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camachogabriel

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 #31 

Very interesting job, Will be nice to see also SPO2, to see the O2 saturation.

Can you describe what king of workout you perform, of if was at rest state, just to get a better picture of the results.

Sorry to ask this, but I will like to know a good software to graph results, since I will like to post some test I perform, but I will like to show nice graphs.

I like Juerg idea about a common language, I think will be nice to try to standardize a bit more what is shown on the post, so anyone can understand more easier

Thanks

sebo2000

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 #32 

Very interesting job, Will be nice to see also SPO2, to see the O2 saturation.

I will do another test like this with SPO2, when I have a moment.

Can you describe what king of workout you perform, of if was at rest state, just to get a better picture of the results.

Just good old seating in the chair, I tried not to move at all, pressing lap button with my left hand not to interrupt Moxy on right hand [smile]


Sorry to ask this, but I will like to know a good software to graph results, since I will like to post some test I perform, but I will like to show nice graphs.

This was from Golden Cheetah, WKO4 now has really nice graphs as well, and you can use Excel as well, but there is a bit more work with that.




camachogabriel

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 #33 
Thanks

Sure I forgot about WKO4 now support moxy.

juergfeldmann

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 #34 
Craig  will be back on your lactate  and  respiration  discussion but    I like to get people   thinking.
 I will open a  new section for  all  readers here now involved in the respiratory ideas. I like to leave the  hyperventilation idea  for  the cycling community as danielle  points nice  out  and  like to  separate  the believe in the exercise  physiology  and the   use  of  terminology   in the respiratory  rehabilitation and  application. This because  hyper ventilation is there a  clinical  picture  with some   health consequences, where    out of  what ever reason in  sport we    simply  not use  that idea.  Hyper ventilation as a clinical picture  is  used  since over  100 years  and  Friedrich Miescher  ( nobel prize winner and father of the CO2  ideas    had a clear definition for the different  respiratory  terms.
 So  I will  give some feedback  for the physio  and   respiratory therapists  engaging more and more on my email and   reading on here  and how   NIRS is used  to support  therapy and   live feedbacks  when we  do  physiological  stimulations.
ryinc

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 #35 
Daniele would you mind to post the VL muscles file?
DanieleM

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 #36 
VL file is attached (please let me know if you need the .fit file as well).






 
Attached Files
csv vl_cp_20170404.csv (71.96 KB, 7 views)

ryinc

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 #37 
Thanks Daniel, based on your feedback, i had wanted to check whether it did actually confirm no venous occlusion on the VL muscle. To do this, i put together the following bias graph. Given that "amplitude" of the HHb looks to be exactly the inverse of the O2Hb - i agree that there doesn't seem to be any evidence of HHb pooling at the muscle, and therefore no evidence of occlusion.

Thanks for sending the file.

11 April 2017 VL Bias.jpg 


DanieleM

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 #38 
thanks ryinc

I would like to summarize here my analysis:
First 20/22 minutes balanced/homeostasis.
Then we can see different reactions:
1. RF is getting more involved (tHB rise and SmO2 drop)
2. VL is also probably getting more blood flow and it is desaturating to even lower values at the end
3. The Respiratory Frequency (and likely) the Ventilation which is correlated to VCO2 start to increase peaking a quite high value at the end (46 breaths per minutes).

My assumptions are:
VL oxydative fibers are reaching their limit and Type IIb start to be involved both in VL and RF.
This will create a large accumulation of metabolites (H+, Pi), decrease of ph and accumulation of CO2 with the associated need to release it.
It could well be that the respiratory system is not so efficient as before but, for me, the root cause of the homeostasis disruption is at muscular level.





juergfeldmann

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 #39 
Nice  work 
 Here some interesting points 
 The Respiratory Frequency (and likely) the Ventilation which is correlated to VCO2 start to increase peaking a quite high value at the end (46 breaths per minutes).oints

 
This  just as  an example, where VT  ventilatory threshold   may be due to respiratory limitation  or  due to respiratory  compensation.  If  it is  due to  respiratory limitation than the classical idea that  LT  and VT  is  the same  is close  to the   reality . if   the VT  is produced  due to   respiratory  compensation than LT   may be due  to muscular    limitation and   respiration can push out  the performance  drop  due to compensation.  Than  LT is    no  VT.
 Here  a number example.

  a) VE 100 l / min  RF  50  TV 2 L
b ) VE 100 l/ min  RF 25  TV  4
 so  a  reaches  the  VT  so his  TV  starts  dropping  to 1.9 / 1.8  and so on  and  to maintain 100 L  his  RF  will o up.
 
