Sign up Latest Topics
 
 
 


Reply
  Author   Comment  
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #1 
This is a  respond  to a great   feedback by Kotinos  in the  certified  training center  section to Andris  interesting Webinar on HIIT.
 I like to give some feedback here  due to the lack of   most likely time   on the certified  center   page  a so regular readers  can  follow  this  thoughts.

First  I do not like  the idea  that  using SmO2   makes it easier  for starter  to use  NIRS  for  strength  and or interval or  any workout.  BUT
That's  just me  and  does not mean it is  right. My  experience is, that  when we  try to make  something easier  so it sells  better we  take  a big risk  to  loose  the actual value  of the  feedback  and in fact may  trigger many  wrong  conclusion  which than  suddenly  will be  a  rule. 
Example is  the  trend in SmO2  after  a load  when it   increases  relative  slow. There are impression out there, that that is  an indication of a respiratory  limitation.  Based in the  increased  slope  in SmO2  we have no  clue   why a or what  does that mean  and only know , that the  reoxygenation due to  what ever  physiological reason is slower  than   perhaps a precious  load  or  compared  to another   person. That's  it.
 The only  interpretation possible  and if  we like to get more feedback  we either need VO2  datas   with it like RF / TV/ VE  therefor  and   possibly gas exchange information like CO2  .

This  can be nicely  done  with the great datas Stuart  sent us  with NIRS  and VO2 feedback of  his athletes and himself.

So  Back  to Kotinos  point of  some interesting  questions on the SmO2  trends  you see in the Webinar.
  I  could not give  Kotinos  answers   which would make sense  to  his  questions.
Why ?  Because I  have no  great answer  but   could  just keen  somewhat talking about it. What Androi offered here is a  very basic starter  idea on what  could be done if  you decide  to start using   NIRS  for strength or interval.  I hate  this idea but that is just me.
 I  believe  strongly  that  using  this   interesting   ideas of NIRS  has   some risk   when we  try  to k jump on it fast   and not really give it some deeper thoughts.  Yes a  starter  cook book  and your kitchen blows  up  due to the wrong ingredients.

I  strongly believe  if we like to integrate  NIRS  successful and meaning full into  a future  training  idea and concept    we have to take to take the  time  and  think through it  to recognition  weaknesses  first  but  as well strength of  this incredible  great  ideas of  NIRS/ MOXY

This includes  me  but   even more successful and established  coaches  and physiologist , who often have the trend  to make a  fast shot   due to the  name we or  they have   and  do not think  the consequences  this  has  for a promising great tool,  when we  than  create a   very  wrong direction.

I am sorry  to bring this up here, but an example is  the   back  down of  BSX  on their idea on LT1  and  NIRS. As many readers   or users  are not happy  with the  LT1   found  by  BSX  and they complained   the company simply chnage  under that pressure and  now use  +- 75 %  of  their   LT2  as  the LT 1 and a message  that they are working on it.

Business versus  trying  to understand  the   possibility  or impossibility s to actually find a  magical  not existing and scientific never explained  LT1  with NIRS. Nirs   looks  at trends in O2   delivery  and  utilization  that's it. Lactate is a   blood  values   with an unknown    time of   production, unknown  place of   production in an amount  which may show up or  not  , unknown  amount  of   lactate used  before it shows up  and in many cases not even related to hypoxia. 

 Enough ranted. In short  I  do not like to rush  to  create something we than have steady to correct as we know   that  what we  try to simply  fly  will blow  up in our  own  face  as there are many  smart thinking coaches  and readers out there.
 Kotinos    shows  this nicely  with his  questions.


AGAIN  this  forum is here to learn to  make interpretation  with NIRS  data  and  how  to combine them  with  existing information you may have. Again Stuart is  doing this very successful using NIRS interpretation and  than his great  knowledge  of  his VO2  equipment. Others may combine NIRS  and Physio flow   or NIRS  and lactate. As  you learn   here the interpretation you can see, whether  what you use   make sense in the combination and if not   you than  ca change   one or  the other idea.


So back  to  HIIT  and SmO2   alone.
I ne  ame it  for myself   HIIT  and MISS. Why  . Because I  do not  use  performance  alone  9 High intensity )  to actually stimulate  physiological reactions. In a HIIT  w ehave  ZERO  ideas   who is  the  limiter  and  who may condensate  and   who is really overloaded. That's  why I use MISS  . Maximal individual  systemic stimulation.  A  HIIIT is if  I go hunting  with a  shot  gun . No  clue  exactly  which  bullet hist  my target    and where   I only known I have a big chance  that something is getting hit.

