Re: Sleep Apnea . . could it be low Glutathione?

[Guest guest]

On Aug 21, 2006, at 3:21 PM, Sue T wrote:

> Hi Rich,

>

> A couple docs have suggested I get a " Sleep Study " performed.

> Do you think there is a link due to low Gluthathione? How about a

> relationship to Neuroinflamation.

Sleep studies are reputable and important for PWCs.

Even back in 1997, when I began looking for cures, Teitelbaum was

sending people out for sleep studies as one of their very first steps.

The doctor who did my study -- one of the world's leading experts in

apnea -- said he believed that it was a significant factor in over

60% of all FM cases.

Getting my sleep fixed with CPAP (I loved your CRAP acronym -- am

gonna remember that ) was perhaps the first big breakthrough I had

with my CFS, and still one of the most important ones.

> If the brain is working correctly . . . then it will not tell the

> body to breath properly, etc. NOt to get personal, but have you

> ever got down to the bottom of why

> you have sleep apnea.

>

> Could CFS cause sleep apnea?

Yes. PWC have very messed up central nervous systems, and sleep

problems are one of the key symptoms of the disease. There are

several forms of apnea; most are treatable by knowledgeable sleep

doctors.

I don't know about glutathioine connections, but neuroinflammation in

general seems like it would play a role here.

Sara

[Guest guest]

I don't know about apnea per se, but concur, sleep disorder is at the top of

ME/CFIDS/CFS.

The number one most consistent problem is not getting the right level stage 4,

restful sleep. And the brain cannot wake up all the way either. Cannot go all

the way to sleep, cannot wake all the way up. (Ciguatera and Zombies is some

interesting reading)

Some of us are walking? around almost in theta lol.

Another very common problem is reversed circadian cycle...awake at night/sleep

in day. lots of us.

But some, up in day + nap +early to bed.

Another is inability to stay asleep once asleep. I'm not having that now...I

recently slept 15 hrs straight...twice. No sleeping pills, or aids. WHen I

remember I take 1/2 Klonopin at bedtime. I am also on Trental, but it's not for

sleep.

I used to sleep 10 hours straight every single day.

Yet other times, now, I am up sometimes almost 2 days straight...but actually

up...not trying to sleep.

Or falling asleep at keyboard...typing in my sleep...dangerous as you have seen.

So very screwy, but not the nightmare of some to sleep.

One study CFS study saw NO melatonin!. Even people in acave for 5 days would

have melatonin.

Read about " Sleep Hygiene "

That really helps. Use bedroom only for sleep, etc.

If normal people are sleep deprived for only 2 or 3 days, they experience body

pain.

Apnea is a specific problem that needs specific help. I have never been tested

for it. A " sleep " EEG was mildly abnormal in 90s.

In 1991, my friend from our support group---if people interrupted his sleep, he

met them at the door with a shotgun.

It's that precious, lack of it , that serious, pursuit of it that diligent for a

PWC LOL.

Katrina

>

> > Hi Rich,

> >

> > A couple docs have suggested I get a " Sleep Study " performed.

> > Do you think there is a link due to low Gluthathione? How about a

> > relationship to Neuroinflamation.

>

> Sleep studies are reputable and important for PWCs.

>

> Even back in 1997, when I began looking for cures, Teitelbaum was

> sending people out for sleep studies as one of their very first steps.

>

> The doctor who did my study -- one of the world's leading experts in

> apnea -- said he believed that it was a significant factor in over

> 60% of all FM cases.

>

> Getting my sleep fixed with CPAP (I loved your CRAP acronym -- am

> gonna remember that ) was perhaps the first big breakthrough I had

> with my CFS, and still one of the most important ones.

>

> > If the brain is working correctly . . . then it will not tell the

> > body to breath properly, etc. NOt to get personal, but have you

> > ever got down to the bottom of why

> > you have sleep apnea.

> >

> > Could CFS cause sleep apnea?

>

> Yes. PWC have very messed up central nervous systems, and sleep

> problems are one of the key symptoms of the disease. There are

> several forms of apnea; most are treatable by knowledgeable sleep

> doctors.

>

> I don't know about glutathioine connections, but neuroinflammation in

> general seems like it would play a role here.

>

> Sara

>

[Guest guest]

Hi Sara,

Thanks for you response and sharing your experience.

I have an appt scheduled with Kaiser. I hope they have a good program.

Sorry about the mispelling of CPAP .

Was it hard getting used to the machine?? How long did it take to feel a

difference?

Thanks again for your help.

Sue T

Mercuria <mercuria@...> wrote:

On Aug 21, 2006, at 3:21 PM, Sue T wrote:

> Hi Rich,

>

> A couple docs have suggested I get a " Sleep Study " performed.

> Do you think there is a link due to low Gluthathione? How about a

> relationship to Neuroinflamation.

Sleep studies are reputable and important for PWCs.

Even back in 1997, when I began looking for cures, Teitelbaum was

sending people out for sleep studies as one of their very first steps.

The doctor who did my study -- one of the world's leading experts in

apnea -- said he believed that it was a significant factor in over

60% of all FM cases.

Getting my sleep fixed with CPAP (I loved your CRAP acronym -- am

gonna remember that ) was perhaps the first big breakthrough I had

with my CFS, and still one of the most important ones.

> If the brain is working correctly . . . then it will not tell the

> body to breath properly, etc. NOt to get personal, but have you

> ever got down to the bottom of why

> you have sleep apnea.

>

> Could CFS cause sleep apnea?

Yes. PWC have very messed up central nervous systems, and sleep

problems are one of the key symptoms of the disease. There are

several forms of apnea; most are treatable by knowledgeable sleep

doctors.

I don't know about glutathioine connections, but neuroinflammation in

general seems like it would play a role here.

Sara

[Guest guest]

Hi Katrina and all,

Thanks for sharing too. I am surprized (maybe I missed it) that Rich has not

suggested that all PCWs have a sleep study done.

I am really curious if this could be an issue with me . . . I have a feeling

it is.

BUT, if it is the BIG questions WHY!!!???

Again. . . I want to get to the bottom(genetics, toxins, bugs, etc?). Why,

why, why??

Best wishes,

Sue T

kattemayo <kattemayo@...> wrote:

I don't know about apnea per se, but concur, sleep disorder is at the top of

ME/CFIDS/CFS.

The number one most consistent problem is not getting the right level stage 4,

restful sleep. And the brain cannot wake up all the way either. Cannot go all

the way to sleep, cannot wake all the way up. (Ciguatera and Zombies is some

interesting reading)

Some of us are walking? around almost in theta lol.

Another very common problem is reversed circadian cycle...awake at night/sleep

in day. lots of us.

But some, up in day + nap +early to bed.