 in b this athletes may have  3.5  TV  and as he   start to compensate  he  keeps  TV inceaisng  and RF  stable.
  Now  the key  numbers are  again he %  of  dead space  chnage.
 In the static  number  
 a)  250 ml dead space  x  50 
 b)
 so a very different amount of  air  with no gas e chnage  has to be  moved  as well  at the mouth piece  despite  the same amount  of VE  there is  different  O2  / CO  concentration in this   athletes . The  difference  despite the same VE is seen in the  SmO2  reaction  due to a different O2 disscurve  reaction.250 ml dead  space  x 25.
 For all VO2   equipment use  super easy to  see live.
  Keep VE  the same as  you see it live  and  chnage  RF and accordingly  the TV  so once  RF  double  TV  half  and vica  verca  and look at  NIRS  reaction and look t  CO2  and FeO2  reaction on he screen.   Very nice  to play as wlel with Spiro Tiger. Calculate  VE  you like to move  and  take  RF and adjust the bag size  accordingly.  This  way  you as well can find your optimal   and most efficient  RF  and  TV    amount.   As  you will see  very different in different sports  so  running  very different  efficient  RF  compared  to  cycling  o  cross county skiing.

 Summary :  fun  would be to see how by 46  the  TV  was compared  to  let's  say by 30 RF
DanieleM

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 #40 
Quote:
 Summary :  fun  would be to see how by 46  the  TV  was compared  to  let's  say by 30 RF


Agree, it would be...and I would be curious to see your analysis.

Anyway, let's make a quick calculation, unfortunately we don't have VE and TV values...so we need some assumptions that could be close or far to reality.

VE(1) at 20 minutes = RF(1) x TV(1)= 32 x TV1
VE(2) at 32 minutes= RF(2) x TV(2) = 46 x TV2

So VE(2)/VE(1)= 1,43 TV2/TV1 and TV(2)/TV(1)=0,7 VE(2)/VE(1).
Assuming that my case falls exactly as the average group of the study mentioned before the increase in ventilation from 60% to 100% was around 30% so VE(2)/VE(1)=1.3
TV(2)=0,7 x 1,3 TV(1)= 0,9 TV(1) 
So possibly a 10% drop.

VE is closely associated to VCO2
VE=863xVCO2/[PaCO2x(1-Vd/Vt)]

So if Vt decreases and PaCO2 decreases as well it will just mean that ventilation to exhale the same amount of CO2 has to increase.

But let's leave the speculations and go back to the reason of the RF (respiratory frequency) reaction:

The respiratory chemoreceptors work by sensing the pH of their environment through the concentration of hydrogen ions. Because most carbon dioxide is converted to carbonic acid (and bicarbonate) in the bloodstream, chemoreceptors are able to use blood pH as a way to measure the carbon dioxide levels of the bloodstream. 

The main chemoreceptors involved in respiratory feedback are:

  1. Central chemoreceptors: These are located on the ventrolateral surface of medulla oblongata and detect changes in the pH of spinal fluid. They can be desensitized over time from chronic hypoxia (oxygen deficiency) and increased carbon dioxide.
  2. Peripheral chemoreceptors: These include the aortic body, which detects changes in blood oxygen and carbon dioxide, but not pH, and the carotid body which detects all three. They do not desensitize, and have less of an impact on the respiratory rate compared to the central chemoreceptors.
Since in this case study there was no respiratory manipulation, the increase in RF in the last minutes was a pure reflex of the above(s) (VCO2 increases and ph fall -> RF increases as reflex -> PaCO2 (possibly decreases) and Vt (possibly decreases) -> need further VE so RF.



juergfeldmann

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 #41 
Nice   and great summary.
 There is one  part which is often overlooked  by  respiratory  " mathematicians "
The  location of   the  ventilation and  with it perfusion  an diffusion  quality.
During  an event like  a longer high intensity ride we not only push  locomotor  muscles to  a high   performance level  ( limitation ) but  as well the cardiac  and in this  discussion  the respiratory muscles.
 Now  the inspiration   main muscle  (  diaphragm)  is  a  biog part of   high intensity  performance as the main  core  stabilization muscle. So even in  cycling   we will have  a  dilemma  of  core stabilization  when we  " fatigue  "  with locomotion  and  respiration.
 If  the respiration is a limiter  than   we loose   core stability  and therefor the optimal function of the muscle sling. if   locomotor  muscle  are   the limitation we may  try  for a  while to compensate  with  the diaphragm but  time limited.
 So  what we  than  see is  that we loose   basal   respiration  ability  so  we  shift  air into the medial  lobe  are and  even apical  where we have a much  less developed  perfusion and diffusion   ability  than basal  and we  will have a different  CO2  accumulation. ( see  the   graph  I showed a few  times  already on the forum.

 If  you use  a bio harness in  cycling TT  you will see this  changes  easy and live as well or you can use a  NIRS in the   Costal7 C8  area  for assessing the   reactions as well.

