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Given how important exercise is to our long term health, it’s no surprise that several exercise programs have been created. Simon Perikles’s is the latest one.
One of the more disturbing things from a long-term health perspective for people with diseases like chronic fatigue syndrome (ME/CFS) and long COVID is the difficulty and, oftentimes, inability to exercise. Given that, it’s not surprising many efforts have tried to find a way to do that.
THE GIST
- One of the more disturbing things from a long-term health perspective for people with diseases like chronic fatigue syndrome (ME/CFS) and long COVID is the difficulty and, oftentimes, inability to exercise.
- Given that, it’s not surprising several groups have tried to find a way to do that and we’ve come a long way from the blunt and unsophisticated graded exercise programs of the past. From Workwell’s precision oriented, heart rate-based approach to Putrino’s autonomic nervous system rehabilitation, we can now add an anaerobic exercise approach from Perikles Simon, a German exercise physiologist.
- Simon came across his long-COVID patients when his lab was contacted by an insurance company that wanted to assess their ability to exercise and functional capacity. While Simon didn’t say so, the nature of their job and their early exposure to the full force of the coronavirus probably left them worse off than later ones. None of them were able to work.
To say that he was impressed and shocked by his findings is probably to understate things. Simon reported that his group of long-COVID patients were “truly and severely physically affected” even 12 months later – despite being in “perfect organ health”. - Speaking about the “massive changes in the breathing physiology” he found in long COVID, he said, “we have never seen values like this before” and that their values of CO2 can get so low that you can’t produce them by purposefully hyperventilating – you would faint first.
- Simon believes that the oxygenated arterial blood is not flowing correctly through the capillaries that provide blood to the muscles. This is-a situation that one typically begins to see in older people – and asserted that the people in his study had suddenly gone from middle-aged to 80. Once the breathing centers in the brain pick up the oxygen deficit, they cause the body to breathe more releasing too much CO2 and potentially causing many of the symptoms of ME/CFS.
- The key theme of his anaerobic exercise plan is to exercise in very small chunks, and rest. When we exercise, our anaerobic exercise system kicks in first, and then after about 30 seconds, hands most of our energy production off to the aerobic energy system. It’s the anaerobic energy production that Perikles wants to focus on.
- Simon suggests exercising for up to 30 seconds at a time – about the time the anaerobic energy system can supply energy without producing lactate. The idea is to exercise your muscles in ways that keep them from being oxygen-deprived, causing you to overbreathe and lose CO2. (He recommends the same for mental exertion. He believes too much stimuli, lights, sounds, mental activity can produce the same results.)
- He often starts at 10-second intervals of standing – 10 seconds of sitting – and then adds 1 second a day. If you can get to 30 seconds without feeling breathless or that you are hyperventilating (taking deep rapid breaths), then you can try prodding your aerobic energy system a bit with 1 minute exercise then I minute rest, then 2 minutes – 2 minutes rest, then 4…
- One key is to exercise different muscle groups. For instance, if you take dishes out of the washing machine – always use different muscles to do that – bend down (or pull up a chair) and take the dishes out for say, 30 seconds, then rest.
- There are no hard and fast rules – just make sure that you get 30 seconds to a minute of rest in between sessions. (There’s no need to rest for more than a minute.) He noted that checking for increases in one’s pulse doesn’t always work because the pulse doesn’t rise for everyone.
- Because overexertion can cause all sorts of symptoms, it’s helpful to keep a written journal of your symptoms so that you can tell when you go over. Most patients on the 30-second program notice a boost in cognitive functioning within 2 weeks. Noticeable physical improvement often takes months.
- Simon acknowledged that his exercise program will only get many ME/CFS / long-COVID patients so far – but asserts it can help. He reported that at the beginning of the program, the nurse that had the capacity to work 0.5 hours a week had the capacity to work 5 hours a week at the end of it. That was not enough to resume her work but still a major improvement.
- The Workwell Foundation uses exercise testing to determine the heart rates at which things go south (i.e. toxins start building up) during exercise. In this way, they can provide a more precision, tailored exercise program.
- A case report found that a year of heart rate monitor use, deep breathing, flexibility and short-term endurance exercises, and consistent rest breaks one patient reported substantial improvements in general functioning and, importantly, some of her physiological measures notched upwards. She was not well but her long slide into disability had stopped and she had improved significantly.
- David Putrino’s autonomic rehabilitation program emphasizes breathing, and a very slow ramp up of exercise using anaerobic exercise at first and, if the patient is able to tolerate them, eventually aerobic exercise activity. (See a Health Rising blog for more.)
- While none of these programs promise a cure, it’s clear that they can improve fitness in some.
- While we don’t know exactly what is causing these problems, it’s notable that problems with oxygen extraction and low CO2 levels have shown up repeatedly in the last five or so years in ME/CFS and now long COVID patients. They don’t affect everybody but do appear to affect a majority of patients and could play key roles in these diseases.
The Simon Approach
(The material from the Simon section of the blog comes from Dr. Simon’s Vimeo presentation at 46:32 and the r/cfs superb overview on reddit)
Dr. Perikles Simon – About a year ago, Perikles Simon PhD, a well-published neurobiologist and exercise physiologist, and the head of the Division of Sports Medicine, Rehabilitation and Disease Prevention at the Johannes Gutenberg-University in Mainz, Germany, gave a talk at a long COVID at a conference put on by Mess Dusseldorf.
Most of Simon’s recent work has centered around professional athletes and he’s recently been exploring which blood-borne biomarkers could best explain an athlete’s training status. He came across his long-COVID patients when his lab was contacted by an insurance company that wanted to assess their ability to exercise and functional capacity. While Simon didn’t say so, the nature of their job and their early exposure to the full force of the coronavirus probably left them worse off than later ones. None of the patients in the cohort were able to work.
Strange Days
Dr. Simon is taking a different approach to long COVID than I’ve seen before. He’s focused on the levels of cell-free DNA (cfDNA) that gets released from cells when they are damaged (and from immune cells). Cell-free DNA levels explode in people with acute COVID (COVID-19). He believes they’re producing microclots that clog up the capillaries all over the body.
His research suggests that levels of cell-free DNA, while variable, correlate well with both COVID-19 severity, and with fatigue in healthy controls. His most recent study suggests that cell-free DNA (cfDNA) probably reflects the “primary muscle damage” that occurs during exercise rather than the secondary muscle damage that inflammation causes. Instead of inflammation, it appears to reflect a loss of muscle function. (Exercise always produce some damage – which our bodies are usually well-equipped to deal with.)
Exercise also increases the production of this factor dramatically but not nearly to the extent found in a COVID-19 infection. In healthy people, levels of cell-free DNA (cfDNA) rise 10-20 fold after exercise but typically fall within 90 minutes and then, interestingly, often drop below baseline. Exercise, as Dr. Perikles noted, is quite a stressor for the body, but in most people, it makes them stronger over time.
We are used to seeing chronic fatigue syndrome (ME/CFS) and long-COVID studies present bizarre and unexpected findings, and so it goes here: where we might have expected cfDNA levels to explode after exercise in long COVID, smaller increases than normal were seen (!). Perikles didn’t explain that, but it perhaps it fits in with findings indicating that instead of producing a normal response to it, the bodies of people with ME/CFS just don’t respond much to it. Perikles did not explain what he thought was going on.
“We have never seen values like this before”
Simon next moved on to Inderjit Singh’s and David Systrom’s work at Yale and Harvard which showed that long-COVID patients had “decreased exercise capacity combined with exaggerated hyperventilatory response” during exercise. (Throughout the talk, Simon will note that similar findings show up in ME/CFS.)
Perikles said he had never seen readings like he saw with his long-COVID patients. (From John Pierce CCO via Wikimedia Commons)
To say that he was impressed and shocked by his findings is probably to understate things. Simon reported that his group of long-COVID patients were “truly and severely physically affected” even 12 months later – despite being in “perfect organ health”.
Speaking about the “massive changes in the breathing physiology” he found in long COVID, he said, “we have never seen values like this before” and that their values of CO2 can get so low that you can’t produce them by purposefully hyperventilating – you would faint first.
