Article: Post-Exertional Malaise: Cause and Effect By Jennifer M. Spotila, J.D.
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What I get from the Kinesophobia section is that even in people who have it - it doesn't seem to be affecting their activity levels much - so it can't be the cause of their low activity.
How lovely that they found no difference in physical conditioning between CFS patients and sedentary people and that only CFS patients showed drops in metabolic functioning after the first exercise test. (It all seems so clear when Jennie writes this - why doesn't the research community really get it? I don't know.....Jennie, I think you should write them a letter
)
How lovely that they found no difference in physical conditioning between CFS patients and sedentary people and that only CFS patients showed drops in metabolic functioning after the first exercise test. (It all seems so clear when Jennie writes this - why doesn't the research community really get it? I don't know.....Jennie, I think you should write them a letter
)
I think the difference in perception of effort could be a brain problem if, as some studies have suggested, the motor planning sections of the brain are not functioning well. We noted that CFS patients brains have difficulty screening out innocuous stimuli and that the inability to do that makes it harder for them to focus on one item at a time. Basically they have to work harder to focus than normal people. The same thing could apply for movement; because there is a problem planning movements CFS patients brains have to work harder and get tired more easily when they move their bodies.
The oxygen consumption problem seems like it's the most clear-cut; energy is a function of oxygen consumption and if your cells are not consuming oxygen they are not to be producing energy. I really don't know why the research world is in jumping at this - hopefully at some point they will be.
Thanks for this great series of articles, Cort.
Thank GOODNESS someone is looking at C4a besides Dr. Shoemaker.
It is one of the cytokines that skyrocket when people get biotoxin poisoning.
I think we could learn a lot by studying it.
Also, I've heard CFS described as "partial paralysis". I think that makes a lot of sense. It takes an effort to make my body move every time I want it to do something. Even lifting a toothbrush to brush my teeth takes effort.
I think we people with CFS get used to making this additional effort to move every body part, and we might forget how easy it is for healthy people. But we feel the aftereffects of that effort.
At my worst, moving felt very similar to having oxygen sickness at the top of a high mountain. (I had that experience in my younger days)
Thank GOODNESS someone is looking at C4a besides Dr. Shoemaker.
It is one of the cytokines that skyrocket when people get biotoxin poisoning.
I think we could learn a lot by studying it.
Also, I've heard CFS described as "partial paralysis". I think that makes a lot of sense. It takes an effort to make my body move every time I want it to do something. Even lifting a toothbrush to brush my teeth takes effort.
I think we people with CFS get used to making this additional effort to move every body part, and we might forget how easy it is for healthy people. But we feel the aftereffects of that effort.
At my worst, moving felt very similar to having oxygen sickness at the top of a high mountain. (I had that experience in my younger days)
I like the 'partial paralysis' idea, it sometimes seems like 'body shutdown' - you are telling your muscles to move and your body is saying "I don't want to"; its like its digging its heels in and saying "No"!
I almost feel like there are two commands going on - the conscious command to move that arm and another commanding say- don't move it..its like trying to push a car with its brakes on.
I almost feel like there are two commands going on - the conscious command to move that arm and another commanding say- don't move it..its like trying to push a car with its brakes on.
Mitochondrial dysfunction was mentioned in the comments for the first or second part of this series.
I've been reading an old 80's science book that discussed the then newly hypothesised role of brown adipose tissue (brown fat) in weight gain and cold adpation.
For those of you unfamiliar, your endowment of brown fat (amount and efficiency) can determine the extent to which you burn off excess calories and can tolerate cold temperatures. Those 'deficient' in brown fat will put on weight easily, and in cold weather cannot burn calories to create heat and therefore can become dangerously cold. Exercise, or lack of, actually contributes very little to the rate at which we burn calories compared to normal metabolism.
The point is, brown fat is possibly the body tissue richest in mitochondria.
I wonder how many PWCs have either a history of easy weight gain and cold intolerance or developed these symptoms post ME/CFS.
If it is hypothesied that there is a mitochondrial dysfunction in ME/CFS it seems likely that this dysfunction would be generalised rather than specific and should therfore also show up in brown fat dysfunction.
It would be relatively simple to test a cohort of PWCs against controls for brown fat efficiency using either infra red scanning or a hood calorimeter in reponse to adrenaline infusion (I know we don't tolerate adrenaline well).
While this wouldn't explain why, it would at least help confirm that mitochondrial dysfunction is a key part of the illness.
C
I don't have to get aerobic to set off PEM. Mental stress, which may or may not even increase my heart rate, will set it off without getting anywhere close to aerobic. The same is true of light weight muscle exertion....I don't even have to increase my heart rate and it will set it off. But yes, aerobic exertion is by far the worst offender.