Another is inability to stay asleep once asleep. I'm not having that now...I

recently slept 15 hrs straight...twice. No sleeping pills, or aids. WHen I

remember I take 1/2 Klonopin at bedtime. I am also on Trental, but it's not for

sleep.

I used to sleep 10 hours straight every single day.

Yet other times, now, I am up sometimes almost 2 days straight...but actually

up...not trying to sleep.

Or falling asleep at keyboard...typing in my sleep...dangerous as you have seen.

So very screwy, but not the nightmare of some to sleep.

One study CFS study saw NO melatonin!. Even people in acave for 5 days would

have melatonin.

Read about " Sleep Hygiene "

That really helps. Use bedroom only for sleep, etc.

If normal people are sleep deprived for only 2 or 3 days, they experience body

pain.

Apnea is a specific problem that needs specific help. I have never been tested

for it. A " sleep " EEG was mildly abnormal in 90s.

In 1991, my friend from our support group---if people interrupted his sleep, he

met them at the door with a shotgun.

It's that precious, lack of it , that serious, pursuit of it that diligent for a

PWC LOL.

Katrina

>

> > Hi Rich,

> >

> > A couple docs have suggested I get a " Sleep Study " performed.

> > Do you think there is a link due to low Gluthathione? How about a

> > relationship to Neuroinflamation.

>

> Sleep studies are reputable and important for PWCs.

>

> Even back in 1997, when I began looking for cures, Teitelbaum was

> sending people out for sleep studies as one of their very first steps.

>

> The doctor who did my study -- one of the world's leading experts in

> apnea -- said he believed that it was a significant factor in over

> 60% of all FM cases.

>

> Getting my sleep fixed with CPAP (I loved your CRAP acronym -- am

> gonna remember that ) was perhaps the first big breakthrough I had

> with my CFS, and still one of the most important ones.

>

> > If the brain is working correctly . . . then it will not tell the

> > body to breath properly, etc. NOt to get personal, but have you

> > ever got down to the bottom of why

> > you have sleep apnea.

> >

> > Could CFS cause sleep apnea?

>

> Yes. PWC have very messed up central nervous systems, and sleep

> problems are one of the key symptoms of the disease. There are

> several forms of apnea; most are treatable by knowledgeable sleep

> doctors.

>

> I don't know about glutathioine connections, but neuroinflammation in

> general seems like it would play a role here.

>

> Sara

>

[Guest guest]

On Aug 21, 2006, at 5:00 PM, Sue T wrote:

> Hi Sara,

>

> Thanks for you response and sharing your experience.

>

> I have an appt scheduled with Kaiser. I hope they have a good

> program.

They should. Kaiser's historically been pretty up on this stuff.

>

> Sorry about the mispelling of CPAP .

No, no, really -- I smiled.

> Was it hard getting used to the machine?? How long did it take to

> feel a difference?

Some people have a hard time. Much of it can be alleviated if you get

a proper-fitting mask. Some clinics just have one or two kinds of

mask, which they stick on you, take it or leave it. And, too often,

their patients leave it.

But you can look on the Web (google " CPAP Store " for one big place)

and see the wide variety of solutions there are. Dozens and dozens --

and, with persistence and a good respiratory therapist who's willing

to work it through, there's no reason you shouldn't find one that's

perfectly tolerable.

After seven years, I literally will not, can not, fall asleep without

my mask on. My body panics at the very thought. I have a permanent

dent in my forehead where the bridgepiece of my gel mask sits. I

don't care. I sleep.

I started feeling the difference after the very first night. At the

end of two weeks, my FM was pretty much gone (and I was still

sleeping 10+ hours a night -- my poor carcass couldn't get enough,

and was making up for decades of lost time.) Over the first six

weeks, I felt strikingly better day by day. By three months, my whole

body was just happier, better cognition, better organ function. It's

amazing what a difference a little sleep can make.

Not all PWCs have obstructive sleep apnea. Many have central apnea --

make sure they test for both!

Sara

[Guest guest]

Hi Sara,

Again, thanks for sharing!

Appreciate your input.

Pleasant dreams with your C__P machine! :<))

Sue T

Mercuria <mercuria@...> wrote:

On Aug 21, 2006, at 5:00 PM, Sue T wrote:

> Hi Sara,

>

> Thanks for you response and sharing your experience.

>

> I have an appt scheduled with Kaiser. I hope they have a good

> program.

They should. Kaiser's historically been pretty up on this stuff.

>

> Sorry about the mispelling of CPAP .

No, no, really -- I smiled.

> Was it hard getting used to the machine?? How long did it take to

> feel a difference?

Some people have a hard time. Much of it can be alleviated if you get

a proper-fitting mask. Some clinics just have one or two kinds of

mask, which they stick on you, take it or leave it. And, too often,

their patients leave it.

But you can look on the Web (google " CPAP Store " for one big place)

and see the wide variety of solutions there are. Dozens and dozens --

and, with persistence and a good respiratory therapist who's willing

to work it through, there's no reason you shouldn't find one that's

perfectly tolerable.

After seven years, I literally will not, can not, fall asleep without

my mask on. My body panics at the very thought. I have a permanent

dent in my forehead where the bridgepiece of my gel mask sits. I

don't care. I sleep.

I started feeling the difference after the very first night. At the

end of two weeks, my FM was pretty much gone (and I was still

sleeping 10+ hours a night -- my poor carcass couldn't get enough,

and was making up for decades of lost time.) Over the first six

weeks, I felt strikingly better day by day. By three months, my whole

body was just happier, better cognition, better organ function. It's

amazing what a difference a little sleep can make.

Not all PWCs have obstructive sleep apnea. Many have central apnea --

make sure they test for both!

Sara

[Guest guest]

Hi, Sue.

I'm glad to hear that you are getting a sleep study done.

Yes, I do think that there can be a link between low glutathione and

sleep apnea. I actually have held forth about this in the past on

the list, but I think it has been quite a while since I last did.

Here's how I think it could work, updated using information from the

ATP Profile tests and the Translocator tests from Biolab:

Glutathione causes mitochondrial dysfunction in CFS in several

ways. When the onset first occurs, the drop in glutathione in the

skeletal muscles particularly, but perhaps in some other tissues as

well, allows hydrogen peroxide to rise in concentration. Because of

what's called " product inhibition " in chemistry, this backlog causes

the superoxide dismutase reaction to slow down, and that causes the

superoxide concentration to rise in the mitochondria. Depending on

the concentration of nitric oxide, this may also cause peroxynitrite

to rise in concentration. Superoxide and possibly peroxynitrite

then react with the enzyme aconitase in the Krebs cycle, and in that

way produce a partial blockade there. This is the rapid way in

which glutathione depletion produced mitochondrial dysfunction.

In addition to this, as time goes by, with low glutathione, toxins

are allowed to build up, and they inhibit enzymes in the

mitochondria. Also, infections are allowed to get going, and it

appears that viruses are able to block the mitochondria as well.

