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sebo2000

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 #1 
Just came back from weekend racing at Calabogie with a lot of cool data.

large Master 2 field, over 50 people, tons of old farts having great time [smile]

One Moxy on left Medial Deltoid and second on right VL

I went in the break a bit too early, stay there for 4 laps about 30min, Moxy was just amazingly instrumental and usefull in allowing me to stay there for 30 min. and giving it all, break NP almost 340Watts

If you look at the data W prime was negative! (but I did't have it on my Garmin or I would simply get scared and drop off) instead I was watching my Deloid Smo2 numbers and pulling without going too deep.  This was the longest effort with negative W prime I ever had without bonking.

(I know someone will say my CP was set incorrectly...)

HR goes way up, smo2 down on both sensors, and VL tHb goes up, I'm assuming venous occlusion or tHb is up because HR went up?

final sprint nobody dropped me, I finished nicely with the pack again taking bad line that cost me few places, didn't win but got some points in new stronger field. Could not be happier.

The end was strange from respiratory perspective. I did my blood shift trick, stood up on the pedals for 10 sec to prime my hamstrings, pulled with hamstrings for 30-40sec  to get VL rested, and sprinted all out with VL, at the end after crossing finish line I thought I will choke, I could not catch my breath for 2-3 seconds, I'm breathing but I was not absorbing any oxygen. Deltoid Smo2 hit the bottom.

I looked at the data at home, but I can't see hemoglobin curve shift to the right, It looks smo2 curve raising before tHb increases, I can't explain why I could not catch my breath for few seconds, any idea what happened in final sprint?

VL data (blue area breakaway)

CalabogieVL.png 


VL (first two charts) and Deltoid (last 2 charts)

CalabogiDeltoid.JPG 









 
Attached Files
csv Calabogie.csv (737.62 KB, 2 views)

ryinc

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 #2 
Cool data Sebo. I reckon you are on the bleeding edge of practical use of Moxy data.

By definition if W' bal goes negative, you either have CP set to low, or W' set too low. I assume you have set W' specifically are not just using default W' = 20 000? I have no problem though accepting that Smo2 deltoid, a physiological indicator, is a better guide for gauging efforts than a performamce based mathematical formula - thats fairly logical to me, provided you can find the right physiological marker and you have done that!

What would be interesting is to do a 20 min FTP test pacing according to smo2 deltoid, not power and see the power result.
bobbyjobling

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 #3 
Well done Sebo and interesting data.
I never used CP and W' because I found it to laborious to set the thing up correctly.
I get a better feedback using Moxy [smile]
Stuart percival

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 #4 

I looked at the data at home, but I can't see hemoglobin curve shift to the right, It looks smo2 curve raising before tHb increases, I can't explain why I could not catch my breath for few seconds, any idea what happened in final sprint?

During the max effort sprint SEBO you would have created a big build up of C02- we all know about hypercapnia and the associated problems - So usual imbalance of homeostasis here that correcting quickly

The big deep breathing removes the excess C02 - Hyperpnoea (not hyperventilation) - the bodies attempt to return to normocapnia  as soon as possible

So you were in fact 'catching your breath' even though you felt out of breath......never short of 02 ...just too much C02

Its C02 that drives respiration normally.

I will post some Moxy and V02 data on here for you to see what happens with peak end tidal C02 (PETc02)during exercise.
PETC02 is the amount of C02 in the final part of your expired air- its generally agreed that this represents the arterial C02 at the lungs (paC02)
So during V02 assessment we can estimate arterial C02 levels from expired air.

juergfeldmann

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 #5 
PETC02 is the amount of C02 in the final part of your expired air- its generally agreed that this represents the arterial C02 at the lungs (paC02)

and  don't  forget  we  have  a CO2 in the arterial  blood   and  a  CO2  level  in the alveolar  air  and then  at the mouth  with the  full discussion on dead  space  regulation and   breathing localisation. 

Unfortunately  not  true  but it  is sold  that  way.
 PaCO2  PACO2  and  EtCO2  are  close   to the same    at rest or minimal  activity and than  it has to be balanced  out  over a  8  plus minute  time frame. That is  why a  resting metabolic  rate  test is  15 min long.