Simon explained that the oxygenated arterial blood did not appear to be flowing correctly through the capillaries – a situation that one typically begins to see in older people – and asserted that the people in his study had suddenly gone from middle-aged to 80. He talked about a former nurse whose exercise study indicated she has the capacity to work about 20 hours a week in a sitting position and 0.5 hours a week as a nurse.
Once the breathing centers in the brain pick up the oxygen deficit, they cause the body to breathe more. Simon is attempting to develop better technology to measure this situation but is confident this is a major contributor to long COVID and ME/CFS.
Simon’s Anaerobic Energy Program
Simon – who has helped develop exercise programs for several other diseases – has developed one for long COVID and ME/CFS. His statement that, “Many are not aware of the situation they are in”, was so reminiscent of what Staci Stevens at the Workwell Foundation has been saying for years.
The goal is to restore the ability of the circulatory system to get blood to the tissues. The key theme of his anaerobic exercise plan is to exercise in very small chunks, and rest. When we exercise, our anaerobic exercise system kicks in first, and then after about 30 seconds, hands most of our energy production off to the aerobic energy system. It’s the anaerobic energy production that Simon wants to focus on.
Simon suggests exercising for up to 30 seconds at a time – about the time the anaerobic energy system can supply energy without producing lactate. The idea is to exercise your muscles in ways that keep them from being oxygen-deprived, causing you to overbreathe and lose CO2. (He recommends the same for mental exertion. He believes too much stimuli, lights, sounds, mental activity can produce the same results.)
Perikles suggests exerting different muscle groups.
He often starts at 10-second intervals of standing – 10 seconds of sitting – and then adds 1 second a day. If you can get to 30 seconds without feeling breathless or that you are hyperventilating (taking deep rapid breaths), then you can try prodding your aerobic energy system a bit with 1 minute exercise then I minute rest, then 2 minutes – 2 minutes rest, then 4…
People who have trouble standing should try to stand for 30 seconds (or until you feel unwell and/or start hyperventilating (breathing deeper and faster), and then rest and repeat.
One key is to exercise different muscle groups. For instance, if you take dishes out of the washing machine – always use different muscles to do that – bend down (or pull up a chair) and take the dishes out for say, 30 seconds, then rest. Stairs are particularly difficult. He recommends taking 3 steps and resting.
There are no hard and fast rules – just make sure that you get 30 seconds to a minute of rest in between sessions. (There’s no need to rest for more than a minute.) He noted that checking for increases in one’s pulse doesn’t always work because the pulse doesn’t rise for everyone.
Because overexertion can cause all sorts of symptoms, it’s helpful to keep a written journal of your symptoms so that you can tell when you go over. Most patients on the 30-second program notice a boost in cognitive functioning within 2 weeks. Noticeable physical improvement often takes months.
Simon acknowledged that his exercise program will only get many ME/CFS / long-COVID patients so far – but asserts it can help.
He reported that at the beginning of the program, the nurse that had the capacity to work 0.5 hours a week had the capacity to work 5 hours a week at the end of it. That was not enough to resume her work but still a major improvement. Her lactate accumulation and heartbeat also went down over time.
He did mention a professional athlete, though, with severe enough long COVID that he was experiencing rapid heartbeats even when lying down. Very disciplined, he started with lying in bed and raising 1 arm. When he could handle that, he did 2 arms, and so on. He was back to perfect health in 6 months.
Apheresis?
If beta-adrenergic or ACE-2 autoantibodies are the culprit, it’s been thought that apheresis that targets them and filters them out could help. Citing a partner at a hospital though, who said that five treatments were needed to produce what appeared to be pretty modest results, he said the thought the autoantibodies were probably buried too deeply in the tissues for the aptamer to reach most of them. Perhaps repeated infusions could get rid of them, but he didn’t sound excited about that treatment.
He didn’t seem that excited about the autoimmunity approach – stating that if autoimmunity was the primary cause, he would have expected to see more young people get the disease.
Other ME/CFS and Long COVID “Exercise” Programs
Other “exercise” programs have shown up in ME/CFS and long COVID over time.
Workwell’s Approach
The exercise physiologists and physical therapists at the Workwell Foundation – one of whom has ME/CFS – have been working on rehabilitation programs for ME/CFS for a long time. Workwell’s approach is unique in that its ability to physiologically improve things in ME/CFS was documented in a case report. Workwell uses exercise testing to determine the heart rates at which things go south (i.e. toxins start building up) during exercise. In this way, they can provide a more precision, tailored exercise program.
In this case, the 28 year-old was getting steadily worse and was having trouble doing her household chores. Every time her heart rate hit a preset number, she was to lie down. She was also provided with flexibility, resistance, and short-term endurance exercises. Because the muscles moving the lungs use up a lot of energy and can quickly become exhausted in ME/CFS, diaphragmatic breathing was encouraged and gentle upper body stretches were included to reduce pain levels. The resistance exercises were done while lying down. Yoga, meditation, and other disciplines that focus on breathing, as well, to slowly drop the heart rate, reduce stress, and reduce pain were recommended.
After a year of heart rate monitor use, deep breathing, flexibility and short-term endurance exercises, the patient reported substantial improvements in general functioning and, importantly, some of her physiological measures notched upwards.
Parts of her body began to respond more normally to exercise. During an exercise test, her respiratory rate (the number of breaths she took), the amount of oxygen she inhaled, her heart rate, and her blood pressure went up dramatically.
Her aerobic energy production system was still broken – but her ability to use her anaerobic energy production system to produce energy increased significantly. She was able to be active at a significantly higher level (about 20 heartbeats higher) without triggering a negative response. Even though she was still limited aerobically, it was as if her cardiovascular system had emerged from a state of partial hibernation.
The Workwell Foundation provides disability testing for ME/CFS and long COVID and provides many resources on exercise and rehabilitation.
Putrino’s Autonomic Nervous System Rehabilitation Program for Long COVID and ME/CFS
Putrino’s program is the only one put to the test in a study. Like Workwell, Putrino puts an emphasis on breathwork but to a greater extent – using the Stasis program to first get the breath under control. Similar to Perikles, Putrino limits exercise (done in the supine position) to 30 seconds with rest periods in between.
After 4-6 weeks – if the patient is able to – isometric exercises begin. If the patient is able to tolerate those, then aerobic exercises and walking begin at low levels. The goal is to be able to complete a 6-minute walk test (6MWT) without increased symptoms. If that goes well, then a 3-month-long progressive aerobic exercise program on a bicycle is next.
Both Putrino’s and Workwell’s programs employ deep breathing techniques.
Forty percent of the people in the study were able to complete the full program. Overall, the participants went from feeling “very fatigued” to “moderately fatigued”.
Conclusion
None of these programs state they can cure ME/CFS, and all recognize that (with some exceptions) a substantial block to producing energy remains. Instead, they try to work within the limitations imposed by these diseases in hopes of increasing one’s tolerance of exertion. All three programs call for short exercise periods followed by rest. Perikles adds the interesting idea of being aware of exercising different muscle groups. Workwell and Putrino both include breathing exercises. Workwell – using the results from exercise tests – takes a more personalized approach. While these programs do not promise a cure, it’s clear that they can improve fitness in some.
Getting Closer? The Breathing / Oxygen Extraction Problem in ME/CFS and Long COVID
But what is causing these exercise problems? Two themes have cropped up recently: problems with extracting oxygen from the blood and getting it into the muscles; and breathing patterns that reduce CO2 levels.
Simon is only the latest researcher to glom onto the problem that low CO2 level and problems getting oxygen into the tissues may be playing a major role in these diseases. Note in the review below that no one finding can explain what’s going on in every ME/CFS and long-COVID patient – a mixture of problems exist. That said, low CO2 levels and problems with oxygen extraction are showing up again and again in a significant proportion of people with these diseases.
The first person to study low CO2 levels in ME/CFS, Benjamin Natelson was way ahead of the crowd when, in 2006, he found evidence of hypocapnia in 21% of people with ME/CFS. It took the field years to catch up, but eventually it did. In a 2022 follow-up study, Natelson found that 60% of people with ME/CFS exhibited hypocapnia and hyperpnea – deeper than normal breathing upon standing – and called the condition POSH (postural orthostatic syndrome of hypocapnia).
- Check out two simple at-home tests to see if you are hyperventilating or if you have “POSH”: postural orthostatic hypocapnia syndrome; i.e. low CO2 levels upon standing.