The net effect of all these things is that the mitochondria are not

able to burn fuel to produce carbon dioxide and water, as well as to

produce ATP as well as normal. One result of this is that the cells

put carbon dioxide into the venous blood at a lower rate. This

causes the concentration of carbon dioxide to be lower in the blood,

including the arterial blood. Since the enzyme carbonic anhydrase,

which is present in the red blood cells, converts carbon dioxide to

carbonic acid, the lower carbon dioxide production will mean less

acid in the blood, so that the pH will rise somewhat above normal

(i.e. in the alkaline direction).

The respiratory center in the brainstem has the job of controlling

the rate and depth of breathing. In order to do this, it monitors

the level of carbon dioxide and the pH of the blood that it

receives. When it finds that the carbon dioxide level is lower than

its set point and the pH is higher than its set point, it cuts back

on the rate and depth of breathing. When a person is awake, they

can notice if they are short of breath (which really means short of

oxygen), and they can consciously increase their rate and depth of

breathing. However, when they are asleep, they can't do this. What

happens is that the respiratory center stops the breathing in an

effort to get the carbon dioxide level up to normal and the pH down

to normal. However, because the skeletal muscle cells are just not

putting out enough carbon dioxide, because of the mito dysfunction,

what happens is that the oxygen level in the blood drops too low

before the carbon dioxide comes up enough to satisfy the respiratory

center. This triggers an alarm reaction in the respiratory center,

because it also monitors oxygen. When this happens, a signal is

sent to the adrenal medulla to put out adrenaline. This " takes

over " control and causes the person to start breathing, sometimes

even to gasp. Sometimes there is a panic attack associated with

this, because the adrenaline goes up high.

I think that's the origin of the sleep apnea in many cases of CFS,

and it it isn't either obstructive sleep apnea or a real central

sleep apnea. I would call it a metabolic sleep apnea, but I have

just made up that term, so no one else will recognize it.

The last I heard, Kaiser gives people a recording pulse oximeter to

take home, clamp to a finger and sleep overnight with. This should

detect whether there is a sleep apnea, but I don't think it will

tell what type it is. By far most sleep apneas in the general

population are obstructive, and I think Kaiser has opted to assume

that's what it is if they detect one this way, and to give the

person a CPAP machine. In most cases, this does the job. If it

doesn't, they probably look into it further. Will a CPAP machine

help for the type of sleep apnea I've described? I think it can, but

I don't have a lot of data about that. I think it's also true that

some PWCs have obstructive sleep apnea.

The CPAP machine works well for obstructive sleep apnea, which is

the type I have. It's wonderful! You asked whether I know what

causes mine. No, I don't. I'm not particularly fat (6 feet tall,

185 pounds or so), but I do have a neck size of about 17 inches.

Men who are fat and particularly if they have a big neck size are

more at risk for obstructive sleep apnea, because there is more

tissue in their neck area to block their windpipe when they lie down

and fall asleep. Lying on the back is the worst situation. When a

person falls asleep, it's up to the autonomic nervous system to keep

the airway open. For some reason, it doen't do that so well in some

people. The back of the tongue can sag down and block the windpipe,

and other tissue can intrude as well, when the muscles in the neck

are not actively holding the airway open under the action of the

autonomic nervous system.

I hope they are able to do you some good on this issue. I can

certainly echo what Sara said about how wonderful it is to get a

CPAP machine if you really need one.

I tried several types of masks, and they have their pros and cons.

I've settled on the type that clamps on your head, and has a duct

coming down the front of your face, between your eyes. It has two

big cannulas that mate with your nostrils. My sister-in-law the

respiratory therapist refers to it as a " cannula on steroids. " She

recommended this type, but, being stubborn, I tried two other types

before this one, and I was not able to sleep on my side with either

of them, which I like to do, because the mask would come off because

it would hit the pillow. My wife is not thrilled about this one,

because it shoots air out forward, so if I'm facing her, it blows on

her and is irritating. There are some things about it that are not

ideal, but it's really great to be able to sleep soundly and wake up

feeling refreshed, without a headache and ears that sound as though

there's a threshing machine running inside them! It's also really

nice to be able to remember what happened yesterday in detail, and

to be able to drive without blanking out and running through red

lights. I am really glad my wife insisted that I get checked out.

It was really life or death, and for her, too, if she rode with me

in the car while I was driving. I really had no idea that's what I

had, but the pulmonologist I was referred to had no trouble figuring

it out.

I hope this is helpful.

Rich

>

> Hi Rich,

>

> A couple docs have suggested I get a " Sleep Study " performed.

> Do you think there is a link due to low Gluthathione? How about a

> relationship to Neuroinflamation.

>

> If the brain is working correctly . . . then it will not tell the

> body to breath properly, etc.

> NOt to get personal, but have you ever got down to the bottom of

why

> you have sleep apnea.

>

> Could CFS cause sleep apnea?

>

> I know a in Calif doc who had CFS for years and spent $300,000 on

> treatments then finally got 75% better once he figured he had

sleep

> apnea and got a CRAP(?) machine.

>

> How would this all relate?

>

> Best wishes,

> Sue T

>

[Guest guest]

Hi, Sue.

One more thing I forgot to say, which I found to be very important.

Get a chin strap to hold your mouth closed when you are sleeping.

Now, of course, I'm assuming that you can breathe through your

nose. If you can't, then you have to get a mask that covers your

mouth and your nose, and you have to get a humidifier. But if you

can breathe through your nose, just get a mask that feeds air to

your nose, such as the cannula type I mentioned, and then get a chin

strap to hold your mouth closed. If you don't have a chin strap,

what happens is that your mouth is forced open by the air pressure

coming into your nose after you fall asleep. The result is that the

CPAP machine blows air into your nose and out your mouth, and your

whole throat and mouth get very dried out. You wake up in the

middle of the night feeling like you are in the Sahara. But if you

can hold your mouth shut with a chin strap, then this doesn't

happen, and you won't have to mess with a humidifier, which is a

hassle, which cuts down on the air flow, and which has to be

cleaned, filled, etc. Avoid the humidifier by getting a chin

strap. That's my advice about that!

Rich

> >

> > Hi Rich,

> >

> > A couple docs have suggested I get a " Sleep Study " performed.

> > Do you think there is a link due to low Gluthathione? How about

a

> > relationship to Neuroinflamation.

> >

> > If the brain is working correctly . . . then it will not tell

the

> > body to breath properly, etc.

> > NOt to get personal, but have you ever got down to the bottom of

> why

> > you have sleep apnea.

> >

> > Could CFS cause sleep apnea?

> >

> > I know a in Calif doc who had CFS for years and spent $300,000

on

> > treatments then finally got 75% better once he figured he had

> sleep

> > apnea and got a CRAP(?) machine.