It sure seems there would be an easy treatment for PEM. Something like an immune modulator...or something that blocks the cytokine storm, etc.
It sure seems there would be an easy treatment for PEM. Something like an immune modulator...or something that blocks the cytokine storm, etc.
Actually for me weight lifting of any type is the worst. I can do some aerobics (walking) but the other stuff is more difficult. Taking showers does as well. I can handle cognitive work OK. I actually find that some exercise helps me cognitively; that is, my muscles can be in pain but my mind is actually sharper. Too much, of course, effects everything.
A terrible and irresponsible article. People with ME/CFIDS do not have kinesiophobia, and there is no good evidence they have ("likely" isn't a scientific statement) deconditioning as remissions and fluctuations occur with a rapidity and autonomy that severe deconditioning can't allow for. (Anyone who has experience with ME should know this). Even if people did have deconditoning it's made so irrelevent by mito disease, cardiomyopathy, brainstem softening, spinal inflammation etc etc, why confuse by crediting it at all?
The tiny amount of supposed evidence for kinesesophobia is worthless due to criterion contamination, illegitimate comparison with something vague like lower back pain, the ever present patient selection doubts plus De Merlier's bias in coming from an exercise physiology background. It's vintage Wessely school. De Merlier has a CBT/GET pseud at his clinic but all the people with ME only see Dr M for biomedical tests and treatments as appropriate.
It is EXTREMELY irresponsible and DANGEROUS to put forth accusations that a vague group of very vulnerable suffering patients are irrationally afraid of exercise! It matters not a jot whether you say it's not the cause or not, others think it is so your validation will be useful to them. Shame on Spotila and the CAA, and all the more as you likely can't see why!
Without these very damaging assertions this could have been a useful article.
The tiny amount of supposed evidence for kinesesophobia is worthless due to criterion contamination, illegitimate comparison with something vague like lower back pain, the ever present patient selection doubts plus De Merlier's bias in coming from an exercise physiology background. It's vintage Wessely school. De Merlier has a CBT/GET pseud at his clinic but all the people with ME only see Dr M for biomedical tests and treatments as appropriate.
It is EXTREMELY irresponsible and DANGEROUS to put forth accusations that a vague group of very vulnerable suffering patients are irrationally afraid of exercise! It matters not a jot whether you say it's not the cause or not, others think it is so your validation will be useful to them. Shame on Spotila and the CAA, and all the more as you likely can't see why!
Without these very damaging assertions this could have been a useful article.
I think this article demosntrates the dangers on relying on too little evidence which has arbitrary conclusions based on insufficient data. As an example, the faulty high perception of effort sense is based on what, heart rate and other "mundane" (suitable for people without exertional disease or healthy even) tests? Did they check ejection fraction? Did they check NMH/POTS? Oxidative stress? Inflamed glangia? The immune dysregulation the article mentions later? Probably not! What with James Jones of the CDC saying we've just got faulty perceptions, that doesn't need any encouragment on such a flaky basis.
I'd like to see this applies to testing mental activity/fatigue too. After all, the defining feature of this illness is not tiredness/weakness, but fatigue and fatiguability ie how quickly we run out of gas. I suspect this is the main reason that many studies have failed to find consistent problems with neurocognitive activity in CFS patients. Anyway, great to see this new focus on PEM.
References for this article posted here for those that are interested:
1 Part 2 of article series: http://www.cfids.org/cfidslink/2010/080402.asp
2 Nijs, J, De Meirleir, K, & Duquet, W. (2004) Kinesiophobia in Chronic Fatigue Syndrome: Assessment and Associations with Disability. Archives of Physical Medicine and Rehabilitation, 85: 1586-92.
3 Nijs, J, Vanherberghen, K, Duquet, W, et al. (2004) Chronic Fatigue Syndrome: Lack of Association Between Pain-Related Fear of Movement and Exercise Capacity and Disability. Physical Therapy, 84(8): 696-705.
4 Nijs & De Meirleir (2004).
5Gallagher, AM, Coldrick, AR, Hedge, B, et al. (2005) Is the chronic fatigue syndrome an exercise phobia? A case control study. Journal of Psychosomatic Research 58: 367-373.
6 Bazelmans, E, Bleijenberg, G, van der Meer, JWM, et al. (2001) Is physical deconditoning a perpetuating factor in chronic fatigue syndrome? Psychological Medicine, 31: 107-114.