Systrom’s invasive exercise studies found that 45% of patients had low oxygen extraction that was probably produced by hyperventilation and/or mitochondrial issues. Another large group demonstrated hyperventilation without problems with oxygen extraction. Fifteen percent of the group were simply mysteries.
In a large study Vermeulen reported that low oxygen uptake by muscle cells caused exercise intolerance in a majority of ME/CFS patients. In a very large study, Van Campen et Al. found evidence of hypocapnia during a tilt table test in 80% of ME/CFS patients but concluded that it did not play a role in the reduced blood flows to the brain that the group has repeatedly found. (They believed the poor oxygen extraction did.)
The largest exercise study done to date (n=413) – the Cook/CDC study, which did the deepest dive into breathing yet in ME/CFS – found that people with ME/CFS were breathing more deeply and slowly during exercise, presumably in an attempt to get more oxygen into the muscles. Cook did not find increased lactate levels. Cook believed that oxygen extraction problems were probably key, though, and said he’d wished he could have done every mitochondrial test possible.
Natelson recently showed up again (with Mancini) in a long-COVID study of people with shortness of breath. Almost 90% exhibited, in one form or another, strange breathing patterns (dysfunctional breathing) that got worse as the exercise session went on. Mancini and Natelson commonly found hypocapnia (low CO2 levels), and/or an excessive ventilatory response to exercise (elevated VE/VCO2 slope). In both cases, they were moving more air than was necessary.
Wust’s recent muscle biopsy long-COVID study also found evidence of oxygen extraction issues and hypocapnia. Those features were paired with multiple findings indicating that the people with long COVID were depending more on anaerobic energy production. A recent fibromyalgia study found evidence of hypocapnia in about a third of FM patients.
Problems with oxygen extraction (i.e. problems getting oxygen from the blood into the tissues) has become a key theme. Why that’s happening is unclear but could include microclots that block the flow of blood, small fiber neuropathies that shunt blood away from the capillaries, mitochondrial problems that prevent the oxygen uptake from the blood, damage to the microcirculation, and probably others.
The promising thing is that these problems are showing up consistently. What we above all want in these fields are consistent findings that researcher then dig more deeply into thus getting us closer to answers.
This was all extremely interesting. I shall try the exercises suggested and take notes. After months of not understand at all what is really wrong with my body and having doctors that “don’t know anything about Long Covid” , I shall also make them aware of all these findings. These are very hopeful discoveries and shed new light (for me at any rate) on the problems with Long Covid).
Dear Cort, and all dear followers:
I think that Cort did a STUPENDOUS job in analysing this subject through the studies upon which he focused.
It may be that that previously I did not absorb key points as well as today because Cort was not yet including an audio transcription of the text!
My emphasis here is on the fact that because Cort interpreted the information, with vocal stresses on what he found novel, I was MORE engaged than normal. I absorbed MORE facts than usual from the points that Cort was stressing, and with his guidance through vocal intonation I could much more easily sense his logical direction.
This was game-changing for me.
HERE IS MY MOST CRITICAL COMMENT: (not of Cort’s analysis, which was excellent,
but of the German study)
1. For some unknown reason,
let’s call it the ME/CFS RAISON D’ETRE,
the CFS/ME reader’s body begins, usually, with AEROBIC metabolism in the cell.
BUT !!! :
SOMETHING HALTS IT. The studies say that the muscle cells reverts PREMATURELY to anaerobic energy production. This means: prematurely — compared with muscles in unaffected subjects.
2. The Perikles (mysterious ancient Greek overtones here….) experiment,
INSTEAD OF attempting to solve a LACK of AEROBIC respiration in muscle cells,
says:
OK !: the muscle cells are not into Aerobic.
what are they INTO? ANAEROBIC metabolism/respiration.
**KEY POINT: **
Normal exercise seeks first the AEROBIC glycolysis of Glycogen stored in the muscle cell.
BUT: !! in a body in which there is inflammation in the brain, and encephalomyelopathy…
there is possibly also a brain-central problem with Myelin. The degradation of Myelin on the EFFERENT nerves that send motor instruction to the muscle cells , in CFS, but MORE IMPORTANTLY IN FIBROMYALGIA…. , needs to be repaired.
)))
Ok.
Then Perikles accepts the unwillingness of the muscle cell to generate ATP aerobically.
Perikles then decides to work WITHIN the new paradigm, since the cell has its mind made up already.
Perikles leverages the anaerobic generation of ATP, while respecting a known limit.
As Perikles progresses with the patient, Perikles MAXIMIZES the use of Anerobic ATP creation in the cell.
This could be the brick wall….
or…
this could be the stimulus to re-awaken the mitochondria
Lastly:
If the Hypothalamus (HT) is forbidding the muscles to use AEROBIC GLYCOLOSYS to generate the MAXIMUM possible ATP load for exertion,
there may be a reason why: The brain is inflamed and is too hot already, too close to its maximum
HOWEVER: the DYSAUTONOMIA leading to this state may be keeping the Hypothalamus/Pituitary/Adrenal gland axis
(HPA axis) at LOW FUNCTION because it has become UNAWARE of improvements.
OR
The HPA axis will only improve FULLY when the requirements for each of the linked 3 systems are met.
It is is very clear to me that: if there is not a viral onslaught in the body, then the HT does not need to either set its temp point for fever or for Hypothermia.
However, as in Sepsis, if the HT DID need to reset its set point for Hypothermia,
then the solution lies in reducing and resolving those conditions which keep it on alert.
————
In this manner I am saying that I think that Cort got the GIST:
That the brain is saying NO ! to exertion since that will generate heat.
Since the cells are STUCK in phase 3 of the Cell Defense Response,
INTERVENTION IS REQUIRED to loosen the cells’ CDR.
Maximizing Anaerobic ATP generation may be the first step,
and I can only guess that when the cell realizes more is expected of it,
with Anaerobic hitting the ceiling… that the cell may resume AEROBIC.
But there are various related deficiencies that need to be FIRED UP ! AGAIN.
But they can’t be kick-started. They need to be nurtured back to health
I totally forgot a key point regarding dopamine:
Yes, dopamine runs our reward system for productive and protective behaviour.
But it is also the chemical that allows CONTINUED EXERTION.
Case in point: a distance runner. The legs begin to stiffen, but the person wants this somewhat unpleasant stress of being winded and tiring. Wanting/procurement triggers dopamine release in the brain. The brain sends the signal for dopamine release in the skeletal muscles. This relaxes the muscles compared with if they had NOT received this dopamine.
In one of the CFS stress tests it was found that while the brain said no, the muscles said yes.
That is, the brain tells the body, by withdrawing the dopamine supply early to stop exerting before one would actually have to fall over. This allows the person to get to safety or appropriate resting place. The test showed that the muscles were still capable of further exercise, but the cognitive brain did not feel capable.
Dr. Klimas has/had an exercise protocol that was 2 min. on, 2 min. off (resting), and never got your heart rate above the anaerobic limit. I used that successfully after stents for several years, with a timer and a heart rate monitor and a rowing type of exercise machine in my basement – working up from two cycles to about 5.
Then we moved to a retirement community, and I haven’t reinstated it yet.
Good to hear. I did my CPET with her :).
I’ve never met her, or seen her (I don’t do videos – can’t parse), but somehow cobbled that bit together from things people said she recommended.
I really need to get back to that. But the energy hasn’t been there. Moving, and the pandemic, and just existing through the days – plus my writing Pride’s Children – take everything I have.
Did you have a set routine that you did/followed? Or did you work with a physical therapist?
Just aimed for doing up to 5 cycles of this three times a week – in my pjs. No PT, no doctor – but I worked up to it, kept it up for several years after the stents, and need to get back to it.
It helped that the machine was in my basement. I had several dollar-store kitchen timers and a chest-strap heart monitor.
Easy – never had the benefit of it measured in any way. I did my own because going to the local hospital for their cardiac rehab program was an incredible time waster – I gave up their after two sessions when I realized that I had to sit in their waiting room for a half hour ever MONTH to redo the paperwork, drive there and back, and it was designed for healthy people, not our kind. I could do the whole thing in my basement in about a half-hour total; going to the hospital took two hours the first time and wiped me out completely for days after.
