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ryinc

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 #1 
I am trying to force myself to do at least one physiologically based training session a week.

For this session, i used a basic breathing resistance tool while cycling. Basically the workout consisted of cycling at a low wattage for about 2 mins normal breathing, then about 1.5 minutes at the same wattage using the breathing resistance tool (i could not manage longer intervals at this stage). I did this 6 times.

I have a few questions:
  • As expected, THb increased and Sm02 dropped.
  • HR increased, which is actually the opposite i was expecting and hoping (i was hoping that HR would actually stay the same or fall due to a SV increase due to the increased bloodflow).
  • So it seems to me this workout was effective at working on respiratory system but no SV. Is that a reasonable conclusion to draw
  • How would i know that the increase in THb is due to to the respiration change, and not simply due to the higher HR
  • In one or two other workouts I have tried the reverse i.e. short shallow breathing to go hypocapnic. In those cases, i notice that Sm02 seems to go up i.e. opposite reaction of hypercapnic, but tHB doesn't seem to change
  • Picture of the relevant part of the relevant workout below.
  • Target Respiratory.png

juergfeldmann

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 #2 
Hmmm Ryan  you are getting  a nice  c  chef here  starting top  "cook " with different  ingredients.  NOW . that is exactly  where we  can use bio feedback  for. To get feedback  whether the theory  fits  the  actual reactions  and that  what you are doing here. So let's go step by step  though your cooking list  and see what the   data show  and what the expectations was.
  1. used a basic breathing resistance tool

So the  question is  what Resistance   a) inspiration  resistance or expiatory Resistance  or both ? b)
 than what muscles  are  you triggering  Auxiliary muscles  or  key muscles. and  where is  your respiration location. ? Apical or basal.
 Thna  let's look  your first  result.


As expected, THb increased and Sm02 dropped.
 Iam not sure  whether  with resistance  respiration  we woudl expect  this. BUT  we  had this results.
 This means  the resistance  really an minimal to do with it but rather the  fact , that you  where under breathing ( hyperventilation as in contrast  to hyper ventilation )  so you did not  moved  as much air  as needed to stay normocapnic  (  CO2  37 +- mmHg ) so CO2  accumulated  ( possibly  above  40 mmHg  and  the O2  disscurve shifted  to the right  so easier O2  release  and  vasodilatation  due  to  CO2 increase. ( If  you have  a SpO2  sensore  you possible  dropped  SpO2   below 95 /94 %Now  this can  be done easy without  any resistance.  in respiration.

HR increased, which is actually the opposite i was expecting and hoping (i was hoping that HR would actually stay the same or fall due to a SV increase due to the increased blood flow).

Not really  you used a resistance  device  and added   more  work  to about  60 %  of  your bodies  muscles  depending how  you where breathing . You may have reduced the wattage but mostly  added much more  muscles  for  a higher O2   needs  so  CO  had to go up therefor. I may be worng but if you still biked  you where most lily sitting free handed   so you could hold the respiratory device  at least  with  one hand.
 The is  creates much higher   demand  for core stability  and will as well reduce  your  SV  from aero position to up right position. In fact free handed cycling will create some problems  for a  proper diaphragm  respiration  Why ?

So it seems to me this workout was effective at working on respiratory system but no SV. Is that a reasonable conclusion to draw

May be  depending what  muscles  do you sused for respiration  auxiliary muscles  or key respiratory muscles. ?  Hard  breathing or better  moving  air  in and out under resistance  can be  as well an trigger  for  the ro  wrong respiration muscle as  you may use  auxiliary muscles. Best exampel are  people  with  exercise   induced  asthma,a  or  COPD  people or  any athletes  going  though the finish line  after a very hard  race. They  use  anything to mi9ve  air  but in  many cases  not the   great respiration muscles  as they now just have to try to survive by getting CO2  back into balance.
 ( See  after middle  distance races  and so on. Their  respiration muscles are  so  tired , that  they use  anything to o move the  air. but the   proper respiration  muscles.

How would i know that the increase in THb is due to to the respiration change, and not simply due to the higher HR.
 