Or  you go  with a one bullet  gun  and you either HIT  and you know with  what or  you MISs but  you know  why .

\ So using SmO2  alone is  a   HIIT  but  you may have  often a MISS.
  I use  either  2  NIRS   or I use one NIRS but integrate   tHb or  any other  simplke  marker  like HR  or  RF  and so on . (  if more in details I use    a capnometer or SEMG feedback  as a fast option. 

BUT lets stick  with just SmO2  for now.But 2  MOXY's


hard load  wiht O2  shift.jpg 
Above is a  "HIIT"  which is  really a HIIT  as we pushed  so hard, that  the  actual delivery systems  could not keep  up as the  goal was to  trigger the ability  to shuttle   O2   form  nonprioity  muscle  to the priority mussels  to sustain a longer  high intensity.
 You  can see  as well how  we  than look at the recovery  time , do we like to recover  non priority  muscles or not  what is the goal and what is needed in the activity you like to improve. What do we gain if we recover all  and what  do we loose if we recover all.?

Now below a  "HIIT"  but  if  it would be a HIIT it  would be a miss. So it is a MISS. Target  a   optimal all  overload  of  a leg  muscle group  but  without integration of a non priority upper body muscle  or a  shift of
blood.





localleg only  O2  utilization.jpg


respiratory  O2  reaction systemic.jpg 
A
bove now  a  MISS  where we  used a  very low  load  to  target  O2 utilization  and thna tried  to integrate  as well the upper body  in the  O2 utilization process by  shifting  O2  dissociation curve  to the right.  . Goal  was a 2.3  DPG  stimulation .


All the above  example s are actually live  demonstration  during a presentation in Joshua n Tree ( California) with   Mary Ann Kelly in the 5  Star  fitness center   in Yucca  valley a while back. The fun part of all of  this is  it is NOT theory  we do it  and we can see it live and we  can  make  an interruption and can change to what ever we like to  try out.  It is  all  physiology   theory   under attack and see, whether we can back up  what we learned and read or whether  we  have some  questions to the current liveliness  in practical live  applications.

To  end this  fun    part here. 
 I  can already read the  email I have only one MOXY. So here  an example  when   you have one  how tHB  can help   and we  have  in the forum all possible interpretation of  combination of thB  and SmO2  just needs  some effort  and time  to  carry this  together  as  Ryan   and   some grate   brains  are doing it  daily  in here.

What  can you read out of  this it was a  HIIT  or  perhaps a MISS  as I  can  create this  picture  with a  very high intensity but as well with a very low  intensity.

thb smo2 systtemic.jpg 
 Now  just  for  fun. This above   picture  who shows a  >>>>>>> limitation was  done  with a  very low intensity.
 Meaning we  tried  to get rid  of  the  compensation by the cardiac system.  below  you can see  how that looks like   when we  try to reduce CO  during the  actual load.

hr smo2  leg respiration  with lines.jpg

R
ed is  HR  and  this  was done  with a   cardiac limitation  client  where we  where not allowed  to move  HR above  120  but  the  goal was  to  keep  the  utilization ability  going in his muscles. You can see his MISS was very successful in the first  load    and somewhat less optimal  in the second load so the workout  was over. e  now  6  weeks in can  repeat  the  first reaction over  10   times  till we  loose the quality of the workout.

True it takes  time but  again the goal is  to avoid   a mess  as we have this  days  with LT ideas  so that NIRS  can slowly   (  slowly ) be  a  great  part in future  coaching courses and ideas.

 Kotinos  thanks  for your inspiring  questions  which triggered  this responds  with a very very poor  help  to your  questions.  from my side..

ryinc

Development Team Member
Registered:
Posts: 369
 #2 
Juerg thanks for posting and sharing.