One   more fun part to  calculate  if we  calculate is  the  change in air  moved in dead space  due to the  10 %  change.  And  the     blood flow change  due to change in VE  for the repsiratroy system itself. ( Again graph on the forum )
juergfeldmann

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 #42 
And here a   additional  question  readers  may have .

So if Vt decreases and PaCO2 decreases as well it will just mean that ventilation to exhale the same amount of CO2 has to increase.


1. Why  would  PaCO2  decrease  when VT  decreases.

VT  4 l   dead space  250 ml   
VT  3 L  dead space  still  250 ml  Where is it easier to get rid  of  the CO2  which is coming  from PaCO2  than  it is PA  CO2  and  final it is  EtCO2  at the mouth piece.  So  could it be  that  TV  reduction  and the same  activity may in fact increase  PaCO2  as well as  PA  CO2  but  may  initially see a  lower EtCO2  ?.  Now  we may  actually see a  compensation if  still possible of  an increase in RF  to  try to increase  VE. But  before  we see that   at the mouth piece  level  form any VO2  equipment  we  may see in NIRS  something  earlier and different . What  doe we  see.
  This is in fact a fun experiment we  very often   do in our   high school  class  to show the relative  time lag  of a   external feedback system like a VO2  and  a  direct feedback  form NIRS  and even better would be a   blood sampling of  blood gases but   somewhat too complicated  in   real  sport activities.  Another  real life  experiment  to show  how   often  calculations  can not work is  to show   the change in EtCO2  and  NIRS  reaction by changing  respiration location. So breath abdominal  and than breath apical the same  TV  and RF.  If  you have problems  to  do this  use a  kidney belt  around  your    abdominal area  so  you have a problem to let the    belly  drop out if  you try  to do  diaphragm  respiration. Another way to   test it is  to move  yourself in a  tight   abdominal pressure position like you breath  in a  semi   abdominal  crunch position so your  rectus  abdominalis is  contracted.

All this  " experimental  " ideas  are really used   during physiological  training stimulation   depending on what we  try to  stimulate  and or achieve.
 The later is an integral  part in many  sports like  wrestling , boxing  but as well in  sports  like ice hockey  where we use  this inhibition to create  specif   physiological stimulation  during a workout  as they will for sure  show up in the   sport  during competition.
DanieleM

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 #43 
Quote:
 If  the respiration is a limiter  than   we loose   core stability  and therefor the optimal function of the muscle sling. if   locomotor  muscle  are   the limitation we may  try  for a  while to compensate  with  the diaphragm but  time limited.
 So  what we  than  see is  that we loose   basal   respiration  ability  so  we  shift  air into the medial  lobe  are and  even apical  where we have a much  less developed  perfusion and diffusion   ability  than basal  and we  will have a different  CO2  accumulation. ( see  the   graph  I showed a few  times  already on the forum.

I agree and basically the purpose of the study posted was to show a strong correlation between respiratory muscles endurance and performance.

I think we have few options:
1. Muscular limitation -> Large production of CO2, H+ production ->Respiratory acts as compensator (as much as it can) driving possibly down PaCO2
2. Respiratory limitation > Respiratory fatigues, VE is not effective (probably in this case the RF increase is associated to a similar decrease in TV) and CO2 may accumulate driving PaCO2 up -> right shift of dissociation curve with an evident decrease of PaO2.

SpO2 measurements may give us some hints for the options above or perhaps we can use the non-involved muscles (if SmO2 drops without a sign of vasocostriction, we may think that the drop is caused by the drop in PaO2).


 


juergfeldmann

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 #44 
Thanks  Daniele  perfect summary great  short  and clear  thanks  so much.
DanieleM

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 #45 
As promised, last week I've done the test increasing the power of just 10 watts compared to the "CP" level.
Same environment conditions and approx same level of training status (both test/workouts have been executed in a well rested condition).

Result: Time to exhaustion was 20 minutes (compared to 32 min).
First 20 minutes was a warm-up with a 4 minutes steps and short high intensity(30s)
Test started at minute 20 (timestamp 1200)

Very interesting the respiratory frequency pattern:
At 3 min: 32
At 6 min: 42
At 9 min: 42
At 12 min: 44
At 15 min: 46
At 18 min : 46

VL
cp_plus_10_vl.png 
RF:
cp_plus_10_rf.png 
From my point of view this is indicating very well the concept of critical power: this small increase in power reflected in a condition of no homeostasis at all (perhaps just a short moment between minutes 6 and 10)
VL SmO2 remained very stable during the interval but this was due to the continuous increase of HR and VE (central) and tHB (local) 
RF SmO2 showed a small drop only in the last minutes.

tHB reaction in VL was different from the "CP test" with an overshoot at rest before starting a decline.

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