By finding a  system  where you actually   maintain HR  or  drop it  and  still see an increase in tHb but as well a  drop in SmO2  and as  you  quite  the SmO2  will still drop or stay low  and tHb  goes up as in the picture  I showed in  Stuarts  case.


In one or two other workouts I have tried the reverse i.e. short shallow breathing to go hypocapnic. In those cases, i notice that Sm02 seems to go up i.e. opposite reaction of hypercapnic, but tHB doesn't seem to change

short shallow breathing

 It may create  hypocapnia  but it could as well create hypercapnia. Shallow breathing and short  may  just move a lot  of dead space but reduce  gas exchange  and you may actual accumulate  CO2 in the lungs  and therefor as a  time lag  as well exchange from  blood to lungs  is getting worse  and you actually  may go  hypercapnic.
 To be sure you go hypocapnic  you have to  hyper ventilate  not  hyper respirate.  People  at the end of a  race  do NOT hyper ventilate.  If  they could do this  they  would pass out  as CO2  woudl  drop rapidly . They  hyper respiration as  CO2  forces  them  and as soon CO2  is balanced  they go back to normal respiration.
 So  breath as usual  and you either breath a higher RF  but same TV  or  you breath  same TV  but higher RF  to increase VE  above   balanced  and you will get  rid of  CO2  and  will feel somewhat dizzy if  you drop too low. 
Hope  that helps 
ryinc

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Posts: 369
 #3 
Juerg more like the kid flipping burger at McDonalds that has found his way into a proper chef's kitchen and does not know what he is doing...[crazy]

To answer your questions:
  • It is a very basic resistance device - it provides resistance on inspiration and expiration. It is basically a mouthpiece, so both hands can stay on the bars while cycling. I had it on the easiest setting which was still quite hard while cycling (even at an easy load).
  • I have no ideas what muscles i was triggering - auxillary vs key, or apical vs basal or even what these terms mean. Please can you refer me to a good resource to read up on the differences.
  • I expected Sm02 to drop and tHb to rise, because i expected a C02 build up and shift of diss curve which seems to have occurred.
  • In the short shallow breathing i was increasing RF. I do think i was going hypo and not hypercapnic. There was evidence of diss curve to the right but there was evidence of diss curve to the left (since Sm02 increases) but the reduced C02 does not seem to lower THb in the same way that increased C02 seems to raise THb.

By your reply sounds like i am not doing this right, any clues or hints (even if by email) on what i should be experimenting with to make this more constructive???? Feels like i am trying to solve a maths problem by chewing bubblegum.

Thanks Ryan (rehabilitating McDonald's burger flipper).

juergfeldmann

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 #4 
I may  have to start to give some more inside in respiratory integration  for  activities  as I have more and more  people  e mailing similar questions. I  try to keep up  with all the   fun interest  so will try  first  to get Stuarts  section over  with  and BOBBY's  and your  feedback's on the  cardiac limitation we discuss in Stuarts  case. Thna we  can shift towards  the respiration  and how we  can use  MOXY   to see  what  actually may happen.
 Thanks  so much  for   all your  great  fun  and open feedback's.
juergfeldmann

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Posts: 1,501
 #5 
Ryans great  respiratory graph  got  viral  and I got   1  email  with a  request.  Basically.
 Can I show a respiratory  manipulative  workout in a graph, where  tHb goes up  and HR  goes  down.  Sure  an it is super easy  as  when ever  you reduce load  tHb will go up  and  HR  down  and it does not proof  anything  about  what you are looking for.
 The key as so often  but so little we see in  research studies  or  discussion is .
SmO2  alone  or tHb alone  do  often not  give any answer  they are  strongly interlinked.
 So  the  question is. Can we   for example  change  load  down so easier load , which will increase  tHb  and  drop  HR  but if  we  use respiration as a manipulation  we have a different SmO2  reaction. Simple  reducing  load  will  as mentioned increase tHb  as muscle contraction is less so  easier  for CO  to  try to keep   tHb  up  but as well HR will drop  but SmO2  as we reduce load  will go  up as well. In a respiratory manipulation physiological workout  we lie ot create  different ideas, The workout  I  like to show you   has the goal  to reduce  HR  but increase  SV.  Below the graph .