> >

> > How would this all relate?

> >

> > Best wishes,

> > Sue T

> >

>

[Guest guest]

Hi Sue,

Just wanted to add a few comments since I just had a sleep study done

at the Stanford Sleep Disorders Clinic. I have had CFS for 2.5 years,

but only recently started developing disrupted sleep. I thought it

might be from apnea since a couple of times I awoke gasping for

breath. Even still, they were very iffy about giving me the study

since they told me that apnea doesn't just come on suddenly, but

occurs gradually over time. If you don't snore and don't have

excessive sleepiness during the day, you apparantly aren't a likely

candidate. You can get a list of symptoms online to help you decide

if you are candidate.

Based on Rich's comment that Kaiser gives you a home test, I would

press for an overnight study where they can monitor you. I tried to

get a take home test from Stanford, but they said it isn't as accurate

and not as helpful - at home test measures 4 things, while in the

clinic they can measure 16 things. I imagine Kaiser gives you the

take home test to save money - the sleep clinic was $6,000.

As it turns out, they were right and I don't have apnea, but what they

did find out was that I have pretty severe limb movement, something

that a home test won't tell you. I am waiting for the complete write

up to see everything else.

Cheers,

Chris

> The last I heard, Kaiser gives people a recording pulse oximeter to

> take home, clamp to a finger and sleep overnight with. This should

> detect whether there is a sleep apnea, but I don't think it will

> tell what type it is. By far most sleep apneas in the general

> population are obstructive, and I think Kaiser has opted to assume

> that's what it is if they detect one this way, and to give the

> person a CPAP machine. In most cases, this does the job. If it

> doesn't, they probably look into it further. Will a CPAP machine

> help for the type of sleep apnea I've described? I think it can, but

> I don't have a lot of data about that. I think it's also true that

> some PWCs have obstructive sleep apnea.

[Guest guest]

>I think that's the origin of the sleep apnea in many cases of CFS,

>and it it isn't either obstructive sleep apnea or a real central

>sleep apnea. I would call it a metabolic sleep apnea, but I have

>just made up that term, so no one else will recognize it.

Rich,

I had them for years, very scary, they were not obstructive apnea (I am thin and

husband says I don't snore). I sure can relate to what you are describing and I

like the name " metabolic sleep apnea " . I called them WIFs (for Wake In Fright).

>In addition to this, as time goes by, with low glutathione, toxins

>are allowed to build up, and they inhibit enzymes in the

>mitochondria. Also, infections are allowed to get going, and it

>appears that viruses are able to block the mitochondria as well.

Long term abx cured me of that. Glutathione might've cured me as it might've

helped me fight my infections. Chiken or egg?

Nelly

[Guest guest]

Hi Rich,

Does this all then imply that those with this problem (metabolic sleep

disorder) would have alkaline pH due to low carbon dioxide ? I ask b/c

I have this and my blood pH is not alkaline, if anything, it is a bit

too acidic. Is the low carbon dioxide the main factor or the pH ?

Re: Sleep Apnea . . could it be low

Glutathione?

Hi, Sue.

I'm glad to hear that you are getting a sleep study done.

Yes, I do think that there can be a link between low glutathione and

sleep apnea. I actually have held forth about this in the past on

the list, but I think it has been quite a while since I last did.

Here's how I think it could work, updated using information from the

ATP Profile tests and the Translocator tests from Biolab:

Glutathione causes mitochondrial dysfunction in CFS in several

ways. When the onset first occurs, the drop in glutathione in the

skeletal muscles particularly, but perhaps in some other tissues as

well, allows hydrogen peroxide to rise in concentration. Because of

what's called " product inhibition " in chemistry, this backlog causes

the superoxide dismutase reaction to slow down, and that causes the

superoxide concentration to rise in the mitochondria. Depending on

the concentration of nitric oxide, this may also cause peroxynitrite

to rise in concentration. Superoxide and possibly peroxynitrite

then react with the enzyme aconitase in the Krebs cycle, and in that

way produce a partial blockade there. This is the rapid way in

which glutathione depletion produced mitochondrial dysfunction.

In addition to this, as time goes by, with low glutathione, toxins

are allowed to build up, and they inhibit enzymes in the

mitochondria. Also, infections are allowed to get going, and it

appears that viruses are able to block the mitochondria as well.

The net effect of all these things is that the mitochondria are not

able to burn fuel to produce carbon dioxide and water, as well as to

produce ATP as well as normal. One result of this is that the cells

put carbon dioxide into the venous blood at a lower rate. This

causes the concentration of carbon dioxide to be lower in the blood,

including the arterial blood. Since the enzyme carbonic anhydrase,

which is present in the red blood cells, converts carbon dioxide to

carbonic acid, the lower carbon dioxide production will mean less

acid in the blood, so that the pH will rise somewhat above normal

(i.e. in the alkaline direction).

The respiratory center in the brainstem has the job of controlling

the rate and depth of breathing. In order to do this, it monitors

the level of carbon dioxide and the pH of the blood that it

receives. When it finds that the carbon dioxide level is lower than

its set point and the pH is higher than its set point, it cuts back

on the rate and depth of breathing. When a person is awake, they

can notice if they are short of breath (which really means short of

oxygen), and they can consciously increase their rate and depth of

breathing. However, when they are asleep, they can't do this. What

happens is that the respiratory center stops the breathing in an

effort to get the carbon dioxide level up to normal and the pH down

to normal. However, because the skeletal muscle cells are just not

putting out enough carbon dioxide, because of the mito dysfunction,

what happens is that the oxygen level in the blood drops too low

before the carbon dioxide comes up enough to satisfy the respiratory

center. This triggers an alarm reaction in the respiratory center,

because it also monitors oxygen. When this happens, a signal is

sent to the adrenal medulla to put out adrenaline. This " takes

over " control and causes the person to start breathing, sometimes

even to gasp. Sometimes there is a panic attack associated with

this, because the adrenaline goes up high.

I think that's the origin of the sleep apnea in many cases of CFS,

and it it isn't either obstructive sleep apnea or a real central

sleep apnea. I would call it a metabolic sleep apnea, but I have

just made up that term, so no one else will recognize it.

The last I heard, Kaiser gives people a recording pulse oximeter to

take home, clamp to a finger and sleep overnight with. This should

detect whether there is a sleep apnea, but I don't think it will

tell what type it is. By far most sleep apneas in the general

population are obstructive, and I think Kaiser has opted to assume

that's what it is if they detect one this way, and to give the

person a CPAP machine. In most cases, this does the job. If it

doesn't, they probably look into it further. Will a CPAP machine

help for the type of sleep apnea I've described? I think it can, but

I don't have a lot of data about that. I think it's also true that

some PWCs have obstructive sleep apnea.