How did you know what the anaerobic limit was? thanks
I believe I used something like this – but can’t find my notebook, so I’m NOT SURE. Ask your doctor.
—
Anaerobic Heart Rate Example
First, determine your max heart rate. Subtract your age from 220 to determine your max heart rate.
Next, determine your anaerobic level. Calculate your anaerobic heart rate by multiplying your max heart rate by 80-90%.
—
There’s a calculator here: https://calculator.academy/anaerobic-heart-rate-calculator/
At 65, it calculates mine as having been 131 (which agrees with my memory)
I’m now 74, so it comes up with 124.
By subtracting my age from 220, my maximum heart rate would be 146 now. I used the multiplier of 85%, which gives 124.
Thanks for making me go back and calculate it.
I will use 124 as my target heart rate when exercising for each 2 min. period, never go above that, and then rest completely for 2 min. in between exercise periods.
But I have no idea when I’ll have the energy to start this whole thing up again – even a short period alternating 2 min. on, 2 min. off several times, three times a week, is a big commitment. When I do, I will do only 1-2 exercise periods (with rest) for a week or two, to make sure it isn’t too much, and then add an exercise period and a rest period every week or so until I’m doing 5 pairs.
Sorry this is muddled – late in the day.
USE ME/CFS MULTIPLIER of 55%
[Ignore the 85% multiplier in previous response – that’s for healthy people.]
Here’s what I found when I googled ‘Dr. Klimas exercise protocol for ME/CFS using anaerobic limit’:
What is the anaerobic threshold for CFS?
Heart Rate Thresholds to Limit Activity in Myalgic …
For ME/CFS patient-pacing purposes the heart at the anaerobic threshold is set at 55% of the peak heart rate. A popular formula to determine the heart rate at the anaerobic threshold is the calculation: 220-age * 55%.
https://www.scirp.org/journal/paperinformation?paperid=100333#:~:text=For%20ME%2FCFS%20patient%2Dpacing,220%2Dage%20*%2055%25.
Which makes mine 80 now.
Good news: I always exercise this way and for me it definitely works! Just a note: Many of us avoid gluten due to allergy. I experienced muscle aches due to lack of glycogen – which athletes usually get from pasta and other wheat derived food. So, I was advised to eat potatoes daily in order to supply enough glycogen. It works great! (I could not get enough glycogen from eating fermented brown rice)
Thanks for the comment! I can’t eat too much carbohydrates like pasta (for me it’s always sauce with a side of pasta, not pasta with a side of sauce :-). I’ll give potatoes a try! How much of them do you it in a day?
Hi JR, Just one large potatoe per day is enough for me.
One single potatoes chip sends me into a very bad state for a week or more…ONE SINGLE POTATOE CHIP!!!
same with booze
Great, that sounds manageable! Is there anything else to know about potato medicine :-), like do you have to eat it for breakfast already?
Hi JR, I like to cook a few potatoes at a time and then eat it over a few days. I slice the potatoes up, before cooking it in the microwave – so I eat slices all through the day. I store it in the refrigerator after it cooled down and eat it cold. The AI says: “Eating cold potatoes can lower the glycaemic index (GI) compared to eating them warm. The GI measures how quickly a food raises blood sugar levels. Cold potatoes have a lower GI, which can be beneficial for individuals managing blood sugar levels, such as those with type 2 diabetes. Cold potatoes release sugars more slowly, which can help regulate blood sugar levels. This is particularly beneficial for individuals with blood sugar management issues. Cold cooked potatoes contain resistant starch, which is a type of fiber that is resistant to digestion in the small intestine. Instead, it is fermented by beneficial gut bacteria in the large intestine, producing beneficial compounds like short-chain fatty acids (SCFAs). These SCFAs have anti-inflammatory properties and support colon cell health”
You really do have potato science down!! Though I actually don’t like cold potatoes too much for the very reason that the starch changes, I will definitely try now! Thanks a lot!
I can’t imagine just eating plain cold potato slices. Now a German style potato salad with a bit of vinegar, a few spices, some sliced scallions, chopped celery… you get the idea…;-)
Now I’m hungry 🙂 due to not tolerating raw scallions and raw celery, I might just end up with the potato slices, hehe :-)!
Yum!
Cool ! Intelligent choice
I will read it better further on, but I wonder about “lifting one arm …” Do these people otherwise lie completly bedbound doing nothing or is the excercize added to normal ADL?
I’m quite sedentary, but as it is I have to cook, clean (minimum) dress myself. Are these programs added to that, or is it someone that’s not doing these everyday chores (albeit on minimum level)
I don’t know about the person mentioned in the article, but yes, there are people who cannot lift an arm without setting off severe symptoms, to the point they are bedbound and have to lie completely still in order not to cause themselves pain, or PEM, or tachycardia, or nausea etc. etc. (depending on which condition they are suffring from).
Yes, I know. I have phrased the question wrong. I wondered at what level excercize they started, quess it was “at their own level”.
They probably start at the level their on at the moment … Maybe it was a stupid question.
No, not a stupid question at all I think.
I thought that these people must have carers so they can limit their daily exercise to seconds.
I’ve been severe for a couple of months but without carers, so any minimum of daily chores like getting food or washing dishes means exercise beyond limits.
Maybe I should break up chores into 30 second chunks ;).
I can confirm that switching between sides helps – e.g. switch from scrubbing dish with right arm to left arm. I even think I got this idea from an early article about Perikles Simon’s findings and could not remember his name – so, thanks for the blog!
Here https://www.fasynation.de/das-hochwirksame-30-sekunden-training-bei-long-covid-und-me-cfs/ for example I just found an article on how to apply his approach to daily tasks (use google translate).
The way I understood Prof. Simon in his videos, it is really ONLY doing that little.
E.g. sitting down every 30 sec. Or stopping after every 30 sec on a walk.
For someone who needs to lie down or avoid sensory input in order to count the pause as rest, this might be difficult to put into practice, especially without carers doing chores etc.
It’s a bit of a mystery to me how people make this program work.
But it can serve as a reminder to take things really slow and pace well.
Thanks for another well-researched article, Cort.
I’m from Germany and had heard about this approach before. Just want to point out that the professor’s name is Perikles Simon (Simon being the last name and Perikles the first).
Ha! Thanks – fixed. I wonder where Perikles comes from. As Christopher said – strong Greek overtones 🙂
https://www.wikiwand.com/en/Pericles
High V me (oops, that’s Roman) 😉
Thank you for pointing out again that muscular exercise is a physiologic assault to the muscle tissue. This assault is normally buffered and “healed” through the physiologic stress response. Obviously, this does not happen in ME/CFS where the body´s stress response is basically out of service – leaving the body´s tissues unprotected after exertion (of any kind). As to the muscle damage, a recent finding from Maureen Hanson´s team could be of interest: they showed that, in healthy people, exercise causes a rise in several proteins which are thought to protect muscles against damage from exercise as they can induce repair processes in muscle cells (like actin cytoskeletal proteins). This surge – obviously typical for the recovery phase of the stress reponse in healthy people – seems to be lacking in ME/CFS patients. ((https://pubmed.ncbi.nlm.nih.gov/38173127/ )) Just nice to see findings converging in ME/CFS research.
Yes, indeed! More on that here
https://www.healthrising.org/blog/2024/06/08/chronic-fatigue-syndrome-extracellular-vesicle-exercise/
Another comment: the very low CO2-levels observed again and again in ME/CFS. It would be great to know what happens clinically if these low levels were corrected, wouldn´t it?
Now, luckily, there is a simple device developed for migraine therapy which is able to do just that – you can basically dial in your CO2 level with your smartphone: https://www.rehaler.io/
It´s hazzle-free, simple, easy to use – and would probably answer many questions regarding ME/CFS pathobiology. Possibly, it may even lead to clinical improvements as it would be able to increase cerebral blood flow.
I have suggested numorous times that researchers try this device, the company would probably be more than happy – yet, no takers so far, which is unfortunate.