Use  an I stat and check  blood gases  and   look at the mask or  screen and you will  have  an instant  confirmation.  It is  the    difference between RQ  and RER  and why we see  RER  above 1.0
  Here  from an  ACSM  seminar  many many years back

assumption rer  rq.jpg 
This  is  well accepted  but we simply  push it under the table as it is very inconvenient  for many  test ideas  and   handouts.   This is  as well the reason  why  so many struggle with the difference in reaction we see in an indirect feedback over a VO2  equipment or  classical  finger    lactate  testing.  and  a  NIRS  equipment.
 The  whole idea of intervals of  short duration like  15 +  seconds  suppose to be  anaerobic  so no  O2 involved  and alactacid so no lactate   is  measured  at the finger is the reason  for  what  many still believe , when in fact  they are highly  oxidative and highly lacticid it is just not  enough time to show up in the older ideas like VO2  and lactate. 

ryinc

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 #6 
Stuart the problem is that might not reconcile to the data. Too much C02 would be a right shift of disa curve with sm02 rebounding after thb - Sebo says he was seeing the opposite.
Stuart percival

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 #7 
Thanks Juerg

Do you have some I stat data ?

Are we saying that blood C02 at lungs and does not match ETC02?

If so whats happening metabolically to drive the ventilation --I cannot take arterial blood samples [smile]
juergfeldmann

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 #8 
Are we saying that blood C02 at lungs and does not match ETC02?

Yes  it  can match  close  but in a  3 min step test  or  interval it  does not. It is very easy  to assess  and it is one  of the first  critical  feedbacks I   show  the   grade  10 - 12 students here. Simply  change  dead space  ventilation  and  you see the  delay of  CO2  reaction  or the FeO2  %  manipulation.
 . We  showed  I start in  the forum  form some great    work  from Red Bull  ( Per )   As well   when we   use VO2  equipment there is a  big difference on the  way we  collect    at the mouth . Full face mask  or  mouth  breathing  only  or  nose  breathing only . Very different  end results in    step tests.  as well on this forum  shown  a few  times. Again very easy  to show  and proof  with a  capno meter alone  and  then the  three  respiration  options  as  above     with  a   tube in the mouth  free  nose  and mouth  and a    nose  clip.   same  wattage if  you do in biking  and very different reactions    at the mouth  and  on NIRS . Why   and in blood  when you sample  lactate. Thank  you add body position to it   like upright  aero position and  inversion  and  you  will be even more surprised  how  VO2    and information at the mouth  have to be taken  with a lot  of  critical  looks. Very important  when  you us e Physioflow as a  confirmation   as  soon  we  work  with paraplegic    people  and  we have to look at the cardiac  hemodynamic  as well or in   non injured people once  you start playing  with  specif cardiaca stimulation like loading more  right or left  ventricle. 
sebo2000

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 #9 
Thank you all for comments, 

Stuart for sure my blood was loaded with CO2, whenever I do "blood shift trick" I dig deeper than ever.

Ryan I'm positive my CP was set correctly on the trainer just week ago (I keep updating my data just to have full picture and see how and when Moxy differs from power etc),

W' values are at 29000 and Pmax 1151. I totally understand when people have negative vales it must be wrong setting...(I would say the same), however I think from my limited tests moxy seems to be far more superior than WPrime model. or I gained 25W in 6 days [smile](unlikely)

This is exactly what I was thinking of doing 20min power test but only driven by Moxy, so really 20min moxy denaturation test not power test. This will be super interesting, but I need to wait we have race after race and I want to be fairly fresh.

Again when I crossed the finish line, for luck of better words, I felt not only out of breath, but it felt my lungs turned in to little nuts, I took 3-4 breaths and didn't feel them at all. My first thought was: Wow this will be super visible hemoglobin curve shift, I was actually excited to see it.

This is how final section looks like, slight very slight tHb move while Smo2 is flat before increases, but I was expect way more.

Red arrow indicates when I stopped peddling.




finishcalabogie.JPG 






juergfeldmann

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 #10 
I will  try to be back today and show  you how  you use   a  less  priority muscle in any sport t actually  control intensity  for  workouts and or racing  as Seboo relates  to. Seboo  do you have  a csv  file from the last section after the race I like look somewhat closer. What was  your  possibly  RF  and  do you have a  oxy  meter  for SpO2 . ?
sebo2000

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Posts: 227
 #11 
Thanks Juerg,

CSV attached, I stopped pedaling in 6665 second for a minute, right leg down, rolling for a minute then stopped completely.

It was a race so no oxy meter, RF hard to say, max effort. I have noticed one thing this year: ever since I started training my breath hold and hypoventilation drills, I breath not enough... It sounds strange, but initially I do not feel the need and then Smo2 is too low, I really have to concentrate to get it correctly. Last year many times I was out of breath while still in full swing sprint (this was really bad) this time it was after, I can't complain about this new situation since this is perfect, I'm just puzzled why I can't see it in data, or I most likely missed it.




 
Attached Files
csv Calabogie.csv (440.71 KB, 3 views)

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