The CPAP machine works well for obstructive sleep apnea, which is

the type I have. It's wonderful! You asked whether I know what

causes mine. No, I don't. I'm not particularly fat (6 feet tall,

185 pounds or so), but I do have a neck size of about 17 inches.

Men who are fat and particularly if they have a big neck size are

more at risk for obstructive sleep apnea, because there is more

tissue in their neck area to block their windpipe when they lie down

and fall asleep. Lying on the back is the worst situation. When a

person falls asleep, it's up to the autonomic nervous system to keep

the airway open. For some reason, it doen't do that so well in some

people. The back of the tongue can sag down and block the windpipe,

and other tissue can intrude as well, when the muscles in the neck

are not actively holding the airway open under the action of the

autonomic nervous system.

I hope they are able to do you some good on this issue. I can

certainly echo what Sara said about how wonderful it is to get a

CPAP machine if you really need one.

I tried several types of masks, and they have their pros and cons.

I've settled on the type that clamps on your head, and has a duct

coming down the front of your face, between your eyes. It has two

big cannulas that mate with your nostrils. My sister-in-law the

respiratory therapist refers to it as a " cannula on steroids. " She

recommended this type, but, being stubborn, I tried two other types

before this one, and I was not able to sleep on my side with either

of them, which I like to do, because the mask would come off because

it would hit the pillow. My wife is not thrilled about this one,

because it shoots air out forward, so if I'm facing her, it blows on

her and is irritating. There are some things about it that are not

ideal, but it's really great to be able to sleep soundly and wake up

feeling refreshed, without a headache and ears that sound as though

there's a threshing machine running inside them! It's also really

nice to be able to remember what happened yesterday in detail, and

to be able to drive without blanking out and running through red

lights. I am really glad my wife insisted that I get checked out.

It was really life or death, and for her, too, if she rode with me

in the car while I was driving. I really had no idea that's what I

had, but the pulmonologist I was referred to had no trouble figuring

it out.

I hope this is helpful.

Rich

[Guest guest]

Hi, .

I think there are other things that can affect the blood pH as well,

such as lactic acid, if it's elevated. Some people who have

mitochondrial dysfunction have elevated lactic acid, but that doesn't

appear to be true of you, based on your organic acids analysis.

I must have forgotten your blood pH. It's probably buried in the

file. When was it measured, and what was the value? Was it venous or

arterial pH?

I'm not sure what dominates in the respiratory center. I think it

looks at both CO2 level and pH. I'll have to dig into that some

more.

Rich

>

> Hi Rich,

>

> Does this all then imply that those with this problem (metabolic

sleep

> disorder) would have alkaline pH due to low carbon dioxide ? I ask

b/c

> I have this and my blood pH is not alkaline, if anything, it is a bit

> too acidic. Is the low carbon dioxide the main factor or the pH ?

>

>

>

>

[Guest guest]

Hi

Thanks for your response.

I will comment below

Hi Sue,

>

> Just wanted to add a few comments since I just had a sleep study

done

> at the Stanford Sleep Disorders Clinic. I have had CFS for 2.5

years,

> but only recently started developing disrupted sleep. I thought it

> might be from apnea since a couple of times I awoke gasping for

> breath.

*** Yes that is what I do and have been doing a couple times a

month for a few years. Sometimes I wake up witha spasm in my throat

and can not stop coughing(I never or rarely cough during the day)

Even still, they were very iffy about giving me the study

> since they told me that apnea doesn't just come on suddenly, but

> occurs gradually over time.

**** Yes, that is me!

If you don't snore and don't have

> excessive sleepiness during the day, you apparantly aren't a likely

> candidate. You can get a list of symptoms online to help you

decide

> if you are candidate.

*** I do snore I will look up more symptoms online . . .Thanks

>

> Based on Rich's comment that Kaiser gives you a home test, I would

> press for an overnight study where they can monitor you. I tried

to

> get a take home test from Stanford, but they said it isn't as

accurate

> and not as helpful - at home test measures 4 things, while in the

> clinic they can measure 16 things. I imagine Kaiser gives you the

> take home test to save money - the sleep clinic was $6,000.

*** Yes . .. it's all about money with Kaiser. I figure I will try

this first and if tKaiser does not find anything I will push harder

there or elsewhere.

>

> As it turns out, they were right and I don't have apnea, but what

they

> did find out was that I have pretty severe limb movement, something

> that a home test won't tell you. I am waiting for the complete

write

> up to see everything else.

**Please keep us posted and glad you do not have sleep apnea!

Best wishes,

Sue T

>

> Cheers,

>

> Chris

>

>

> > The last I heard, Kaiser gives people a recording pulse oximeter

to

> > take home, clamp to a finger and sleep overnight with. This

should

> > detect whether there is a sleep apnea, but I don't think it will

> > tell what type it is. By far most sleep apneas in the general

> > population are obstructive, and I think Kaiser has opted to

assume

> > that's what it is if they detect one this way, and to give the

> > person a CPAP machine. In most cases, this does the job. If it

> > doesn't, they probably look into it further. Will a CPAP

machine

> > help for the type of sleep apnea I've described? I think it can,

but

> > I don't have a lot of data about that. I think it's also true

that

> > some PWCs have obstructive sleep apnea.

>

[Guest guest]

Hi Rich,

There you go again . . . with a wonderful detailed explaination! You are

GREAT!

Thank you for all your suggestions, too.

It was very helpful and I have it filed away for future reference.

Best Wishes, Sue T

rvankonynen <richvank@...> wrote:

Hi, Sue.

One more thing I forgot to say, which I found to be very important.

Get a chin strap to hold your mouth closed when you are sleeping.

Now, of course, I'm assuming that you can breathe through your

nose. If you can't, then you have to get a mask that covers your

mouth and your nose, and you have to get a humidifier. But if you

can breathe through your nose, just get a mask that feeds air to

your nose, such as the cannula type I mentioned, and then get a chin

strap to hold your mouth closed. If you don't have a chin strap,

what happens is that your mouth is forced open by the air pressure

coming into your nose after you fall asleep. The result is that the

CPAP machine blows air into your nose and out your mouth, and your

whole throat and mouth get very dried out. You wake up in the

middle of the night feeling like you are in the Sahara. But if you

can hold your mouth shut with a chin strap, then this doesn't

happen, and you won't have to mess with a humidifier, which is a

hassle, which cuts down on the air flow, and which has to be

cleaned, filled, etc. Avoid the humidifier by getting a chin

strap. That's my advice about that!

Rich

> >

> > Hi Rich,

> >

> > A couple docs have suggested I get a " Sleep Study " performed.

> > Do you think there is a link due to low Gluthathione? How about

a

> > relationship to Neuroinflamation.

> >

> > If the brain is working correctly . . . then it will not tell

the

> > body to breath properly, etc.