Fascinating that the same problem may persist in migraine – which is often found in ME/CFS and FM as well. So many similarities: cerebral hypoperfusion, local tissue hypoxia can trigger migraines!;
From their website
Clinical studies have shown that by increasing the CO2 level and oxygen/energy supply to the brain, a large percentage of migraine attacks can be stopped or alleviated
Imaging studies show that cerebral hypoperfusion is the norm before and long into migraine with aura (MA) and possibly many migraine without aura (MO) attacks (
Local tissue hypoxia (as will result from a pronounced hypoperfusion) reliably triggers MA and MO attacks in migraine patients (Arngrim 2016) and migraine-like headache in healthy individuals (Broessner 2016), as well as triggering Cortical Spreading Depression (CSD) in brain tissue (Ayata 2015).
CO2 is a well-documented and strong cerebral vasodilator, increasing cerebral blood flow (CBF) by up to a factor of two (Claassen 2007). If normal oxygen saturation is retained, moderate, well-tolerated hypercapnia increases brain oxygen/glucose delivery by up to 50% or more (Johansen 2017).
… even more surprising that this simple device hasn´t been picked up by ME/CFS researchers, isn´t it?
It does seem to have real applicability. I signed up for theire newsletter – here’s to their getting FDA approval.
I hope this comment will make many say “Oh ya, that’s right !”
The byproducts of Aerobic metabolism of glucose are fairly harmless:
CO2 and water.
The CFS body switches, prematurely, in stress tests (exercise being a positive form of stress) to ANAerobic metabolism.
The main byproducts of ANAerobic is lactic acid, with a CONSPICUOUS LACK of Co2 and water.
Only from this blog today do I realize how that would indirectly reduce brain oxygenation .
I knew that Hemoglobin moves CO2 to the lungs, but just reading up on it now, I see that only accounts for 10% of the transport, while 80% would normally be “chaperoned,” if you will, by water. Meaning that the Co2 binds with H2O into HCO3− and H2CO3. The other roughly 10 percent is simply dissolved in the blood. Someone more knowledgeable will have to say what will happen if there is LITTLE C02 and no water produced.
In covid infection we know that the alveoli in the lungs are at low capacity for the EXCHANGE of C02 for Oxygen. This is because they are inflamed and emitting liquid. I am not saying that it remains this way in CFS-like long covid, nor that it must have remained this way in influenza pandemics for the chosen few. Correct me if there is a chance that it would.
So, just trying to be logical, then, in response to you, Cort, if you go prematurely anaerobic, then you prematurely produce too little CO2 and water for the main transport vehicle of CO2.
If Aerobic glycolysis is the preferred method of ATP generation, and it is, and given that ANAerobic
One thing to keep in mind about Hemoglobin moving either Oxygen or CO2 is the word “affinity.” Healthy hemoglobin is 90% iron and has 4 binding sites for Oxygen– or for CO2. The affinity of the Hemoglobin unit for one or the other is in constant flux depending, I guess, on whether you are inhaling or exhaling. And whether you are sitting or exerting. I know that the Hemoglobin is less willing to release oxygen that it’s carrying when you don’t need it, but loses some affinity for it when you exert. Long story.
So my main point is that CO2 should be a potent vasodilator, as you stated, and going Anaerobic prematurely is going to create a shortage. As I understand it from your blogs, hypoperfusion results from low blood pressure in CFS, and that starves the muscle cell, cognitive brain cell, limbic cell of oxygen.
To me vaso-action dysfunction (renin-angiotensin-aldosterone system dysfunction) or incorrect systolic/diastolic is the cause of CFS which is an endothelial damage issue. The preload of the heart with oxygenated blood is reduced when the vessels won’t push back adequately to the heart. That’s the cause for the tachycardia, to make up for the loss of help.
To me that’s a good enough cause to derail exertion support.
Lastly, allow me to repeat that one can help to stimulate the vagus nerve, and in so doing switch more from fight-or-flight to rest-and-digest, by stomach breathing. Again, it artificially pulls down the diaphragm, creating a vacuum in your chest cavity, which draws more oxygenated blood into the preload.
I hope this helps.
Myoglobin and Neuroglobin, blocked or destroyed, progressively, but only when its oxygen storage site is empty
Just a conjecture, but only a computer CPU designer of my age would ask the question that led to that line of thinking
Yeah, I know, people are getting tired of me saying this
Well… !! Call me a Windows expert and tech support star…
but iiiiiiI would like to hear more about this !!
I offered the hypothesis to the NIH NINDS ME/CFS crowdsourcing effort back in February/March at
https://ninds.ideascalegov.com/c/idea/31814
If you want to discuss further (let’s get this off Cort’s site) I have a copy up on Medium at
https://medium.com/@FStevenChalmers/heretical-hypothesis-to-nih-ninds-me-cfs-crowdsourcing-web-site-d6cf8a7a2d4a
It’s very good Steven.
I get it, but need to read it twice more.
There was one paragraph or two right in the middle which I felt was bang-on.
I disagree with some points and can clarify others. Some of what you said was not covered in medical literature actually is covered.
We can talk off-site for sure.
But I would like to stress something to you that I said higher up or lower down on this page:
Affinity: The hemoglobin have more or less affinity to oxygen or to CO2 depending on dissolved blood gas levels. You said that the hemoglobin readily gives up oxygen to the muscle cell. Well, in CFS it might not be. A you said: yes at first when you are at rest, but things go wrong when exertion starts. Even in a healthy situation, there are moments when the hemoglobin is UNwilling to give up the oxygen. Has a higher affinity.
Typically that occurs when the muscle cell is NOT exerting– the wisdom being, I am guessing, that too much oxygen is toxic, so the hemoglobin hangs on to some oxygen. You are right that atoms and molecules all have charge/stickiness of a positive or negative value and in that sense it definitely compares to a switch opening or closing on a motherboard.
But I think the main problem is the failed shunt of oxygenated blood from some organs over to exerting muscles, cognitive cells, limbic cells.
Yes, maybe there is enough glycogen stored in the cell or in the nearby astrocyte. But we still have to work in the relevance of the insulin resistance found in the CFS patient: ie. why, or to what end.
Thanks for linking me.
Steven, I do think you should write to Perikles Simon (contact information see https://healthycampus.uni-mainz.de/univ-prof-dr-dr-perikles-simon/ ) about your hypothesis that antibodies block/impede myoglobin and neuroglobin binding sites, thus preventing oxygen extraction from the blood (right?).
Being the director of Uni Mainz sports medicine research department and having a definitive interest in Long Covid / ME/CFS / PEM, Prof. Simon could be just the person with the interest & ability & possibly even a patient cohort to confirm or exclude this hypothesis contributing to the problem of ME/CFS, and – if so – discovering a new mechanism impeding athletic performance to boot. Mainz University has a neuroimmunological department, too.
I still think your hypothesis is worth looking into, in particular as from diagnostic technology I think we know anti-myglobin antibodies do exist. So, I hope you do go ahead contacting him, and maybe you’ll to let us know if you do! Kind regards!
My brain can’t quite follow the dots, but…
I recently started doing a stop start excercise program. A “Strength in Menopause” program because I was worried about bone loss. (Fibromyalgia for over a decade, two bouts of covid, and some back problems had left me with minimal exercise ability)
The program involves 40 secs excercise, 20 secs rest for 20 mins.
To start I couldn’t do the 20 minutes, or even to full 40 seconds. But I built up, and felt that I had found a program that suited me and I could do at leastb3 or 4 times a week.
Then a few weeks ago I saw an unrelated thing on Creatine, and how we may not have enough of it as we age. I went down a rabbit hole of research and found it linked to cellular energy, excercise recovery, and may be of use in fibro and long covid. It can also be neuroprotective and improve concentration.
So I decided to try it and I think I see an improvement. Better recovery from my sessions, and improvement in brain fog.
Could it be linked to this study at a cellular level?
As I said, my brain can’t quite link the dots, but maybe someone else can?
Please follow your instinct on this and share your results.
I am confused between creatine and creatinine. Kidney? Liver?
But you knew what you were doing.
Please amplify your search for us all.
”it’s notable that problems with oxygen extraction and low CO2 levels have shown up repeatedly””
I think it is a key finding. If we know what causes this then we you know the cause of ME/CFS.
There is also a simple and reliable test that allows you to immediately see for yourself whether you are breathing incorrectly.
It’s called the Control Pause.
This is how you measure the Control Pause:
(1) Sit quietly on a chair for a few minutes. Breathe very normally, and through your nose.
(2) After a normal exhalation, pinch your nose closed (so you stop breathing).
