To Matt

[Guest guest]

Hi, Matt.

I've sent this twice, but it didn't go through. Here's antother try.

Rich

>

> 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