> > NOt to get personal, but have you ever got down to the bottom of

> why

> > you have sleep apnea.

> >

> > Could CFS cause sleep apnea?

> >

> > I know a in Calif doc who had CFS for years and spent $300,000

on

> > treatments then finally got 75% better once he figured he had

> sleep

> > apnea and got a CRAP(?) machine.

> >

> > How would this all relate?

> >

> > Best wishes,

> > Sue T

> >

>

[Guest guest]

Rich

It's been a while since I've studied the Krebs cycle and the ETC,

but I don't see how CO2 production and O2 consumption can be

decoupled, as your model implies. That is, you say that CO2

production is reduced in PWCs relative to their O2 consumption. How

do you think the TCA and ETC permit that?

You say that the blockade inhibits the ability of the mitochondria

to " burn fuel to produce carbon dioxide and water... "

Isn't the water produced when oxygen is consumed?

" ...the stepwise transfer of electrons from NADH (and FADH2) to

oxygen molecules to form (with the aid of protons) water molecules

(H2O) "

quoted from:

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CellularResp

iration.html

What, then, do you propose is consuming the O2, if not the ETC (with

concomitant production of water)?

And how do you propose that oxygen is consumed without the usual

production of CO2? Isn't O2 consumed in the ETC when the ETC is fed

NADH and FADH2? And aren't NADH and FADH2 produced in conjunction

with the production of CO2? The consumption of O2 seems coupled to

the production of CO2. How are they decoupled in your mind? Since

CO2 production occurs upstream of O2 consumption, I could envision

some production of CO2 in the absence of O2 consumption (for a

while) if the ETC were blocked. But your proposing the opposite.

It would help if you gave an explanation with the aid of a diagram,

as seen in the URL I provided.

Matt

>

>

> The net effect of all these things is that the mitochondria are

not

> able to burn fuel to produce carbon dioxide and water, as well as

to

> produce ATP as well as normal. One result of this is that the

cells

> put carbon dioxide into the venous blood at a lower rate. This

> causes the concentration of carbon dioxide to be lower in the

blood,

> including the arterial blood.

However, because the skeletal muscle cells are just not

> putting out enough carbon dioxide, because of the mito

dysfunction,

> what happens is that the oxygen level in the blood drops too low

> before the carbon dioxide comes up enough to satisfy the

respiratory

> center.

>

> Rich

>

[Guest guest]

Hi, Matt.

Thanks for the comments.

Sorry for the confusion. What I'm suggesting is that in CFS, the

organs do not all behave the same, in terms of how successfully they

can carry on oxidative metabolism. When there is a system-wide

scarcity of glutathione, some organs, tissues, and cells go low in

it earlier than others, because there is a built-in priority system

that is based on a combination of different degrees of access to

amino acid substrates (particularly cysteine, the rate-limiting

substrate for making glutathione) coming in from the diet (the gut

and the liver having priority here) and different degrees of gene

expression for the rate limiting enzyme for making glutathione

(glutamate cysteine ligase) for different cell types, in which the

cells of the heart and other vital organs excel. The skeletal

muscles are at the low end of the totem pole, and when the onset of

CFS occurs, they go low in glutathione first, producing the physical

fatigue. The fatigue is also the last thing to recover on the way

back up, when system-wide glutathione is building, for the same

reason.

The blood from all the organs is mixed together as it passes through

the circulatory system, so the carbon dioxide level that is sensed

by the respiratory center in the brainstem reflects an average of

the production of all the organs. Since the skeletal muscle cells

represent a large fraction of the total cellular mass, when they

produce significantly less CO2 because their Krebs cycles are

blocked as a result of their glutathione depletion, it shows up in

the average value of the blood. And of course, as you point out,

they also require less oxygen than normal. Incidentally, this is

the reason why Dr. Cheney finds that when he puts a pulse oximeter

on a PWC and has them hold their breath for a while, their arterial

oxygen percent saturation does not drop as fast as that of a normal,

healthy person. Their skeletal muscles are not using oxygen as fast

as normal.

Meanwhile, the brain and other vital organs are still trying to

conduct business as usual in terms of oxidative metabolism. That's

the reason PWCs are able to stay alive, even though they are

physically very fatigued. These organs still do need oxygen, though

perhaps not as much as usual, and the respiratory center in the

brain still has a low-oxygen trip point that will call for

adrenaline if the oxygen gets too low, in order to save the person's

life. So it goes along doing its usual job, trying to correct the

low carbon dioxide level that is produced by the low oxidative

metabolism in the skeletal muscles by slowing and shallowing the

breathing, until this gets so low that it causes the oxygen level in

the arterial blood to get too low, and that triggers the adrenaline.

In some ways it's like a government in a country. Different people

have different needs and desires, but they are all in the same

country, and there has to be one government. The more alike the

people are in terms of their opinions about things the more in

agreement they are, the easier job the government has. But when

there get to be major extremes, it becomes much more difficult to

govern, because there is less agreement among the people.

Rich

> >

>

> >

> > The net effect of all these things is that the mitochondria are

> not

> > able to burn fuel to produce carbon dioxide and water, as well

as

> to

> > produce ATP as well as normal. One result of this is that the

> cells

> > put carbon dioxide into the venous blood at a lower rate. This

> > causes the concentration of carbon dioxide to be lower in the

> blood,

> > including the arterial blood.

>

>

>

> However, because the skeletal muscle cells are just not

> > putting out enough carbon dioxide, because of the mito

> dysfunction,

> > what happens is that the oxygen level in the blood drops too low

> > before the carbon dioxide comes up enough to satisfy the

> respiratory

> > center.

>

> >

> > Rich

> >

>

[Guest guest]

Rich

You're saying that the respiratory center in the brain responds both

to elevated levels of CO2 and reduced levels of O2, and that the

concentration of CO2 in the blood reflects an average of the

production of all the organs. Doesn't the concentration of O2

likewise reflect an average of the consumption of O2 by all organs?

As you say, the respiratory center in the brain responds to the

levels of CO2 and O2. Why would it matter what the various

contributions of CO2 production and O2 consumption are by the

various tissues? If the respiratory center responds to blood

levels, why discuss specific tissues?

You're implying that PWCs consume O2 more rapidly than they produce

CO2. PWCs rely, in your view, more on low O2 to trigger ventilation

than on elevated CO2. You're appealing to the Krebs cycle and the

ETC to support your model. How do you propose that the consumption

of O2 and the production of CO2 are decoupled in PWCs?

Matt

[Guest guest]

Hi, Matt.

>

> Rich

>

> You're saying that the respiratory center in the brain responds

both

> to elevated levels of CO2 and reduced levels of O2, and that the

> concentration of CO2 in the blood reflects an average of the

> production of all the organs.