(3) Wait until you feel the first urge to breathe, and then start breathing again.
The Control Pause (CP) is the time you could comfortably stop your breathing. Without any willpower.
You can use this online stopwatch to measure your Control Break.
Less than 15 seconds
You breathe heavily and deeply. This can cause serious health problems.
We strongly recommend that you calm your breathing again.
Around 25 seconds
You’re still breathing quite a lot. About twice as much as the norm. This can cause many diseases and
cause complaints. You may become ill quickly because your immune system functions poorly.
Around 35 seconds
You’re still breathing a little too much. There is also a danger that during a period of stress your breathing will slow down
becomes much heavier.
Around 45 seconds or more
Your breathing is excellent.
https://www.buteykoluchtop.nl/?page_id=44
Maybe it’s an idea to start a poll. Patients measure their control pause (CP). Then you tick an answer, for example: 0 to 10 seconds, 10 to 15 seconds, 15 to 20 seconds, 20 to 25 seconds, 25 to 30 seconds, above 30 seconds. Something like that.
Gijs: this is a great idea of yours.
I very much agree, having just been introduced to
CO2 as a GOOD THING, which induces oxygen supply to one’s brain.
So… when skeletal muscle stops its CO2/H2O byproduction,
because the muscle cell has — I presume– been UNDERSUPPLIED with OXYGEN,
or UNDERSUPPLIED with Glucose because of Insulin resistance,
or BECAUSE OF BOTH undersupplies,
it reverts, prematurely, compared with healthy exercise subjects
to ANAEROBIC Glycolysis. The payload of ATP is only about 1/12th compared with Aerobic.
—-Sidebar: Rob Phair talks about the Itaconate shunt in the Fatty Acid energy production occurring, and shipping out ATP rather than using it, WHEN the GLUCOSE SUPPLY has already failed.—-
We DO know for sure from earlier CFS studies, that the CFS patient has INSULIN RESISTANCE.
Once again, I have to ask you all two sides of the same glucose coin’s question:
a) If the CFS patient has INSULIN resistance, which is a prediabetes, and obviously also a T2D symptom,
then why is it ignored in CFS talk??
Why is diabetes theory not already encorporated into CFS theory??!!
How can Insulin Resistance be overlooked? when the problem is an anaerobic shift related to glucose? The skeletal cell prefers glucose, and needs Oxygen for maximal ATP production (at least 12x what anaerobic can muster)
b) WHY would the cell shun Insulin?
Who told it to NOT generate much ATP? I would say that most likely the Brain was Inflamed, and the HT knew that an increase in core body temperature would push the brain PAST it’s upper temperature limit, after which damage occurs.
It is ONE THING for the body to go into low production of energy during an infection, and the human just needs to sleep, or not function physically or mentally.
It is quite another for the BRAIN, who orchestrated the preceeding state,
to go into an unwelcome state of FEVER,
and thus become UNABLE to be the wisdom and regulation of the body.
If that were to occur, then the vagus nerve control of the organs would fail,
resulting in an ordered shutdown of organs, until only the brain and heart/lungs remained.
That is why, BRAIN-DEAD is the marker for true death in a hospital.
At the moment that brain damage begins to occur, and brain functions are ceasing to occur, this is because the heart and lungs have shut off.
Yes, some doctors revive them.
My point is to describe why DAUER ===== AVOIDS brain death… and actually gives the creature the ability to RESPOND to better nutrition/climate conditions, and gradually build itself back to full function.
This points DIRECTLY to the need for nutrient interventions (donations through supplements)
as well as
what has been described here:
a SLOW AND GENTLE APPROACH to reviving the creature that would otherwise be dead.
The talk above about 20 seconds exertion, building up to 30 seconds exertion,
and people finding that this WORKED !!!!
…unfortunately….
means that IMPATIENCE or rushing is not permitted in CFS recovery.
We may have battered our bodies, then succumbed to a virus or bacterium,
in the goal of 100% Up-time, or 110% effort at work.
Which is unreasonable…
But if we now have CFS to reverse….
then the REVERSE approach will be required.
CD
In a fever, the energy is channeled to HEAT production but shunted from Ribosome replication effort.
I argue that when a pandemic virus SEEMS to fail to be cured …AFTER THE 3 MONTH ACUTE LIMIT
— or when a bacterial infection SEEMS to do the same
…..
That SEPSIS is likely to occur.
The toxins will come from cytokines from the endothelial cells which produce it,
as we now agree:
because these cells are STUCK in an Innate immune response
of fever (and low ATP energy production, but HIGH temp generation)
BUT
the Hypothalamus realizes, as the mastermind of the brain over the body,
when fever plus cytokine storm has failed.
THEN
Because of an overload of Cytokines (ROS, NOS) designed and released by Endothelial cells to poison (react destructively with) the infector,
there is a serious overload of self-harming toxins present. Self-generated and also self-toxic.
If you were not already aware…
This can and will contribute to the Apoptosis or — programmed cell death of the Endothelial vessel cells…
Those cells
1. go anaerobic, and the white blood cells FUNCTION anaerobically, in unison with them
BUT:
2. If it is not working, and the CYTOKINE PRODUCTION PERSISTS: then the killer cells will remove the endothelial cells and take them to Macrophage eaters.
The same process that can SAVE a cell in a mild-to-medium infection,
will
ASK FOR DEATH through Apoptosis
if… the cytokines escalate.
SUMMARY:
The Endothelial vessel cells are the AMBASSADORS or the main agents of the immune response.
BECAUSE of what they emit… and then… the white blood cells knowing what to do, or
knowing when to back off as well, if the fight goes well.
THEREFORE,
if the fever/cytokine reaction has FAILED to neutralize the infector,
THEN,
IF THE HUMAN IS TO STAY ALIVE…
SEPSIS and hypothermia must occur.
The body could NEVER sustain the energy requirement of Fever past 3 months.
HOWEVER ! :
if FEVER (“hyperthermia”) is cancelled by the Hypothalamus temperature set point,
and
revised
to be Hypothermia,
this will CONSERVE energy in comparison.
The drawback
is that where there were 5 cytokines during fever,
the SEPSIS response reduces the body temp,
and reduces the TYPES of Cytokines to only 2 types:
Bradykinin is one (painful)
and I can’t remember the other, but I believe it is NO (Nitric Oxide),
a potent vasodilator.
NO may be the cause of low blood pressure in Chronic Fatigue Syndrome.
NO is, yes, an RNS (reactive nitrogen species)
but it is also a natural and normal, one-of-several, vasodilator.
THEREFOREFORE:
if the CFS body resorts to Low temp, then energy production will be choked. This is similar to FEVER, except that prolonged FEVER would mean DEATH.
Instead, CFS produces DAUER. It is a means to survive, but at low function.
It is a “fate WORSE than Death??” . That is a person values question. Not for me to answer.
—-I often write things to friends, and to you here, and while doing so,
while require myself to be logically sound…and as result… realize a new possibility.
A hypothesis or proposal like this comes from the assumption that LC/ME patients are unable to exercise. They are. The NIH paper on deep phenotyping said so. So does 2-day CPET test. It’s just that they succumb to PEM the next day if they do.
Any exercise protocol, especially high intensity one, should come with caveat emptor warning. I’ve tried 4×10 sec spurt exercise long ago and I gave up because of PEM. Even now after the recovery, I succumb to PEM after 4×50 sec jogging when I’m under the weather.
It may be, though, that it would have worked if you had started with much smaller levels of exertion, rather than what we think of as exercise.
Graded exercise therapy? I’ve tried that too and it didn’t work for me. Only thing that worked was low intensity with frequent rest.
I saw in a blog https://www.fasynation.de/das-hochwirksame-30-sekunden-training-bei-long-covid-und-me-cfs/ that Perikles Simon’s program, though that blog advertises it as “training”, is really more about pacing (like the example that breaks up daily chores like putting a plate into the dishwasher into small bites of 30 seconds), with the aim of never even entering the (malfunctioning) aerobic zone in the first place, but staying withing the 30 seconds that the muscle can function well anaerobically.
i agree that if someone attributes improvement to training, that’s probably incorrect attribution. It would rather be that his programm allows for doing things without impeding regeneration processes in the body. And, probably, reap some of the general beneficial effects of movement (like moving the fascial system) without triggering PEM, as compared to a baseline of either not doing anything, or too much.
