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Exercise Alters Gene Expression Of Adrenergic Receptors In People With Chronic Fatigue Syndrome


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A husband/wife team of scientists in Utah recently have been working on developing diagnostic markers for chronic fatigue syndrome. Story here.

I was reading up on the studies they have done and came across this one. There were some interesting findings:

No gene expression changes occurred following exercise in controls. In 71% of patients with CFS, moderate exercise increased most sensory and adrenergic receptor's and one cytokine gene's transcription for 48h. These postexercise increases correlated with behavioural measures of fatigue and pain. In contrast, for the other 29% of patients with CFS, adrenergic α-2A receptor's transcription was decreased at all time-points after exercise; other genes were not altered. History of orthostatic intolerance was significantly more common in the α-2A decrease subgroup.

So, I have no idea what that means in terms of POTS and OI, but I'm wondering of the blanket recommendation for exercise may be contraindicated as it may be interfering with the receptors' activity, especially for the second group. Also, it's a small study so take it with a grain of salt. (And fluids! ha!)

General stuff on adrenergic receptors: http://www.dysautonomiainternational.org/blog/wordpress/new-evidence-of-autoimmunity-in-pots/

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What does this article mean to the non-scientific reader. It sounds like CFS patients exercised and the result fell into 2 groups. One group had orthotstatic intolerance? Do we know if the orthostatic intolerance is ongoing or just after the exercise?

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What does this article mean to the non-scientific reader. It sounds like CFS patients exercised and the result fell into 2 groups. One group had orthotstatic intolerance? Do we know if the orthostatic intolerance is ongoing or just after the exercise?

I'm not sure exactly what it means, and I don't know if the researchers do either. I posted it because there seem to be a handful of people here with CFS and they might be interested.

The researchers hypothesize that is a compensatory response. This is from the full paper (here):

The large decreases in α-2A mRNA may reflect a particular type of dysregulation of the sympathetic nervous system. For example, activation of α-2A normally causes a decrease in sympathetic outflow (decreased release of norepinephrine). It is possible that the decrease in transcription of α-2A observed is a response to abnormally low levels of sympathetic outflow (or low levels of vascular and cardiac responses to norepinephrine), and resulting decreased cardiac output and possibly global vasodilatation. These effects would cause inadequate blood flow to working muscles and the brain. Thus, this decrease in α-2A transcription may be an attempt to compensate for a dysfunctional sympathetic response (by increasing norepinephrine release) that does not adequately increase blood flow to working muscles and the brain during and following exercise.

So, essentially they don't know for sure but they cited some other studies showing poor autonomic function in peripheral muscle and cardiovascular response to standing in CFS. So, that would be the cause, and the gene expression would be the effect in response to help the body during exertion. But, not everyone who has CFS also have POTS/OI. In the group that showed cytokine expression and changes in all of the adrenergic receptors, 24% had orthostatic intolerance, while 71% did in the decreased α-2A group, yet non-OI people were still having changes in gene expression.

Yeah, generally people who have POTS/OI in CFS have it all the time, but it pretty much all symptoms are more pronounced after exercise or exertion. Anecdotally, my onset of POTS followed a particularly bad flare up of CFS symtpoms.

I'm just wondering if POTS in CFS is different than POTS for previously healthy people or those who had other health issues. It would have been interesting if they included a non-CFS POTS group!

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I was so happy to finally be able to read the research. Tyler is going to be in the bigger study that's coming up. Thanks for posting.

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The problem being it makes me wonder how they select their participants. I've had ME for 30 years and I actually improved in earlier years with diet and mild activity however the longer I have had it the nervous-system related problems became more pronounced. I have noted this has happened to a lot of people I know with long-term ME, the nervous system causes more problems and therefore activity becomes more of an issue.

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I was so happy to finally be able to read the research. Tyler is going to be in the bigger study that's coming up. Thanks for posting.

You meant the POTS autoantibiodies study? I am looking forward to results!

And, I am hoping for the best possible outcome for Tyler. It ***** to be an adult and struggle with debilitating health issues but for a kid who just wants to be a kid, it breaks my heart. Hope he's hanging in there.

The problem being it makes me wonder how they select their participants. I've had ME for 30 years and I actually improved in earlier years with diet and mild activity however the longer I have had it the nervous-system related problems became more pronounced. I have noted this has happened to a lot of people I know with long-term ME, the nervous system causes more problems and therefore activity becomes more of an issue.

I'm pretty sure the Lights get their patients from Lucinda Bateman, who runs one of the few clinics for CFS, and was one of the authors of the International Consensus Criteria (though she's been controversial for her role in the IOM contract), so she's probably good at selecting a cohort.

I've been following the tweets from the Invest In ME conference and Julia Newton said 89% of her ME patients have OI, and she's studying problems with muscle metabolism. It seems like autonomic nervous system dysfunction is a big under-studied part of the illness

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Yes, Robin the Pots Autoimmune antibodies. Tyler is in a study with Dr. Cunningham and is being put in the next study with Dr. Ken at OU. Tyler just had his second round of IVIG treatment. Our cardiologist is thinking that it will take at least 4 treatments of IVIG before we may see any improvement in Tyler. The anti-neuro autoantibodies have been found in Tyler's brain and heart testing. The research is very exciting and there are some other patients going through the treatment if their insurance will approve it. Our cardiologist got our insurance to approve it. I feel bad for anyone that has this condition because this is a nightmare.

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