Exercise

[Guest tearose]

Thank you for your compassion. In spite of the challenges, I keep a positive attitude and use reasonable caution.

( MomtoG, It sounds like your friend has to use the same caution as I do.)

The thread topic of how important exercise is in staying conditioned is valid.

From my experience, it is very important to make clear that there is a problem with lack of adequate blood supply in some of us that leads to disaster if we push to hard.

(futurehope, yes, I actually tore my muscle away from the back wall, internally!)

best regards,

tearose

[MomtoGiuliana]

Yes, in my friend's case it is due to lack of adequate blood and oxygen supply to muscles. That's my understanding from what she told me.

[Dizzysillyak]

I admit I didn't read all of this thread but I wanted to add that I did PT for OI for a couple of months. We only worked on my lower body though and it didn't help my OI at all. I gained muscle strength in my legs of course, but I still got fuzzy headed and winded after 20 minutes of walking / running errands.

One thing I found very interesting was that I could ride the recument bike for a whole 10 minutes only if I rode it very very very slowly. When I tried riding it at full speed, my leg muscles went into spasm and I had to quit. If I rode it a little slower, I got winded and my vision got fuzzy and I had to quit ... only at a very very slow pace could my body keep up ...

My PT said it's because my body couldn't replenish the blood in my muscles like it should ... Makes sense but I have no idea why. I have a Left bundle branch block which I think may be behind this though ...

[ramakentesh]

>Exercise increases the bioavailability of nitric oxide which in a subset of POTS patients was found to be inappropriately low causing increased orthostatic sympathetic activity.

Exercise improves the release, uptake and turnover of NO in the peripheral vasculature.

Inappropriate mopping up of that nitric oxide signal is an important issue, as it points to the associated problem of cleaning up energy metabolism free radicals that can cause aggregate damage in muscle and nervous system tissue.

Think: low glutathione status.

Not even close Im afraid... we are talking neuronal nitric oxide deficits here and not endothelial or plasma nitric oxide.

Low glutathione status seems unlikely given that the contention that nitric oxide and superoxide is unusually HIGH in CFS patients is unlikely given that Stewart et al demonstrated was not the case and that in a subset is was unusually LOW.

Exercise increases the WHOLEBODY bioavailability of nitric oxide. But its has only been found to be abnormally low at the neuronal level and not at the endothelial level.

Unusually high levels of free radicals and oxidisive stress is again only a contention and not proven in CFS patients and in this subset of POTS patients if present are the result of elevated angiotensin II levels which result in increased oxidisive stress and reduced neuronal nitric oxide.

People often get stuck on the concept that energy production is the primary problem. Its not - its the impaired cerebral blood perfusion that causes nearly all the symptoms of POTS and in many cases CFS.

As for peripheral resistance - increases peripheral resistance in POTS results either from hypersensitivity due to angiotensin II mediated potentiation of norepinephrine or it results from impaired clearance of Nor at the synaptic cleft.

[ramakentesh]

An aside: I've been reading this forum on an off for a while. You have a couple of members who have come tantalizingly close to the central metabolic pathway issues underlying the vast majority of autonomic system disorders, back in late 2006 and as late as 2008. For some reason, these clever members put out the critical pointers in posts meet with dead silence from the rest of you.

I find that curious.

I find it curious that people talk definitively about something as if they have access to information that is beyond the scope of us less learned and then in other posts makes statements that suggest otherwise.

Ill give you an answer: Chronic inflammation (long term infection? autoimmunity?), abnormal local vasoactive inate immune responses, aberant promoter hypermethylation of the NET gene, impaired norepinephrine reuptake, impaired angiotensin II catabolism, impaired cerebral vascular control, postural parasympathetic withdrawal, reduced expression of alpha 3 receptors due to a possible autoimmune reaction, unusual blood vessel permiability in the stomach, primary sympathetic activation caused by brainstem disfunction. etc etc.

Each of these guys has some credible research behind it. The kind that gets reviewed.

[ramakentesh]

tearose- to quote a leading doctor in orthostatic intolerance at the moment - 'exercise may be helpful in some, but definately not all, forms of POTS.'

[Mrs. Burschman]

Thank you, Ramakentesh! I wanted to protest a previous post, but wasn't sure how to go about it. I'm glad you did it.

[lmt033167]

I'm glad to read about exercise and ans problems - I have NCS and OI and I thought my problems with exercise was all due to cardiac related issues.

My cardiologist told me not to exercise for now, it's making me worse and causes my heart and ans to do weird things. UGH how do I combat 6k of sodium and fluid retention daily with anything other than exercise... fluids aren't doing it - when I am awake I have something to drink, I drink at least 10-12 20oz water a day - I feel like I'm floating or like I could float the worlds largest cruise ship lol

heck why do I even want to bother with exercise when all it does is make me SICK and tired for days after I try anything. 6 or 8 months ago I was walking/running 5-7 times a week; sometimes more and now I can't even walk on my treadmill.