Could i ask a few questions?:
  1. In the last example, can i check that i am understanding your point correctly. The athlete has a specific limiter (won't put my guess down for now to keep it open for now), and you don't want cardiac to act as the compensator so you are doing a low intensity to avoid CO?
  2. Would it be normal for CO to be a compensator if in itself is a limiter in this athlete (since you mentioned do not want to go over 120)?
  3. Are you saying the 2nd load was less successful simply because did not quite get the same reaction of HR dropping with Sm02 and tHb, and Sm02 did not drop as low? Or something else?
  4. Is tHB dropping in load here because of muscle compression or because the physiological intervention drops HR and therefore CO (looks like the load to me, but trying to make sure)?
  5. Could you give us (or direct us to) a simple to understand explanation/background of what a "2.3 DPG" simulation is? (Seems it relates to the dissociation curve, but not really sure how/why it is different from other factors that would move the diss curve).
Thanks again for time and effort in posting and sharing Juerg.
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #3 
Ryan great questions  and I will take some time  to each question and will add some additional cases to show  how  a  training    planned on SmO2  amplitude  alone  can go   very different if we  do not  use   additional bio markers like HR in one  of the examples  or  tHb   and so on.
As usual I  go backwards.

Could you give us (or direct us to) a simple to understand explanation/background of what a "2.3 DPG" simulation is? (Seems it relates to the dissociation curve, but not really sure how/why it is different from other factors that would move the diss curve).

2.3  DPG is  substance like we  may have hormones  like insulin  or  adrenaline or  testosterone and son on.
 So  exactly  as we have certain   options to  stimulate  all  of them  so  do we  stimulate  2.3 DPG.
 There are  specific  workouts  combined  with  some specific   natural nutritional interventions , where we  can influence  this substances.  Insulin is   most likely the most  discussed one  as we have millions or  people due to the nutrition habits  to overload  this   system  so that it   finally  is the LIMITER  after we  overloaded  it  as a compensator. over many years.  Now  same   can be done  with 2.3  DPG. It is a very crucial  substance  to  help  to actually allow  O2   to move  from the blood into the  cell.
Certain respiratory   limitations  can  be sued  to   get  permission ot  actually  keep racing  and   a part of the so called  " level playing  field " is     really not that level anymore.
 Look at the current discussion on Wiggins  and Froome  and more  . As we  no tallow anymore  delivery  manipulation  over EPO and other  we simply move to the next  delivery limitation or better  release limitation  and get an official  exemption. ( But that is a very different story. )

 2.3  DPG    reactions can be trained  as well as  supported  over nutritional interventions  after a  actual stimulation workout.
  Again it is  a very old idea  and   it is  used in Farming . yes  farming.. If  you have goats  or sheep's  you will learn it.
  My goats  have to  drinking stations called teets.
  In most cases  you ave  twins but  in  some cases and  every time I have young baby goats I have triplets. So   often the first  2  will immediately or have to drink immediately and no problem  the third  one often has a problem.

In the first 5  + days of the life of a goat  or  other animals  including humans we will see  a  8 - 10 fold increase in red cell 2,3-diphosphoglycerate (DPG) concentration . This is a super important adaptation to extrauterine life. In  goats and more  animals the DPG reduces hemoglobin oxygen affinity by the Bohr effect. There are different  biochemical mechanism underlying this DPG increase which  can be the following:
-Change in blood pH
- an increase inn RBC fructose-1,6-diphosphate (FDP) concentration  most lilely due  to an  pH activation of phosphofructokinase;
-An increase in plasma Pi ( inorganic)
-  increase  or  doubling of plasma glucose .
So  many metabolic  reactions  we  can see  as well when we  demand a higher  O2 intracellular. Now   the   natural milk  creates many of  this reactions   and if not possible  you can feed  that as well.
 But  the  way t hey will actually moves has a direct  effect as well.
 So  the above reactions needed  for   increase in DPG  can  be done  naturally with    specific  physical loading ideas  and that's where we  can use feedback on  SmO2  but in connection with  tHb. . You will trigger   energy release differently  depending how  you  load. The best exampel  are  2  simple   30  or shorter seconds  sprint, where   metabolically  the first  sprint  will    use a very different energy  situation     to maintain ATP levels than the second  sprint.

That feeds in one  great  question we may look later  by Kotinos  .Is there  an influence   when we   recover  SmO2   full or   not   all out.
 Answer is  yes  a huge difference in  physiological reactions.
 BUT again. 2  sprints   400 watt . we learn . Same load  as  wattage  is  really objective  and tells us it is the  same  performance.  Is it ? We  are now  so   good , that we  even  can   predict  and calculate fatigue levels based on wattage  or performance. Can we really  do this in physiological  systems ?  The same as we  can l   increase  DPG  levels  so  can we loose them  if  we  do not stimulate  certain  reactions regular. This explains    in some athletes  surprisingly up and down swings.
  Here a    fun section  to read  and you may not find  DPG  ideas in any   or not likely in  exercise physiological literature.  Which  does not mean it does not exists.  The article  will show  you  why there is  so much interest in Dr.Fuentes  blood storage ideas in Spain.(  What  was his  specialty  ?)

