Two-Day CPET in Females with a Severe Grade of ME/CFS: Comparison with Patients with Mild and Moderate Disease. van Campen et al. 2020

Full title:
Two-Day Cardiopulmonary Exercise Testing in Females with a Severe Grade of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Comparison with Patients with Mild and Moderate Disease

https://www.mdpi.com/2227-9032/8/3/192

 

Two-Day Cardiopulmonary testing of severe ME patients?

That's a huge sacrifice they've made for the sake of research.. Maybe too big..

 

"We reviewed the clinical records of 93 females with a diagnosis of ME/CFS who had undergone a 2‐day CPET protocol between June 2012 and November 2019."

 

I think this is the exercise protocol they cite, to me severe ME means mostly/totally bed bound so I don't know they could have done that let alone twice.

 

Mild, moderate and severe are arbitrary definitions and everyone has their own interpretation of them. Presumably in this context it means something like dividing patients they see in the clinic into 3 groups according to severity.

 

I don't understand the logic of requiring severe patients to do this, but...

Given this is another replication, how long can medical doctors and other scientists deny that this is the most consistent finding to date?



It is frustrating that they're not stating the actual max heart rates of participants, I suspect many patients did not achieve a true maximal result, hence the peak workload/VO2 results should be considered with caution.

edit - see also, this previous paper by the same group for males:
https://www.scirp.org/journal/paperinformation.aspx?paperid=98389
edit2 - not sure how this second paper of female patients (this year) relates to the current findings (overlap?)
http://journalcra.com/article/valid...nary-exercise-testing-female-patients-myalgic

 

I'm amazed that people who are 'mostly bedbound' even managed to get to the centre to do the testing, on day one..... never mind do all that again the next day ????

 

Looks more like a grade of very mild, mild and moderate since no way a severe patient could do a CPET. Still it confirms the spectrum nature of the disease and replicates yet again the objective impairments.

I think we are already long past the point that justifies legal procedures for anyone subjected to GET. The evidence of harm is far more consistent and reliable than the illusion of secondary benefits on trivial psychosocial aspects.

To continue promoting this treatment in official settings is simply dereliction of duty. Completely indefensible and yet several medical authorities in multiple countries are currently actively trying to expand and promote this further. Despite there being no evidence whatsoever of any tangible benefits. Despite consistent evidence of deterioration, further damaged by systemic denial of appropriate medical care to compensate for harm done.

The lawsuits will be huuuuge, they will have to hurt bad enough for this to never happen again. There never were any consequences in the past for when conversion disorder had captured a disease that medical research eventually figured out. Terrible failure. There has to be consequences for failure, even more so for harm. This is what happens when accountability is removed entirely, replaced by unethical claims and blatant fraud.

 

I've not been really in the loop in this CPET research so I'm a bit unclear what these results are telling us beyond that people who are more ill reach exhaustion earlier.

I found a similar trial that included a control group, looking at figure 2 it's not clear why the 2nd day is so important, what is that telling us that wasn't apparent from the first day?

 

The rationale is that some people with milder ME might be within the normal range on VO2 max or anaerobic threshold on day one, but then PEM kicks in and their results are lower at the second test, typically the next day. However people with other long-term conditions do just as well, on the second occasion.

The Workwellgroup in USA have done a fair bit of this: Van Ness and others.

 

The inability to reproduce the results of the previous day is unusual. In other people, the results are usually a little better on day 2, or at least don't worsen as much. Having a patient population with very consistent inability to reproduce their results suggests there is a common disease process where exercise interferes with ability to do further exercise. Somewhere along the body systems that are involved in exercise (heart, blood vessels, muscles, mitochondria) something is going wrong. We know the lungs are not the problem.

 

The ventilatory threshold is a physiological set point, the fact that it is reached earlier (in terms of power output) on the second day is objective proof of increased fatigue. Control subjects (sedentary controls and MS patients) are able to replicate their performance at the ventilatory threshold on the second day.

The VO2 peak/peak workload findings are not as interesting because it is hard to control for true exertion limits, though they do suggest that patients find it hard to maximally exert...

 

VO2 max is maximal oxygen consumption, and this is taken as a proxy for your body’s ability to produce energy in response to demand. VO2 max is reached, when even with increased work load the VO2 consumed has levelled out and won’t push up further, with the test subject giving maximum effort.

The significance of failure to replicate day 1 VO2 max on day 2, is that ME patients can’t do this while sedentary controls can.

Like you, I’m a bit confused about the diagrams in the study you cite apparently showing decreased day 2 VO2 max in control subjects, as this pattern is said to be unique to ME/CFS.

 

is 'ventilatory threshold' the same as 'anaerobic threshold'?

 

I found this graph that illustrates ventilatory threshold

 

The study is of course interesting but we desperately need studies comparing ME patients vs other diseases.

 

They're often considered to be the same thing, but I think this is a mistake.

To me, "Anaerobic threshold" is a misnomer since it doesn't specifically reflect what is going on in the muscle fibres. It is also important to note that arterial carbon dioxide pressures remain relatively constant past this point - it is not a point of hyperventilation.

Some are still predominantly relying on aerobic metabolism, some a mix etc. And this is also not the lactate threshold which depends on intracellular and extracelluar buffering and eventually the respiratory compensation point (hyperventilation) when the circulatory pH starts to rise, which is sometimes refereed to as a second ventilatory threshold - the "lactate threshold" always occurs after the first ventilatory threshold and at around the point of the second ventilatory threshold.

More importantly, both the "first" ventilatory threshold and anerobic thresholds are artefacts of ramped increases in exercise output - it is woolly to claim there is some kind of strict anerobic threshold (at a particular heart rate for example) during normal exertion.

Exercise physiologists have long debated the reasons for ventilation depth/frequency, but the strongest argument can be made for it being coupled to central drive. So an earlier ventilatory threshold suggests increased central output for a given power output at or past this threshold on the second day.

A failure to reach the same VO2Peak is easy, just don't work as hard.

The limiting factor for VO2Max is the amount of oxygen that the heart can pump to the muscles.

This can be limited by:
The lungs in people with Chronic obstructive pulmonary disease, and in highly trained athletes which have very high VO2Max can be limited by genetic lung capacity limits (typically VO2Max in excess of 70 mL/Min/Kg).
The blood volume that the heart is strong enough to physically pump.
Heart rate

But reaching a true VO2Max seems to be difficult because it requires the particpant to work increasingly hard during rapid fatigability. (a level of fatigability that I'd speculate that a healthy person does not experience) To compensate the participant must increase central drive at an increased rate.

 

Workwell's studies used sedentary controls and other illness controls and did not find any group like the those with ME.

It is a curious situation. CPET testing is done every day in hospitals round the world; they test patients with lung disease and heart disease in particular including the elderly and those with lots of comorbid conditions. And they all get medical treatment based on ONE test because the results are the same every time they are done. Someone with cystic fibrosis may have a very low score but any change in that score is seen as a deterioration of the disease not the result of too much exercise the day before.

The single, repeatable test result is so well known that the reaction to Workwell's results was that their machine must be broken. They had to include a slide showing that their machines were calibrated when they did talks.

So it is not like other tests where there has to be lots of studies done on other diseases to show that our results are unique. It is like having a peanut allergy. You do not need to do lots of studies looking at different people and diseases to know that allergic reactions are unusual because no allergic reaction is the common position.