7 VanNess, JM, Snell, C, & Stevens, S. (2007) Diminished Cardiopulmonary Capacity During Post-Exertional Malaise. Journal of Chronic Fatigue Syndrome, 14(2): 77-85.
8 Twisk, F & Maes, M. (2009) A review on cognitive behavioral therapy (CBT) and graded exercise therapy (GET) in myalgic encephamyelitis (ME)/chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS. Neuroendocrinology Letters, 30(3): 284-299.
9 Wallman KE, Morton AR, Goodman C, et al. (2004) Physiological responses during a submaximal cycle test in chronic fatigue syndrome. Medicine & Science in Sports & Exercise 36(10): 1682-8.
10 Van Oousterwijck, JV, Nijs, J, Meeus, M, et al. (2010) Pain inhibition and post-exertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome. Journal of Internal Medicine, 2010 Mar. 3 (Epub ahead of print).
11 Farquhar, WB, Hunt, BE, Taylor, JA, et al. (2002) Blood volume and its relation to peak O2 consumption and physical activity in patients with chronic fatigue. American Journal of Physiology – Heart and Circulatory Physiology. 282: H66-H71.
12 De Becker, P, Roeykens, J, Reynders, M, et al. (2000) Exercise Capacity in Chronic Fatigue Syndrome. Archives of Internal Medicine, 160: 3270-3277.
13Jammes, Y, Steinberg, JG, Mambrini, O, et al. (2005) Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise. Journal of Internal Medicine, 257: 299-310.
14De Becker (2000).
15 Jammes (2005).
16 Nijs, J, Meeus, M, Mcgregor, NR, et al. (2005) Chronic Fatigue Syndrome: Exercise Performance Related to Immune Dysfunction. Medicine & Science in Sports & Exercise, 37(10): 1647-1654.
17 Sorenson, B, Streib, JE, Strand, M, et al. (2003) Complement activation in a model of chronic fatigue syndrome. Journal of Allergy and Clinical Immunology, 112: 397-403.
18 White, AT, Light, AR, Highen, RW, et al. (2010) Severity of symptom flare after moderate exercise is linked to cytokine activity in chronic fatigue syndrome. Psychophysiology, 47(4): 615-24.
19 Davenport, TE, Stevens, SR, VanNess, JM, et al. (2010) Conceptual Model for Physical Therapist Management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis. Physical Therapy, 90(4)
1 Part 2 of article series: http://www.cfids.org/cfidslink/2010/080402.asp
2 Nijs, J, De Meirleir, K, & Duquet, W. (2004) Kinesiophobia in Chronic Fatigue Syndrome: Assessment and Associations with Disability. Archives of Physical Medicine and Rehabilitation, 85: 1586-92.
3 Nijs, J, Vanherberghen, K, Duquet, W, et al. (2004) Chronic Fatigue Syndrome: Lack of Association Between Pain-Related Fear of Movement and Exercise Capacity and Disability. Physical Therapy, 84(8): 696-705.
4 Nijs & De Meirleir (2004).
5Gallagher, AM, Coldrick, AR, Hedge, B, et al. (2005) Is the chronic fatigue syndrome an exercise phobia? A case control study. Journal of Psychosomatic Research 58: 367-373.
6 Bazelmans, E, Bleijenberg, G, van der Meer, JWM, et al. (2001) Is physical deconditoning a perpetuating factor in chronic fatigue syndrome? Psychological Medicine, 31: 107-114.
7 VanNess, JM, Snell, C, & Stevens, S. (2007) Diminished Cardiopulmonary Capacity During Post-Exertional Malaise. Journal of Chronic Fatigue Syndrome, 14(2): 77-85.
8 Twisk, F & Maes, M. (2009) A review on cognitive behavioral therapy (CBT) and graded exercise therapy (GET) in myalgic encephamyelitis (ME)/chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS. Neuroendocrinology Letters, 30(3): 284-299.
9 Wallman KE, Morton AR, Goodman C, et al. (2004) Physiological responses during a submaximal cycle test in chronic fatigue syndrome. Medicine & Science in Sports & Exercise 36(10): 1682-8.
10 Van Oousterwijck, JV, Nijs, J, Meeus, M, et al. (2010) Pain inhibition and post-exertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome. Journal of Internal Medicine, 2010 Mar. 3 (Epub ahead of print).
11 Farquhar, WB, Hunt, BE, Taylor, JA, et al. (2002) Blood volume and its relation to peak O2 consumption and physical activity in patients with chronic fatigue. American Journal of Physiology – Heart and Circulatory Physiology. 282: H66-H71.
12 De Becker, P, Roeykens, J, Reynders, M, et al. (2000) Exercise Capacity in Chronic Fatigue Syndrome. Archives of Internal Medicine, 160: 3270-3277.