Top of Form

Storage of red blood cells with improved maintenance of 2,3-bisphosphoglycerate.

Högman CF1, Löf H, Meryman HT.

Author information

Erratum in

  • Transfusion. 2007 Jan;47(1):176.

Abstract

BACKGROUND:

During storage, red blood cells (RBCs) rapidly lose 2,3-bisphosphoglycerate (2,3-DPG) leading to an increase in the affinity for O(2) and a temporary impairment of O(2) transport. Recent clinical evaluations indicate that the quality of transfused RBCs may be more important for patient survival than previously recognized.

STUDY DESIGN AND METHODS:

Glucose-free additive solutions (ASs) were prepared with sodium citrate, sodium gluconate, adenine, mannitol, and phosphates at high pH, a solution that can be heat-sterilized. CP2D was used as an anticoagulant. Additional CP2D was added to the AS to supply glucose. RBCs were stored at 4 degrees C and assayed periodically for intracellular pH (pHi), extracellular pH, glucose, lactate, phosphate, ATP, 2,3-DPG, hemolysis, and morphology.

RESULTS:

Storage in 175 mL of the chloride-free, hypotonic medium at a hematocrit (Hct) level of 59 to 60 percent resulted in an elevated pHi and the maintenance of 2,3-DPG at or above the initial value for 2 weeks without loss of ATP. The addition of 400 mL of storage solution followed by centrifugation and removal of 300 mL of excess solution to a Hct level of 60 to 66 percent further reduced the chloride concentration, resulting in the maintenance of 2,3-DPG for 4 weeks. Hemolysis was at 0.1 percent at 6 weeks.

CONCLUSION:

Improvements in the maintenance of 2,3-DPG were achieved with 175 mL of a chloride-free storage solution with familiar additives at nontoxic concentrations to increase pHi. Adding, instead, 400 mL of storage solution followed by the removal of 300 mL reduced the chloride concentration, increasing the pHi and extending the maintenance of 2,3-DPG to 4 weeks.

 

hmm  Many  may have to  wake  up. Do we really believe  a training idea  based on   wattage and performance has  any chance  to  control  physiological reactions.? There  are  much bigger  reasons  for performance  changes  than   %  of FTP  training  plans.

Do we need this  chemical   help.

 No ,we  can create  with smart  training using physiological  stimuli  a  similar   performance, it just needs more time  and  instead of  a  calculator some physiological  ideas and   information's.  More  later to the  above  questions. This  here is just a very fascinating part as it is  again  all about  survival and very little about  sport  performance.
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #4 
Ryan again great  questions  and I  try to give some   ideas  and  than  come back if  they  are strange or  badly  explained.   I like to start  with a  case  demonstration    I did in a workshop. You see as usual green SmO2  and in this case red  for  HR. You see in 2 loads  the attempt  and goal  to reduce delivery  by  reducing HR  and as  such   CO. In  the  2 other  attempt  we   increased  delivery  during  the load.
 The result  is  that by thee  exactly same load  we had  all 4  times  the  desaturation was very different as you can see. 

