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fitbyfred

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Posted  #1 
Hi. To not interfere anymore with the related topic from Rachel and Sandy, I'll put my question on a separate topic. So the previous reply from Juerg was interesting, but I'm not sure it altogether explained how to note the differences between a decreased O2 supply OVER an increased utilization of O2 ?

Here's a quick experiment yesterday that was conducted with client who has a known supply (respiratory) restraint. I kept the protocol same for the first 4 loads and permitted an extended reload before the fifth. The fifth effort had same load as previous, but I changed the pattern to reduce muscle compression.    
  
Normo - Hypercapnic Reactions.jpg 

So the phenomena that I am now more focused on is that seem with the chart above, is it loading / supply changes more so than an O2 consumption by the measured muscle ?

Effectively same question for the chart that Sandy posted regarding Rachel's (awesome) CO2 Run ? Is it a disrupted loading / supply more so than a local response to "use" more %SmO2 ?

Perhaps someone has some charts / images showing different  (flat, increasing) tHb trend that shows a decreasing %SmO2 ?
ryinc

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Posted  #2 
Fred, as i am sure you have picked up I am new to the interpretations so in my effort to learn (rather than trying to answer your question) can you explain why would the following not be the correct rationale?
The assessment protocol (i.e. rest vs load periods) and speed of changes in Sm02 around these points provide the clues as to whether it is supply or utilization issues. For example,
- if a load commences and Sm02 drops steeply, this would more likely be due to increased utilization than it would reduced supply.
- if a load ends and then Sm02 rises steeply, then the difference at the last point before the load ended and the first points after the load ended is most likely due to utilization differences
- Where a load ends and Sm02 rises more slowly (or even falls) then a reduced supply type of argument may be a possibility.
- After loads, the levels to which Sm02 recovers provides some indications - e.g. if it is a delivery issue then Sm02 peaks after recovery should be lower and lower as supply reduces?

I realise that there could also be some exceptions to the logic above, e.g. muscles not relaxing completely after load etc - could cause a slower Sm02 recovery after load due to utilization rather than due to reduced delivery.

Regards
Ryan
Ruud_G

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Posted  #3 
And an additional remark wrt loads 2/3/4. Guys we are looking at 1%-2% differences. IMHO we are looking at some random error. Just a small extra strain or movement left to right or a breath extra or less (I am exagerating a bit I know), some other minor thing may cause such very very small shifts (or random error). In terms of trends we should look for bigger shifts really.

Attached an example of an interval last week at constant power ouput 300 watt for 15 minutes. Rather flat thb but smo2 trending downward from say 35 to 25. See also the HR which is quite constant - just a tiny going down over the interval.



Attached Images
Click image for larger version - Name: image.jpg, Views: 51, Size: 805.96 KB  Click image for larger version - Name: image.jpg, Views: 45, Size: 826.44 KB 

fitbyfred

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Posted  #4 
Ryan, hi. Thanks for your reply. I'm sure the assumptions around the reactions measured throughout a 5:1:5 and other screening methods are on target. I do aim to practice them regularly in my gym.

The relationship that I'm looking to get better confirmation with is, is % desaturation a direction indication of increased O2 utilization at the cell ?
fitbyfred

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Posted  #5 
Rudd, hi. Thanks for sharing the images re: relatively stable tHb and steadily desaturating %O2, that gradual slope is is the type of image I was looking for.

What do you think is the mechanism behind the desaturation, an increased delivery to cell and utilization OR a decreased supply ?

I see heart rate is steady. Do you monitor your respiration rate or depth ? Or do you measure SpO2 during interval workouts ?
Ruud_G

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Posted  #6 
Hi fred. When riding and saw this picture coming up I had also had some "doubts". But I noticed that along the interval my respiration got much slower (and same time not deeper), supported by the feeiling it got easier, which was however not expressed by very much declincing HR (that stayes quite stable or just a tiny tiny lower). I don't measure respiration but I did notice it.
The 300w is below my (I know Juerg don't like the word) threshold and doing some 15 min at the beginning of a ride is not a hard effort.
fitbyfred

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Posted  #7 
Rudd, thanks for another bit of info. See previously posted image of workout with a respiratory restrained exerciser. Recall these are extremely high compression making loads:

2430973.jpeg

We used an HR monitor, a MOXY and a BioHarness for the live measures, and a finger tip spot checker for the immediate post-load % SpO2 (as an indicator of respiratory / VE performance).

I guess my question remaining is, does a shift over to hypercapnia actually produce an increased utilization of O2 by the cell, or rather does it create some form of dumping phenomena ?    

See top left text circled on image that Juerg shared a while back.