***I believe that's true. The respiratory center normally controls

the breathing on the basis of CO2 level and pH of the arterial blood

it receives. It pays attention to oxygen only if the O2 level drops

pretty low, to the alarm level.

Doesn't the concentration of O2

> likewise reflect an average of the consumption of O2 by all organs?

***It reflects both the overall rate of consumption of oxygen as

well as the rate at which oxygen comes in from the lungs, which is

affected by the rate and depth of breathing.

>

> As you say, the respiratory center in the brain responds to the

> levels of CO2 and O2.

***Yes, but see above. It normally only regulates on CO2 and pH.

Oxygen level normally only comes into play in a low alarm situation.

Why would it matter what the various

> contributions of CO2 production and O2 consumption are by the

> various tissues? If the respiratory center responds to blood

> levels, why discuss specific tissues?

***What I meant to emphasize is that even though the skeletal

muscles don't have as large a demand for oxygen in CFS as normal,

the respiratory center setpoint for the low oxygen alarm is at the

same level as normal. What I meant to say was that it's a good

thing that this is true, because even though the skeletal muscles do

not need as much oxygen as normal, the vital organs still do need

normal levels of oxygen. This mechanism keeps the PWC alive, even

though it's a rather jerky control. Normally this control system

runs smoothly, but in some PWCs, it keeps bouncing off the low alarm

level for oxygen, because it is unable to bring its usual controlled

variable, CO2 partial pressure, into the normal range.

***The problem with breathing regulation in CFS is that since the

muscles aren't producing much CO2, the usual regulatory mechanism of

slowing the breathing doesn't raise the CO2 level as much as it

normally would. The result is that the regulatory center makes the

breathing slower and shallower in an attempt to get the CO2 level up

to the normal range, and it eventually hits the low oxygen alarm

point before it is able to correct the CO2 level.

>

> You're implying that PWCs consume O2 more rapidly than they

produce

> CO2.

***I don't mean to imply that. I'm really not talking about

relative consumption of O2 and production of CO2 at all. What I'm

talking about is the levels of O2 and CO2 in the blood, in terms of

partial pressures, and the lack of correspondence of the different

set points for CO2 regulation and low O2 alarm on the control system

that regulates rate and depth of breathing. The control system does

not control on amounts of O2 used or CO2 produced. It controls on

the levels of these substances in the blood. This is kind of a

tricky concept. The thing that really makes it tricky is that the

actuator of the control system (the lungs) affects not only the

controlled variable, which is CO2 partial pressure, but it also

oppositely affects another variable that triggers the alarm

interlock on the control system, which is oxygen partial pressure,

which is set at a level that does not correspond to the set range of

CO2. Since the set points do not correspond to the same level of O2

utilization--CO2 production (which I agree must correspond to each

other), they don't come into play at the same levels. This has

nothing to do with the stoichiometry or coupling of actual amounts

of O2 used and CO2 produced.

PWCs rely, in your view, more on low O2 to trigger ventilation

> than on elevated CO2.

***I think that's only true if they have developed this kind of

sleep apnea. Not all PWCs suffer from this. I think it depends on

the degree of mitochondrial dysfunction in the skeletal muscles.

This represents a failure mode for the normal control system. In a

normal, healthy person, the low oxygen alarm never comes into play,

because controlling on the CO2 level does not normally require

shutting down the breathing enough to trigger this alarm.

You're appealing to the Krebs cycle and the

> ETC to support your model. How do you propose that the

consumption

> of O2 and the production of CO2 are decoupled in PWCs?

***I'm actually not proposing that. I hope that what I said above

will make this clearer.

>

> Matt

>

***Rich

[Guest guest]

Hi, Matt.

>

> Rich

>

> You're saying that the respiratory center in the brain responds

both

> to elevated levels of CO2 and reduced levels of O2, and that the

> concentration of CO2 in the blood reflects an average of the

> production of all the organs.

***I believe that's true. The respiratory center normally controls

the breathing on the basis of CO2 level and pH of the arterial blood

it receives. It pays attention to oxygen only if the O2 level drops

pretty low, to the alarm level.

Doesn't the concentration of O2

> likewise reflect an average of the consumption of O2 by all organs?

***It reflects both the overall rate of consumption of oxygen as

well as the rate at which oxygen comes in from the lungs, which is

affected by the rate and depth of breathing.

>

> As you say, the respiratory center in the brain responds to the

> levels of CO2 and O2.

***Yes, but see above. It normally only regulates on CO2 and pH.

Oxygen level normally only comes into play in a low alarm situation.

Why would it matter what the various

> contributions of CO2 production and O2 consumption are by the

> various tissues? If the respiratory center responds to blood

> levels, why discuss specific tissues?

***What I meant to emphasize is that even though the skeletal

muscles don't have as large a demand for oxygen in CFS as normal,

the respiratory center setpoint for the low oxygen alarm is at the

same level as normal. What I meant to say was that it's a good

thing that this is true, because even though the skeletal muscles do

not need as much oxygen as normal, the vital organs still do need

normal levels of oxygen. This mechanism keeps the PWC alive, even

though it's a rather jerky control. Normally this control system

runs smoothly, but in some PWCs, it keeps bouncing off the low alarm

level for oxygen, because it is unable to bring its usual controlled

variable, CO2 partial pressure, into the normal range.

***The problem with breathing regulation in CFS is that since the

muscles aren't producing much CO2, the usual regulatory mechanism of

slowing the breathing doesn't raise the CO2 level as much as it

normally would. The result is that the regulatory center makes the

breathing slower and shallower in an attempt to get the CO2 level up

to the normal range, and it eventually hits the low oxygen alarm

point before it is able to correct the CO2 level.

>

> You're implying that PWCs consume O2 more rapidly than they

produce

> CO2.

***I don't mean to imply that. I'm really not talking about

relative consumption of O2 and production of CO2 at all. What I'm

talking about is the levels of O2 and CO2 in the blood, in terms of

partial pressures, and the lack of correspondence of the different

set points for CO2 regulation and low O2 alarm on the control system

that regulates rate and depth of breathing. The control system does

not control on amounts of O2 used or CO2 produced. It controls on

the levels of these substances in the blood. This is kind of a

tricky concept. The thing that really makes it tricky is that the

actuator of the control system (the lungs) affects not only the

controlled variable, which is CO2 partial pressure, but it also

oppositely affects another variable that triggers the alarm

interlock on the control system, which is oxygen partial pressure,

which is set at a level that does not correspond to the set range of

CO2. Since the set points do not correspond to the same level of O2

utilization--CO2 production (which I agree must correspond to each

other), they don't come into play at the same levels. This has

nothing to do with the stoichiometry or coupling of actual amounts

of O2 used and CO2 produced.

PWCs rely, in your view, more on low O2 to trigger ventilation

> than on elevated CO2.