The special thing the program seems to say (based on the abovemention blog) is: based on muscle physiology, in a situation where oxygen extraction by muscles is impaired, 30 seconds of exertion are safe as this is the duration a muscle can safely function anaerobically without hypoxic tissue damage occuring; so it recommends splitting activities up into 30 sec micro-units.
Cort, have you seen this? It’s a research finding about disturbed metabolic pathways;
https://www.biorxiv.org/content/10.1101/2024.06.17.599450v1?ct=
Could be important.
I saw that too and it did look important.
Has anyone tried the supplement with l-ornithine and l-aspartate (LOLA)? I think I will try it.
Thanks – really interesting paper. Working on it 🙂
If I put my legs up the wall before and after I exercise, I can go do better.
It makes so much sense to do short sessions of activity interspersed with sessions of rest that range from short to long in duration, and during these rest periods (especially at the start) to focus on belly breathing and other autonomic resets. The over-response of the autonomic nervous system to each challenge (as Putrino puts it) may not be the root of the problem. It may be downstream from other stressors such as damaged mitochondria or functional autoantibodies. But it happens, and when it does it feeds into a positive feedback loop that worsens PEM. And down regulating that over-reaction seems key to improving ME/CFS. Everything in this article makes so much sense to me.
I’ve wondered about the device linked below for this type of application – it does measure CO2, but I don’t understand things well enough to tell if it could be helpful. Do any of you smarter folks with working brains have any insights? It’s not made for ‘us’ per se, but seems like another ‘athlete’ thing that could possibly be tweaked for us?
I’ve had the 2day CPET, but it’s been a couple of years; I can’t really afford or travel right now to re-test and see if anything has changed, but I’d love if there was a way to see on a regular basis how my metabolism is doing. Does it change day to day, or over time? Am I making any progress? Just not sure if this would be helpful or not. And of course, it seems every potentially helpful device or treatment ends up costing hundreds of dollars, so on a limited budget it’s hard to trial many things, or to know which ones to prioritize. Thoughts?
https://www.lumen.me/
Here’s thought. PEM is a mechanism to protect you. Maybe figuring out ways to exercise is exactly the wrong thing to do. We should be concentrating on finding the cause of ME/CFS and like Jack Palance said in City Slickers, “I think it is just one thing”.
That is not to say that other disabling conditions haven’t been swept into the basket of ME/CFS since there is no way to differentiate it from other things with similar symptoms.
We all know that PEM is a core symptom of ME/CFS. Why keep studying that to death?
Betty,
Please do not lose hope today. Also, please do not view this reply as directed at you.
Rather, please see it as *inspired by your question: why keep studying PEM.
With respect, I must disagree with your dismissal of studying PEM any longer since I have been studying CFS/ME and other autoimmune diseases including long covid since 2020. This has included visiting Cort Johnson’s articles and reviewing the studies he has reviewed. I try to take into account the findings of researchers in case I am incorrect, or, alternatively, in the case they might have the best clue.
In my opninion you have both given the answer or best direction for study into CFS/ME treatment… (the bathwater)
and suggested we throw away PEM (the baby)
To explain my meaning:
You have made a good point: that it is difficult to differentiate ME/CFS from other chronic diseases with similar symptoms. At least it used to be before blood markers were identified in studies since 2020.
It is difficult to differentiate *ESPECIALLY BECAUSE OF: non-restorative sleep, fatigue that will not leave, flare-ups, widespread pain. They occur in Fibromyalgia (more pain but less fatigue), in Lupus, in MS, in Sjogren’s etc.
BUT THAT IS THE BEAUTY OF THE CONFUSION ! : it directs our attention to this state being not authored by one virus or one bacterium or one burn-out period. THIS STATE IS AUTHORED BY OUR IMMUNE SYSTEM.
I have considered renaming ME/CFS, if anyone would licence me, to “Humanness.”
Equally we could rename it “Cell Defense Response-Interrupted.” (CDRI)
That is to say:
a) it is agreed worldwide that the beginning of all disease in inflammation
b) Hypocrates stated that all disease commences in the gut
c) if symptoms *from the infection or *triggered by the burn-out weakness PERSIST,
this is because inflammation is persisting. Inflammation includes Cytokines (chemicals generated by the cell to poison attackers, but which take their toll on self.)
c) yes, this persistent inflammation could be from a cyclical reactivation of an
immune-evasive virus such as Epstein-Barr– and/or of other such viruses.
The END of the disease would be a return from stage 3 of the already established Cell Defense Response (CDR) elucidated by Dr. Bob Naviaux and also by Dr. David Lam and others, to Health — Stage 1.
Naviaux, and I would gather, also Rob Phair see ME/CFS as being stuck in an innate immune response of “kill first, ask questions later”… but later never comes. After antigen/antibody questions had been answered over 4-5 days with most viruses, new antibodies would have been formed and the healthy patient would have HEALED… or returned to stage 1: body happiness.
Therefore, PEM, something that DOES significantly differentiate ME/CFS from other chronic diseases…
(most notably Fibromyalgia in the absence of of ME/CFS co-morbidity… and also Myasthenia Gravis (MG) which can have a comparatively rapid recovery time)
… OUGHT to be the focus.
Here is the key question: Like, okay… the ME/CFS patient runs out of steam quickly. Her body tells her she can not continue the exertion. Yes, lactate acid will pool since the muscle cell resorts prematurely to Anaerobic energy production. This has been proven in stress tests on treadmills. BUT WE DO NOT KNOW WHY.
….BUT: why is there then a PAYBACK for the exertion , AFTER the limit has been reached, and the patient obediently rests? Call that PEM.
Anyone can exercise to their limit. Anyone can fall over from exhaustion in a marathon, regardless of continuing good health. They’ll be sore for a while, but I do not believe that they get PEM.
By asking what is DIFFERENT about PEM, what are we asking?
We are 1st acknowledging that there is not much point tracking symptoms that could come from just ANYTHING. But PEM is rare.
We are 2nd trying to measure chemicals around the cell and in the blood that indicate what has happened to the PEM victim cells– the striated or skeletal muscle cells. But do not forget: it also occurs in the Limbic system (emotion) and the cognitive or executive function brain.
We need to 3rd ask what those 3 Amigos have in common that spares other cells from the same outcome !!
PERFECT vs. IMPERFECT
So a perfectly HOMEOSTATIC body would take the ups and downs and infections, but bring them back down, or back up to normal in a short period. That would be perfect.
The IMPERFECT state has something overtaxed or underpaid. Meaning: too much demand eg. inflammation , or too little nutrition, or too little rest.
Many people might over-exert in every way, feeling that they are just doing good for family or society, but not setting healthy limits for themselves. This is one trigger for ME/CFS that may be predicated on a viral or bacterial infection, but the trigger was the last straw of over-exertion.
Now the brain RESISTS exertion . SEID: same as ME/CFS, but the latest unpopular definition that no one will adopt. Systemic Exertion Intolerance Disorder.
With all of the foregone conclusions made by researchers in this area, and with ME/CFS having had a history of 5-10 years to be properly diagnosed… and even then being difficult to differentiate from other “idiopathic” (no known cause) diseases with no known cure : ie. the Autoimmune Diseases Cohort (to coin a phrase),
PEM seems to many to be about a traffic jam in the space between your nerves and your muscle cells, also nerves and cognitive cells, also nerves and limbic system cells.
What I mean to tell you is that body messengers/chemicals should be ISSUED, then quickly CLEARED.
For the reason that we all seek: why do muscle and other selected cells revert to anaerobic energy creation (pathetically inefficient)(and HIGH in ROS/NOS byproducts)
What I believe we are looking at in PEM is a failure of CLEARANCE of metabolism by-products.
What will be the treatment? A BOOST to all systems. Where they are overtaxed and have depleted their resources,
SUPPLEMENT their resources.