3 loads hyper norm and hypo  hr  smo2.jpg 

Now  to the  questions  
 :
  1. In the last example, can i check that i am understanding your point correctly. The athlete has a specific limiter (won't put my guess down for now to keep it open for now), and you don't want cardiac to act as the compensator so you are doing a low intensity to avoid CO?
  2. Yes and you can see  in case you  compare the  2 last  graphs  so tHb  SmO2  graph  and SmO2  HR graph what happens. As you pointed out  correctly the   goal  was to avoid a  cardiac  involvement but still  trigger a   utilization stimulation. So   we  created a hyepcapnic  high CO2  situation to shift  the  O2  disscurve  to the  right . Thsi  than create  a lag  time in reoxygenation  and the lag  time is directly  dependent on the VE  you are able  to move. So as faster you can balance  CO2  back to normocapnia or  even better in a   sport  to hypocapnia, as faster   you will be able  to load O2  from the lungs to  the  blood. This creates  the  different low points  with   a lag time of  15 - 30 seconds  of SmO2  but an instant increase in tHb. The tHb  has  2   advantages  to increase.. As you stop  you get rid  of  muscle compression  and   high CO2 is a very potent  vasodilatator.
  3. Would it be normal for CO to be a compensator if in itself is a limiter in this athlete (since you mentioned do not want to go over 120)?
  4. That is a  super  great  questions and shows  that  Ryan  really  is  in the Brain mode  we  actually  try to achieve. On the other side for me  this  questions  gives  me  the  ability to show  again  why a cook book is  not  optimal. Now  some may recall this is a cardiac  patient, now  bad  wording  this is a patient  with a   structural  cardiac problem  and not  an actual  muscular  cardiac weakness.
  5.  He  has a   leaking  valve  due to a genetic  reason  Bicupital  versus tricupital So the problem showed up in a assessment  for  cycling due to  bad knees  where he  shifted  to cycling. By a certain HR  or better CO   he  lost performance  dramatically and felt  weak ???? So  by a certain  CO  and a certain SVR  due to the CO  the  arterial pressure in his  Aorta   was  too high  so the back flow  created a  leakage back int the left  ventricle.
  6.  This  than created a   compensator  reaction and his  HR  increased  suddenly    and   so on. This over the years  did not really weakened  his heart muscles   but rather increased the leakage  in cases  where he  tried to push  harder to get back into shape. . So   his actual  LIMITER was the leaking  heart valve.
  7.  His   compensator  was the cardiac  muscle. So  the  120  was  to avoid  that the  compensator HR   would  not kick in  to avoid a back flow    and increase the  damage of the valve. So  this is a great example  of different   " survival " ideas. The  compensation ability  of  his  heart would over time  create  an actual problme   of his heart  in case the   leakage  would increase more and more. . So in this case the key was to avoid a compensation , train  a muscular  deoxygenation.ability  to avoid   the  demand of O2   to trigger a  higher supply  reaction ans   so on. Hope   this makes  sense.  and  as well you can see how this would work in sport. The  highest or  a high risk in  athletes  to create a  valve  damage is  a viral infection. As    deoxygention  in  sport  equals   HIIT  we see that when not properly recovered and to early start  due to races  coming up and   coaches ans  sponsors  are  afraid  to loos money  they go and  do a HIIT  and miss  instead  d  doing a MISS  and than get a HIT. We  can easy   hokd on high end  deoxygenation ability  and  high end  coordination  in very very low intensities.  the intermuscular recruitment pattern  can  be trained  even easier with out a  high  HR  or  high CO.
  8. Are you saying the 2nd load was less successful simply because did not quite get the same reaction of HR dropping with Sm02 and tHb, and Sm02 did not drop as low? Or something else?
  9. Yes  nothing to add here besides   that this  type  of  workout needs practice as any other workout  so over time  the athlete  or patient  can make a few  more  successful  loads  like the first  one see in the  graph above.
  10. Is tHB dropping in load here because of muscle compression or because the physiological intervention drops HR and therefore CO (looks like the load to me, but trying to make sure)?
The tHb   dropping here due to a  drop in  CO  and the load is super low. You can see the " super compensation of  the tHb in the recovery  due to the CO2   reaction If  you look  you can see   hoe tHB  returns  or  drops  after  an initial peak . This is  as soon we  have a  balanced   CO2 elevl  so in the capnometer the  readings  lag behind  so  we have a  mmHg  readings  of 37 +-
  1. Could you give us (or direct us to) a simple to understand explanation/background of what a "2.3 DPG" simulation is? (Seems it relates to the dissociation curve, but not really sure how/why it is different from other factors that would move the diss curve)

ryinc

Development Team Member
Registered:
Posts: 369
 #5 
Juerg firstly thanks for your answer on DPG - I hope you are getting your TUE forms for your goats signed, haha.

Yes i am finding it quite amazing that all top cyclists now all of a sudden suffer from "asthma" - it is making a lot more sense after learning on this forum.

Thanks for your answers on the other questions too. The answers made sense. I just have one question in relation to the workout with the 4 loads you posted in your response. 2 loads with HR dropping, 2 with HR increasing. Are you really keeping HR down or just delaying the increase until after the load? To me it looks as though HR drops during the load, but as soon as the load is finished it spikes up in a similar way to what would occur during a load anyway. So i am not quite sure i understand what the advantage of this workout would be, since it seems to trigger HR response just delayed.



juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #6 
great  comeback. .
 1. Go out  and check  what   kind of a medical test we  do   even with athletes  to decide , that they have  an constructive  respiratory  problem.  Than  I can show  you what the gimmick in all of this  is.

