

not sure what they are using but this is one method that's available clinically in the US - the indicator tracer dilution technique. https://www.daxor.com/how-bva-100-works/

A dose of tracer is injected intravascularly. Once the tracer has fully circulated in the bloodstream, a series of small blood samples are drawn. The [machine] automatically calculates patient blood volume by comparing the concentration of undiluted tracer prior to injection to the tracer concentration diluted in the patient blood samples.

 

Minor point: In order to determine if the diluted tracer concentration indicates that the patient is hypovolemic, you also need to estimate what the patient's normal blood volume should be based on their body size.

 

Thought it worthwhile to provide the following information.

I contacted this study expressing my willingness to participate. After a relatively cursory screening process, a staffer called to inform me that I was rendered ineligible due to the presence of the following medications in my treatment regimen: mestinon, midodrine, hydrocortisone

I would imagine that anyone consuming the aforementioned medications would suffer a similar fate, but it could yield more robust data if others also tried to gain admittance.

 

Note the prior case study:
https://content.iospress.com/articles/work/wor203214

10-15 minutes of exercise isn't going to cause much difference in blood volume, that claim is just speculation by Cort.

The claim about "deep, rapid breathing occurring in people with ME/CFS during exercise" is nonsense too. Dane Cook's recent CPET study found deeper, SLOWER breathing in patients at the ventilatory threshold, but no overall difference in total volume per minute. "Deep and rapid breathing" is hyperventilation which was not found in Dane Cook's study.

In general, a reduction in blood volume could in principle cause a lowering in Peak VO2 between the two days, but I strongly doubt it will explain the findings at the ventilatory threshold.

My expectation is that I see this as an important study that will rule out a potential cause, rather than find a potential cause...

I personally would not accept someone taking such medications if I was running the study either. These studies have limited sample sizes and you don't want unusual medication profiles being potential confounders. Accepting such patients would be useful in much larger followup studies when researchers need to see if the findings are generalisable to all patients.