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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
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I like again to thank  the increasing flood of mails  and like to share    some on here  without names  and  show  how fun it is  to  discuss  open ideas.
 To understand the flow you may start  where the writing is blue  and than follow it through.

see some thoughts below but here a very overall thought.

It is the question of priority for survival.

So to pick up where you ended.

CO2 as it stands may create a vasodilatation.

A high CO2 at the end of a test may create a vasodilatation so top endurance athletes who can push hard often create a low SpO2 at the end due to the ability to really push themselves. So we would combine a vasodilatation due to CO2 paired with a high CO which creates a better blood flow due to pressure and a high vascularisation. All this combined will attack the survival part of central blood pressure and the only way we could react is with a vasoconstriction to maintain the BP. If you start using non-involved muscle groups you may see this much nicer as you may see first of all a tHb drop in the non involved muscle to maintain BP before you may see this in the legs where you still like to run away. So the critical question is which of this mechanism who at the end all try to help survival has the most important t role at that particular moment.. So when we look at assessments we make a priority list of this reflexes and more or less hope our ideas on priority may be okay or may have to change as we go along. 


Thank you for always taking the time…two very short follow up questions…I was able to graph the THb, and sent you in a different e-mail my simplistic view, to try and teach XYZ this new way of thinking and assessing different situations…she is always more skeptical than me, as you may remember from our first LBP testing days in 2001, but she is always open to learning, and she admits that the advice you gave so many years ago has gone along way to helping her have some great success despite being a mother and a speech pathologist, etc.

 
So here the two very short questions…when you say that the O2 is
either not bio available
Not “bio available”, means?
a lack of enzymes to help transport O2 from blood to muscle cells?
a broken membrane structure and possible edema impeding diffusion from the previous days workload?
altered O2 dissociation curve (2,3 DPG, or lower than expected H+)?
Good points. There is somewhere a smart guy out there with the name Shapiro. He made a very interesting definition of hypoxia as the situation, where O2 is not bio available.
meaning that we can have a very high SpO2 and a very high SmO2 but still the muscle may go hypoxic. Hypocapnic respiration can create this nicely and it is nice to use lactate to show how by a steady state load where we may be at lactate steady state or what ever we like to name it ,a change in respiration towards hypocapnia will increase SmO2 but as well lactate and a hypercapnic respiration will reduce lactate, but as well SmO2. So bio available means exactly all the points you list above. Now all this points can be trained with specific intervention functionally, but as well structurally.
 

and or not enough mitochondria who could turn this into additional energy .

That is the interesting part and here what is interesting. We have the same trend information from known top endurance athletes in certain situation as we have from know complete untrained and out of shape patients ( like people with chronic fatigue or fibromayalgia.)

The beauty is we know where structurally the difference is , so we have on one side a structural non existence of blood vessels and mitochondria in the untrained and we have a well developed circulation an mitochondria density in trained

So we know one is caused by a functional situation, the other by a structural non existence.

Now the latter most likely as well will have a functional limitation as they never ever will stimulate this situation . I did some case studies killing in good athletes one leg with eccentric jumps and squatting and keep the other leg relaxed as good as possible. Than did some testing on power cranks just to see, that one leg would nicely desaturate and the other not at all. I am confident that one or the other accepted institution will earlier or later confirm that at it is not very believable when it comes from a goat farm ( Smile )

The other unbelievable data I look here is with so called chronic fatigue people. Under mechanical occlusion they tend to destaurate very very slow and some never desaturated as the pain of the occlusion was too much so we had to quit. They for sure will desturate over time but there is only so much pain you can accept from volunteer patients ( Smile )

So the above will confirm you thoughts below

 
I would think the density of mitochondria in XYZ would be excellent, given our history of training, and her limitations in strength and mobility over the past few years which have really forced her to focus entirely on lower intensity training. She has had a number of chronic injuries, with plantar fascia initially, to achilles tendon, which we finally helped her overcome, only for her to tear her hamstring last year attempting some cartwheels with Kid. She is only now getting her full range of motion back, and able to put strong pressure on the pedals, and easy jog 40 minutes without pain.

tHb indicates a great vascularisation
I presume this development would be developed by a similar type of training that should yield high mitochondrial density.
and a great cardiac delivery.
The possible discussion is above with the so called priority list of survival. What we in sport forget is this simple survival question. The body really does not care about sport it only cares about survival and sport is a tool to try to see how this may work in reality with the exception of extreme survival situations.
We may see at the end a slightly possible CO2 collection tHb reaction
IF she had a CO2 collection, I thought it might shift O2 dissociation curve to right, and unload easier (which may be why she did show a very slight trend in dropping Smo2), but also thought this would result in vasodilation and INCREASE in THb, where the trend was dropping. SO, that was where my confusion really hit a peak [smile]
 
OK, never a short question, and really not expecting you to take time with this. Your help as always has been more than expected.
 
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