First live  peripedal  graph as it developed  and w the client had  an immediate feedback , whether his  physiological stimulation actually  was working.

hypercpnaic  SV  wokrout sT.jpg


Above easy to see. Brown  tHb / green  SmO2  % / Red HR
Goal . Calibration of  todays physiological  balanced  O2  intake and utilization intensity. Once  found . Can you see where ?  than using 25 %  load  to try to maintain  SmO2  level but reduce   HR  but increase  tHb. You can easy see , where we  tried  this  and  that tHb  really  increased but no   or  absolute minimal increase in SmO3  2 meaning  that  by 25  %  lad of  balanced oxygenation we where able to maintain the same  O2  utilization by a much   lower HR  and a much higher tHb  ( Preload )  Now below  somewhat more separated  in graphs.

SmO2 HR.jpg


Above  red HR  and green  as usual SmO2  %. You can see  over  +- 30 min a  stable SmO2 but  with different HR levels.

Below  the   relative loads of  the  10 min +-  segments

smo2  tHb all.jpg

Above  the   SmO2  and tHb  and you can see again 30 min  relative stable SmO2   but very different tHb reaction.  TL  stands  for  target load .  The target load  was  to be 25 %  of  balanced  homeostatic   todays  load.
Any reason  for 25 %  no not  at all no physiological reason just a  demo  on this case  that by  +- 25  %  on what would be  todays  FTP 60 if you are a  cyclist  is a  so low  load  that nobody  would consider  training  there but we have  a  much better SV  stimulation in this veyr low  intensity   than anywhere else.   That is one  reason  why  I  do not like  ideas like HIIT  or   training  intensities  based on performance.
Why because we do NOT need a  heavy load  to create a specific  physiological stimulation  we  simply need the proper preparation  for this.
 This is one  example . Other examples a. Very different out  come. Why.
Example  two sprints  or   other short term loads.  If  I  do 2  or  3 sprints  over  5 - 15  seconds the  2 sprints  will stimulate a very different physiological reaction despite  an absolutely  identical  physical load. Why.
 Do  this  with NIRS  and you will see a different SmO2  and tHb reaction and you have the answer. Will bee back   on the weekend  with Stuarts  cardiac limitation but this  was easy and fast as I have  hundreds  of examples  of  workout's so not lot  of time needed here.


ryinc

Development Team Member
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Posts: 369
 #6 
Juerg - this is the same graph i think that inspired me to try the workout in the first place! So we have come full circle.

Will think through the post. One thing that did pop out at me though - TLx4, is basically approximately FTP for that day if i understood it correctly. Sm02 values look pretty high for someone riding at FTP - am i reading the mark-ups on the graph correctly?

You can come back to this after finished Stuart's case - no rush.

juergfeldmann

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Posts: 1,501
 #7 
Two short feedbacks.
1.The graph  above is a workout I did yesterday with a client so no was never as of yet on the  Forum but  may be some other once.
2. FTP  and  SmO2  .  SmO2  has no  number connection to  FTP  or  a MAX lass , it is simply a  flat  or  balanced intake and output  and can be on any level . It depends  on how  you approach the FTP  or MAX lass or  for us  an  oxygenation utilization an delivery balance. The same is  true  for the classical idea on MAX LASS , as there is no actual lactate level as well but just a stable lactate  over   at least 16 min,  if you go  with the classical school. You can have a  runner or a  person  at  4.6 +-  MAX Lass   but  you can  as well have the same runner  by the same speed  at  2.7 mmol MAX lass +-  again it depends  how  you arrived  at the balanced  metabolic  performance.
 There is some very interesting connection between  classical  believes  on LT  1  and SmO2  which is discussed in some forums  but  from my  take  working on that  the  way it is approached  will most likely  create  more confusion than a solution, but  I promised  to forget  lactate discussions  and VO2 max  discussion. and focus on NIRS  interpretations.
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