  IMG_0990.jpeg         

If I only have a MOXY what's the quickest way to determine the decreasing %SmO2 trend is a faster 'utilization' or a supply restraint ? 
DanieleM

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Posted  #8 
Hi Fred,

regarding to your question:
I guess my question remaining is, does a shift over to hypercapnia actually produce an increased utilization of O2 by the cell, or rather does it create some form of dumping phenomena ? 

If you are in hypercapnic situation, you have a right shift of the Dissociation Curve which means that hemoglobyn can easily releases O2 molecules to the muscle.
In this condition you will see a SmO2 drops. I hope 

PS for all the users of the forum: Shouldn't these kind of questions or specific cases go in the Questions or Case Studies rather than in the Public Webinars section?
If so, the administrator should move them in the appropriate section.
Thanks
fitbyfred

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Posted  #9 
DanieleM, hi. Thanks for your reply. In future I'll be careful to post to more relevant category.

Regarding discussion of increased O2 utilization over a sharp decreasing supply, especially during possible hypercapnic periods, I'm still looking for some more ideas on this? We can see by the many many images posted throughout the forum that SmO2 will drop, but does the drop = increased utilization of O2.

I wonder if any readers could share some NIRS charts/images of exercisers with limited muscular development -vs- exercisers with great muscular development, but both under hypercapnic strain?
DanieleM

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Posted  #10 
Hi Fred,
Not sure I understood your question.
Increased O2 utilization over a sharp decrease of supply...Do you mean artificial occlusion by cuff? Or?

Cheers
fitbyfred

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Posted  #11 
I guess it could be a cuff-induced compression restriction, or any type of loading that sharply restricts a supply to measured muscle. 
juergfeldmann

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Posted  #12 
Super great discussion  and   I love to follow  this form the outside  as this was a very  hard  and is a very hard topic. Here  some ideas. Check it  in a involved  and non involved  muscles  at the same time.
 Than check it    if you have the chance   in a  person, just after  along injury   or long inactivity of  one leg or arm.
 Like  THR  or TKR  after along waiting list. Than look at  a  person  with a  stroke. This  is all nice  to do as we know the limiter and therefor  ca see, what actually happens.
 When we started  out  we  where looking to test mainly people we  had  a very clear idea  of what  was limiting  performance.  examples :
 People  with a lung resection after cancer.
 People with COPD  and  nearly  on permanent  O2  supply.
 Propel after  hearty attacks  or by pass surgery  and or angioplasty.
 People after  strokes  and I had the  "luck " to have a young girl fatter  a stroke  after a birth control  pill with  now  complete recovery.
People in altitude or  eh opposite  with  enhanced  O2  saturated  air ( oxygenator)  Fred points is a great one.  He likes to know.
 Whether  O2 us actually  more use  with or without hypercapnic  or whether as I understand him right it is just used   due to the shift in O2  disscurve.
 So basically if I work out  and I use  so much O2  anyway  and now by the same speed I  add hypercapnia  to it, do I increase the use  of O2    to the already  O2  I use  anyway.
 Fred is this your point. ?
fitbyfred

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Posted  #13 
Juerg, hi. Yes, that's the idea.

Under high compression work (tHb decrease) such as sled push/pull, squat, huge load on bike pedals, steep uphill run/bound, along with the addition of hypercapnia, does the quickly decreasing %O2 indicate an actual sped up ability for the cell to utilize ? Or is this more or less a situation of a quickly unloaded supply ? 

For most I think interpreting the MOXY is more or less an exercise in relationships and there seems to be 'cardinal' reactions associated with the many reactions. If this is the case, which sign or relationship would mark a truly increased utilization of O2 OVER a decreased supply ? 

Thanks for your thoughts to help me be able to identify this for myself going forward.
juergfeldmann

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Posted  #14 
Fred  will be back  with a very intriguing  and head turning option to your question.
 It  will go towards the ongoing  fight between  aerobic  and anaerobic. Hint. O2  is used  for the  glycolytic  reaction. If  as  some  new research  shows the CP.r  is not that involved  but O2  is  very involved in   ATP  maintenance. than the question is  what we  do when we create this hard loads. Do we  ask  for a lot of  O2   and how can the body cope  with this demand   the best. Is it a delivery  limitation    and is it a  highly  aerobic demand    which is supported  by a  CO2   level to allow  a better  use  of O2  form the storage  area. ?  Why  does Gibala  's  studies  of  30 seconds  all out show that great improvement of  aerobic    ability  compared to the classical LSD?
fitbyfred

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Posted  #15 
Juerg, thanks. I've been combing through the forum for some previously posted abstracts re: the milli sec uptake of O2.

What was the end measure of Gibalis (spelling?) study that shows the greater improvements for 30s all-outs over LSD ?

FBF
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