13Jammes, Y, Steinberg, JG, Mambrini, O, et al. (2005) Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise. Journal of Internal Medicine, 257: 299-310.
14De Becker (2000).
15 Jammes (2005).
16 Nijs, J, Meeus, M, Mcgregor, NR, et al. (2005) Chronic Fatigue Syndrome: Exercise Performance Related to Immune Dysfunction. Medicine & Science in Sports & Exercise, 37(10): 1647-1654.
17 Sorenson, B, Streib, JE, Strand, M, et al. (2003) Complement activation in a model of chronic fatigue syndrome. Journal of Allergy and Clinical Immunology, 112: 397-403.
18 White, AT, Light, AR, Highen, RW, et al. (2010) Severity of symptom flare after moderate exercise is linked to cytokine activity in chronic fatigue syndrome. Psychophysiology, 47(4): 615-24.
19 Davenport, TE, Stevens, SR, VanNess, JM, et al. (2010) Conceptual Model for Physical Therapist Management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis. Physical Therapy, 90(4)
A terrible and irresponsible article. People with ME/CFIDS do not have kinesiophobia, and there is no good evidence they have ("likely" isn't a scientific statement) deconditioning as remissions and fluctuations occur with a rapidity and autonomy that severe deconditioning can't allow for. (Anyone who has experience with ME should know this). Even if people did have deconditoning it's made so irrelevent by mito disease, cardiomyopathy, brainstem softening, spinal inflammation etc etc, why confuse by crediting it at all?
The tiny amount of supposed evidence for kinesesophobia is worthless due to criterion contamination, illegitimate comparison with something vague like lower back pain, the ever present patient selection doubts plus De Merlier's bias in coming from an exercise physiology background. It's vintage Wessely school. De Merlier has a CBT/GET pseud at his clinic but all the people with ME only see Dr M for biomedical tests and treatments as appropriate.
It is EXTREMELY irresponsible and DANGEROUS to put forth accusations that a vague group of very vulnerable suffering patients are irrationally afraid of exercise! It matters not a jot whether you say it's not the cause or not, others think it is so your validation will be useful to them. Shame on Spotila and the CAA, and all the more as you likely can't see why!
Without these very damaging assertions this could have been a useful article.
I think you missed the forest for the trees. She is covering all the bases - as she should to write a responsible article - and then showing that even if kinesophobia is present in some patients it could not be a cause of PEM and then pointing out what might be - immune and other problems.
Did you miss the conclusion of the article that it is caused by physiological abnormalities? This article left me heartened about the possibilities present. I guess it depends on what you're looking for.
If this is 'vintage Wessely' honestly I think we'd have alot less problems with Dr. Wessely. I don't see him suggesting that PEM is caused by immune function or metabolic problems or cardiovascular problems - do you?
I imagine that it will. It'll be interesting to see over time how the exercise and the mental subsets break out. I know that for some people mental activity is as exhausting as physical activity. What is the difference between them and people like me, who has trouble with physical exercise but not as much with mental?There's so much to learn in this disorder...I hope I can stick around to see it all.
TempusFugit - You have misread and misunderstood the article. I discuss kinesiophobia and deconditioning under the subject heading "What is not the cause." This section quotes research that proves, in my view, that neither kinesiophobia nor deconditioning is a cause of post-exertional malaise or CFS. This is, of course, why the next section discusses research that may give us a clue as to what the actual causes of PEM might be.
Hi, Jen.
I enjoyed your articles on PEM.
I would like to enlarge a little on the cardiovascular/energy system aspect that you mentioned.
The observed low oxygen consumption, high lactate and oxidative stress in CFS all point to problems with the mitochondria. There is abundant evidence for mito dysfunction in CFS. The most direct evidence is the work of Dr. John McLaren Howard of AcumenLab in the UK. Some of this was described in the paper by Myhill, Booth and Howard showing a correlation between lab measures of mito dysfunction and degree of disability in CFS patients.
Mito dysfunction can easily explain the basic physical and mental fatigue, as well as the diastolic dysfunction of the heart in CFS.
To explain PEM on the basis of a mito dysfunction issue requires a mechanism that worsens the mito dysfunction as a result of placing greater demands on the mitochondria. I'm aware of two possible explanations that have been suggested:
The first is the one embodied in the book by Dr. Stephen Sinatra, called The Sinatra Solution. This explanation has been applied to CFS by Dr. Sarah Myhill. The idea is that when high demand is placed on the mitochondria for ATP, and the mitochondria are not able to keep up with this demand, some of the ADP reacts with other ADP, producing ATP plus AMP. This supplies some ATP temporarily, but the AMP breaks down to adenosine and exits from the cell. Thus, the cell has to start from scratch to build new ADP, and this is a slow process, requiring synthesis of D-ribose. This time lag is what gives rise to the PEM under this hypothesis.