All of this research has pinpointed what is lacking,
ESPECIALLY …. PEM.
again… respectfully, Betty,
Chris
Love the Jack Palance reference! (Remember his Oscar speech when he did one armed pushups! 🙂
These exercise regimens help but, of course, you can go only so far with them. The one thing is still undetermined. I do think we’re getting closer. Interesting paper on that from Wengzhong Xiao that looked at muscle tissue just came out….
https://www.bing.com/videos/riverview/relatedvideo?q=jack+palance+just+one+thing&mid=F679E7556D9C886DA1B5F679E7556D9C886DA1B5&FORM=VIRE
In 2019 after my remission event I was able to increase activity from totally bedridden to 40 min walks over a period of 2 years. Part of the method I used stemmed from the breathing exercises and recommendations in this book. I had a feeling that this method had been key for me but this research suggests i was really onto something. I since declined again due to a mold exposure but movement/activity was incredibly important at the right time and in the right way.
https://oxygenadvantage.com/
More evidence that Long Covid is an autoimmune reaction to the virus:
https://erictopol.substack.com/p/new-insights-into-acute-and-long
This is a summary of four new studies on Covid and Long Covid. The summary:
“SARS-CoV-2 is still evolving, and by selection will continue to find ways to induce (re-)infections despite global complacency. We’re making progress in elucidating the genesis of Long Covid, with a pair of studies that incriminate autoimmunity as a culprit. At the same time, we’re learning about ways to protect from infection (particularly IFN-1) and how to reduce the chances of central nervous system involvement by vaccination. These are all important steps of progress.”
This is awesome. I’m going to try this approach. It makes a lot of sense. And there is no way I’m reading other the comments that will ruin this optimism.
Go for it! it works.
Good for you!
Sounds promising. A lot of good science comes from someone saying “Hmm, that’s odd” and having the nous to investigate.
Cort, could Dr Simon’s testing for cell-free DNA be used in diagnosis? I realise it couldn’t give a definitive diagnosis on its own, but could it assist in the process?
Does anyone know whether testing for cell-free DNA is expensive?
I got the impression that they are developing a test for it. Dr. Simon referred to the fact that they’re developing a commercial product, I think it was, in the beginning of the presentation
Oh good. I had a bit of a Google and cell-free DNA is being used in prenatal and cancer testing (looking for certain types related to those situations). It seemed to be something extra that patients can pay for, rather than part of standard tests.
Simply put, I think poor cellular metabolism including oxygen is a major aspect of ME/CFS – and could also create neurological effects through the effects on neural cells.
I’ve just started a rehab program with an exercise physiologist. It’s interesting, and effective to look at their metrics of heart rate, oxygen saturation, and blood pressure in combination with HRV and my own PEM awareness.
One curious thing I’ve found is that I
apparently do better with recumbent exercise. This has me wondering if in severe cases the increased heart rate associated with POTS and standing is enough to trigger PEM.
The Galloway technique is a variation on the above frequent rest strategies. Dysautonomia folks have had success. I can dig up some references if you like.
I would like !
Recumbent exercise is often the first kind of exercise prescribed in these diseases – so I think you’re on the right track. It’s a particularly big deal in POTS exercise regimens.
It’s great to see a sports medicine researcher tackle exertion intolerance.
Cort, do you know if he has published his case studies and PEM hypothesis? I think he should.
I have slowly built up a routine that I am doing a few times a week. It is not graded exercise but restricting exercise in any muscle group to only a few repeats. as well as restricting the overall cardio demands as any exercise puts demands, however small, on the heart. This routine has improved my muscle tone. I have increased the number of repeats e.g. from 3 to 6 but that is not my main goal. The routine includes some XBX (Canadian Airforce) exercises and stretches that I used to do years ago, squats,upper body exercises and some neck and facial exercises to combat the ravages of aging. (I am soon 87 y.o.). The exercises help with core muscles so my balance is good. CFS/FM adds challenges to aging.
Re breathing, about 10 years ago I visited Waterton park with a friend who is 6’2″ and all legs and on one trail we had to walk up hill to see a waterfall. I knew from past experience that hills were very challenging for me since CFS/FM, so I started deep slow breathing and found I was able to keep up with him (though not talk much) without any problem. I didn’t do the side trip to another vnow of the fall – figured I wouldn’t push it – but suffered no ill after effects. It was only one experience but significant to me. I now do deep breathing as part of my “health” routine,
These exercises combined with supplements have restored me to feeling almost normal at times. I highly recommend starting some exercise/stretching routine, however small – even one repeat.
Re supplements, many say it is individual, and it is, but, there are some general principles that are, I think, valid. The main one, possibly being to take something that calms down the microglia and reduces brain inflammation. A second one is take some supplements to reduce ER stress and support the mitochondria. The third one relates to diet and supplements – be sure your vitamin and mineral intake is good. And fourthly -diet related, take in enough protein. Research has shown It’s been found as your age you need a higher protein intake i.e.75 to 100 gms daily depending on your weight.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4924200/ Bone as well as muscle needs protein. From personal research I am convinced that many bone breaks as people age are due to inadequate protein intake as well as inadequate calcium etc intake. Protein is a major component of bone,
Finally, an aside, I have suffered from IBS type symptoms and recently have started eliminating FODMAP foods from my diet. That seems to have brought improvement, though I am early in the process. Has anyone else found this helpful?
Has anyone tried the supplement with l-ornithine and l-aspartate (LOLA)? I think I will try it.
Is the idea of using a NIRS device, such as the Moxy, applicable here? It is designed to be used on the thigh.
https://www.s4me.info/threads/muscle-oxygenation-as-assessed-by-nirs-near-infra-red-spectroscopy.35172/#post-522944
Woukd it measure the 30 seconds or beyond that’s appropriate?
Hi Cort
Thanks for the City Slicker video. I loved that movie.
For me, PEM is just one thing. But for me, not the most important thing. I have been much sicker and nearly lost my vision from trying to get mast cell disorder diagnosed and treated. The meds used to diagnose mast cell triggered glaucoma and the laser surgery for that was followed by a carotid cavernous fistula. This is where the artery behind one eye ruptures and attaches to the vein behind the other eye. You can have a stroke or lose your vision in that eye.
I had emergency surgery where platinum coils were inserted into my brain to separate the artery and vein. I will have glaucoma and other damage to my left eye for the rest of my life.
I also have been plagued by infections since this horror began. In one case, a tiny cut on my lower leg morphed into painful cellulitis that took 5 months to resolve. They couldn’t figure out what was causing the infection until they finally tested for e-coli, not a normal cause of this kind of infection.
I was left with an ugly scar, but I still have my leg.
I was first diagnosed in 1984 before the name ME/CFS was even used. Two immunologists doing research on immune disorders diagnosed me with chronic encephalopathy and immune deficiency. (This really describes exactly what was going on and is true to this day.) Because they were doing research, I had some immune cell studies that most ME/CFS patients haven’t had.
I had 372 total T cells and a complete reversal of T4/T8. I think the doctors were worried I had AIDS, but I did not.
There are a number of other ME/CFS patients Dr. Paul Cheney was treating and the CDC was monitoring who had the same immune profile I had.
Do I have PEM? Yes, I can go out and suddenly, it is like a ton of cement has been poured on me. I just can’t go any further. This improved a lot while I was being treated by the late Dr. Paul Cheney. But everything fell apart when I got Covid twice this year.
Now I have high blood pressure and A-fib which I never had before.
There is so much more to ME/CFS than just PEM, but it is low-hanging fruit for studies.
Imagine, if this approach really works, having ‘respite and recovery centers’ across the country. Patients could go there for however long it takes, with all the pacing guidance, supportive nutrition and supplementation etc, everything needed in the ideal optimized healing environment. How quickly might we recover (at least to remission) in that setting? And honestly it shouldnt cost that much, as many of us would not need hugely expensive medical interventions with it. Wow! The disability savings alone could probably pay for it!
4 yr+ Long COVID patient: Creatine helped my muscle issues. For 3 years, they felt like they weren’t getting any blood and hurt to use them and would leave me sore for days afterward. One day, I took 2g of creatine monohydrate an hour or so before doing pilates, and it somehow bypassed this issue. I felt like a superhero the first time I took it. I take it every day now and have noticed that my muscles are even less sore than my normal pre-COVID after a workout (just pilates, I’m not doing anything super advanced yet), but still this was a huge improvement. I’ve also noticed low CO2 on my chem panels but no one ever seemed to be concerned about that.
What about people with COPD on Oxygen therapy who also have ME/CFS? How would you figure out an exercise program for them?