***I think that's only true if they have developed this kind of

sleep apnea. Not all PWCs suffer from this. I think it depends on

the degree of mitochondrial dysfunction in the skeletal muscles.

This represents a failure mode for the normal control system. In a

normal, healthy person, the low oxygen alarm never comes into play,

because controlling on the CO2 level does not normally require

shutting down the breathing enough to trigger this alarm.

You're appealing to the Krebs cycle and the

> ETC to support your model. How do you propose that the

consumption

> of O2 and the production of CO2 are decoupled in PWCs?

***I'm actually not proposing that. I hope that what I said above

will make this clearer.

>

> Matt

>

***Rich

[Guest guest]

,

Some PWCS have Lactate spikes in their brain, which are measured by an MRS brain

scan.

There is a doctor in New York who does this testing, and Dr. Cheney does too.

Maybe others. The machine has to be carefully set and monitored because the

machine pulses and so do the peaks (I think I said that right).

Dr. Cheney accompanied me to the hospital In Asheville last year to oversee an

MRS scan. Mine showed spikes in 5 or 6 of 35 " grids " . They are in areas that

correspond with symptoms I have.

Dr. Cheney said these indicate " discrete " injury...metabolic

injury...mitochondria dysfunction. The Mitochondria is supposed to break down

sugars, but is not functioning fully, thusly the Lactate...a by

product...wasteproduct of sugar.

THis is seen in persons with Mitochondria Disease, but far more severely and

with far more severe cognitive deficit.

TC,

Katrina

> >

> > Hi Rich,

> >

> > Does this all then imply that those with this problem (metabolic

> sleep

> > disorder) would have alkaline pH due to low carbon dioxide ? I ask

> b/c

> > I have this and my blood pH is not alkaline, if anything, it is a bit

> > too acidic. Is the low carbon dioxide the main factor or the pH ?

> >

> >

> >

> >

>

[Guest guest]

Hi Rich,

In Feb 2003, it was 7.32. It was venous pH.

Re: Sleep Apnea . . could it be low

Glutathione?

Hi, .

I think there are other things that can affect the blood pH as well,

such as lactic acid, if it's elevated. Some people who have

mitochondrial dysfunction have elevated lactic acid, but that doesn't

appear to be true of you, based on your organic acids analysis.

I must have forgotten your blood pH. It's probably buried in the

file. When was it measured, and what was the value? Was it venous or

arterial pH?

I'm not sure what dominates in the respiratory center. I think it

looks at both CO2 level and pH. I'll have to dig into that some

more.

Rich

>

> Hi Rich,

>

> Does this all then imply that those with this problem (metabolic

sleep

> disorder) would have alkaline pH due to low carbon dioxide ? I ask

b/c

> I have this and my blood pH is not alkaline, if anything, it is a bit

> too acidic. Is the low carbon dioxide the main factor or the pH ?

>

>

>

>

[Guest guest]

Vis-a-vis the relative levels of O2 and CO2 in the blood, would this

not also be affected by the perforated foramena ovales (PFOs) posited

by Dr. Cheney - where, if I understand, correctly, some of the blood

goes back out to the lungs before ever being circulated through the

body? Also, I'm not clear how the brain monitors the O2 - it appears

in some cases that oxygen is freely available in the blood but does

not dissociate into the tissues, thus resulting in low CO2 production

but continuing ample O2 in the blood and a deficit of O2 reaching the tissues.

[Guest guest]

Rich

I'm really not talking about

> relative consumption of O2 and production of CO2 at all.

...level of O2

> utilization--CO2 production (which I agree must correspond to each

> other),

> ***Rich

>

We agree, then, that the production of CO2 and the consumption of O2

correspond to each other. If the putative mitochondrial dysfunction

in skeletal muscles results in low production of CO2, then this must

be matched by low consumption of O2.

What, then, did you mean when you said:

" However, because the skeletal muscle cells are just not

putting out enough carbon dioxide, because of the mito dysfunction,

what happens is that the oxygen level in the blood drops too low

before the carbon dioxide comes up enough to satisfy the respiratory

center. " (Message #105152) ?

If the relative amounts of blood CO2 and O2 are not peculiar for the

PWCs in question (i.e., the reduced output of CO2 will be matched by

a corresponding reduction in the consumption of O2) then why do you

say that O2 will fall low enough to trigger ventilation before CO2

rises enough to do that? In other words, in the absence of

sufficient CO2 to provoke the respiratory center, how does the O2

drop low enough to trigger breathing?

[Guest guest]

Hi, Matt.

The oxygen level in the blood drops because the respiratory center

slows and shallows the breathing. Thus, oxygen is not drawn into

the lungs as fast as normal, and it is therefore not put into the

blood as fast as normal. Since other organs are still using oxygen

at near normal rates, the oxygen level in the blood drops.

Thus, in an effort to raise the carbon dioxide level in the blood,

the respiratory center lowers the oxygen level until it hits the

alarm level.

Rich

> I'm really not talking about

> > relative consumption of O2 and production of CO2 at all.

>

> ...level of O2

> > utilization--CO2 production (which I agree must correspond to

each

> > other),

> > ***Rich

> >

>

>

> We agree, then, that the production of CO2 and the consumption of

O2

> correspond to each other. If the putative mitochondrial

dysfunction

> in skeletal muscles results in low production of CO2, then this

must

> be matched by low consumption of O2.

>

>

> What, then, did you mean when you said:

>

> " However, because the skeletal muscle cells are just not

> putting out enough carbon dioxide, because of the mito dysfunction,

> what happens is that the oxygen level in the blood drops too low

> before the carbon dioxide comes up enough to satisfy the

respiratory

> center. " (Message #105152) ?

>

>

> If the relative amounts of blood CO2 and O2 are not peculiar for

the

> PWCs in question (i.e., the reduced output of CO2 will be matched

by

> a corresponding reduction in the consumption of O2) then why do

you

> say that O2 will fall low enough to trigger ventilation before CO2

> rises enough to do that? In other words, in the absence of

> sufficient CO2 to provoke the respiratory center, how does the O2

> drop low enough to trigger breathing?

>

[Guest guest]

Rich

>

> Hi, Matt.

>

> The oxygen level in the blood drops because the respiratory center

> slows and shallows the breathing. Thus, oxygen is not drawn into

> the lungs as fast as normal, and it is therefore not put into the

> blood as fast as normal. Since other organs are still using

oxygen

> at near normal rates, the oxygen level in the blood drops.

******And don't these organs likewise produce near normal rates of

CO2?

>

> Thus, in an effort to raise the carbon dioxide level in the blood,

> the respiratory center lowers the oxygen level until it hits the

> alarm level.

>

> Rich

*******I wasn't asking why O2 drops. I asked why you think that O2

drops faster than CO2 rises--so much so that for select PWCs it is

low O2 that has to trigger breathing, not elevated CO2.

Matt