The second is one I suggested several years ago, and I think it may still have some viability. The idea is that the mitos are in a state of oxidative stress, as we know. In my hypothesis, this is due to depletion of glutathione. Others have different views as to the cause of the oxidative stress, including Prof. Pall and Dr. Cheney. Nevertheless, I think we agree that there is oxidative stress, as has been shown by many measurements. It is known that the most vulnerable molecules in the mitochondria to oxidative stress are the unsaturated fatty acids in the phospholipid membranes of the mitochondria. These membranes are very important to the production of ATP, because this is carried out by enzymes that are embedded in these membranes. When higher demands for ATP are placed on the mitochondria, the state of oxidative stress worsens, because oxidizing free radicals are a normal product of metabolism, and higher the metabolic rate, the higher the oxidative stress, when glutathione is depleted and thus the antioxidant enzyme system is dysfunctional. I have suggested that this extra demand thus produces more damage to the mito membranes. The cells are able to repair this damage, at least to some extent, but this takes time. I suggest that that delayed repair process could account for PEM, and that this would be consistent with other things we know about the mitochondria in CFS.
Anyway, thank you for writing about a very important aspect of CFS, and I hope your effort attracts more attention to this aspect of CFS, because I think it holds the key to developing a better understanding of this disorder.
Best regards,
Rich Van Konynenburg
I enjoyed your articles on PEM.
I would like to enlarge a little on the cardiovascular/energy system aspect that you mentioned.
The observed low oxygen consumption, high lactate and oxidative stress in CFS all point to problems with the mitochondria. There is abundant evidence for mito dysfunction in CFS. The most direct evidence is the work of Dr. John McLaren Howard of AcumenLab in the UK. Some of this was described in the paper by Myhill, Booth and Howard showing a correlation between lab measures of mito dysfunction and degree of disability in CFS patients.
Mito dysfunction can easily explain the basic physical and mental fatigue, as well as the diastolic dysfunction of the heart in CFS.
To explain PEM on the basis of a mito dysfunction issue requires a mechanism that worsens the mito dysfunction as a result of placing greater demands on the mitochondria. I'm aware of two possible explanations that have been suggested:
The first is the one embodied in the book by Dr. Stephen Sinatra, called The Sinatra Solution. This explanation has been applied to CFS by Dr. Sarah Myhill. The idea is that when high demand is placed on the mitochondria for ATP, and the mitochondria are not able to keep up with this demand, some of the ADP reacts with other ADP, producing ATP plus AMP. This supplies some ATP temporarily, but the AMP breaks down to adenosine and exits from the cell. Thus, the cell has to start from scratch to build new ADP, and this is a slow process, requiring synthesis of D-ribose. This time lag is what gives rise to the PEM under this hypothesis.
The second is one I suggested several years ago, and I think it may still have some viability. The idea is that the mitos are in a state of oxidative stress, as we know. In my hypothesis, this is due to depletion of glutathione. Others have different views as to the cause of the oxidative stress, including Prof. Pall and Dr. Cheney. Nevertheless, I think we agree that there is oxidative stress, as has been shown by many measurements. It is known that the most vulnerable molecules in the mitochondria to oxidative stress are the unsaturated fatty acids in the phospholipid membranes of the mitochondria. These membranes are very important to the production of ATP, because this is carried out by enzymes that are embedded in these membranes. When higher demands for ATP are placed on the mitochondria, the state of oxidative stress worsens, because oxidizing free radicals are a normal product of metabolism, and higher the metabolic rate, the higher the oxidative stress, when glutathione is depleted and thus the antioxidant enzyme system is dysfunctional. I have suggested that this extra demand thus produces more damage to the mito membranes. The cells are able to repair this damage, at least to some extent, but this takes time. I suggest that that delayed repair process could account for PEM, and that this would be consistent with other things we know about the mitochondria in CFS.
Anyway, thank you for writing about a very important aspect of CFS, and I hope your effort attracts more attention to this aspect of CFS, because I think it holds the key to developing a better understanding of this disorder.
Best regards,
Rich Van Konynenburg
Proponents of the kinesiophobia theory seem to lack courage in their convictions. If they were consistent, they would make an argument that cardiac arrest syndrome is an extreme case of chronic fatigue syndrome in which the patient ceases to move at all.