2. Yes  you are right  it  is a delay of  HR  (HR ) but  CO is  HR  x  SV.  so  in the  HR   reaction in this  type of w   workout  we have a  very low  SV  and after the HR  recovers  we than have an incredible nice  preload  as a counter reaction. So  it is a specif  cardiac    reaction  as well.

Below is a   initial try outs , whine we started  this ideas  you can see a lot of years  back. You can pick  the  2 very successful areas  where we  tried  the  manipulation

DESUTTER.JPG



B
y the  way  I love  this  very  great  and  critical  questions.
 What  surprises me , that in any classical  zoning idea  we never see this   needed  positive critical questions. I  still wait  for many answers  form the  wattage  community and the latest is  the  great case  from Stuart  and Sharon  with a 72  %  FTP load  which suppose to trigger a   fat metabolic     situation but  the   data  suggest with a  1.0  RER  otherwise.  What is the  goal  or the reasons  to train in Zone 2   up to 75 %   WHEN IT DOES  A VERY DIFFERENT  METABOLIC STIMULI. how  MANY OF THE  PEOPLE  ACTUALLY KNOW  WHETHER THE SUGGESTED   %  OF ftp  REALLY  TRIGGERS  THE  WRITTEN  COOK BOOK REACTION ?

Kotinos

Development Team Member
Registered:
Posts: 29
 #7 
A.

Quote:
Above is a  "HIIT"  which is  really a HIIT  as we pushed  so hard, that  the  actual delivery systems  could not keep  up as the  goal was to  trigger the ability  to shuttle   O2   form  nonprioity  muscle  to the priority mussels  to sustain a longer  high intensity.
 
You  can see  as well how  we  than look at the recovery  time , do we like to recover  non priority  muscles or not  what is the goal and what is needed in the activity you like to improve. What do we gain if we recover all  and what  do we loose if we recover all.?


I do not have first hand experience. But I suppose there are different ways the body shunts oxygen from a non-priority muscle.

1. Slowly, or
2. Emergently.

Both are in response to critical needs elsewhere. What I am trying to say is that it might be that these are different skills (via different mechanisms). Perhaps the first is less programmed, the second being more fight/flight response. Let me address the extended effort.

It seems that by not recovering fully between efforts that there is less to train with regards to shunting oxygen from one muscle group to other. More oxygen in secondary muscle more oxygen that can be put elsewhere. So a return to baseline allows for a larger shunt and therefore stimulus. 

What is lost by recovering fully? I do not have any great idea. There is less time spent under the strain of being in state where oxygen is distributed non-uniformly. So less adaptation toward holding such a state. Is there something else?

B.

With regards to the other example, that is without consideration of a non-primary mover, how do we compare the stimuli of fully recovered to non-fully recovered. The example given was 30sec sprints at constant external effort. Depending on recovery time different internal mechanisms are stressed. Juerg, or any one, can you say more on the different training stimuli that result?

__________________
Be Water, My Friend.
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #8 
Thanks  for  the great discussion points. First a  small thought  to  Ryans point of  rebound of  HR  after a   drop during the load. As usual  I  ask a  question  as an answer.

What we have to  accept  over time is  that  respiratory  systems is driven by muscle  as well as the cardiac system.. Any muscle   has the  risk if not properly used  to  atrophy or if   used  to  hypertrophy.  Nothing new  just a different mind set  when it comes  to   respiration and  cardiac  involvement in a training  program. The fascinating  part is,  that we create all kind of proven and unproven  muscular  workouts  and  crazy ideas, when in fact  the initial adjustment or  adaptation  has   and will come  from the  vital systems  as the  extremity systems really do not matter too much  for  survival  for us. Now  the questions  or better the   answers  by Kotinos shows  that he is  way into the    thinking of this  reactions. Okay  getting lost. To Ryans  part    with the above start.
 Rebound  after  a  drop  back to  basically normal    HR reaction.
 Question  or idea :
  I  ride  my bike  in a   controlled  easy  load  lets' use the great zoning   Zone 1 (  for Sharon  for sure not  Zone  2   smile )   I ride  and every so often planned or   randomly   I do a really hard  perhaps  all out  sprint  for  30  +- . Or  I use a MOXY  to actually give the all out a  physiological purpose ).  Now lets  stay  with the  30 second  all out  or  using a  wattage 140 %  of FTP. ( despite nobody ever  was able to test 140 %  of VO2 max in many cases  we  may not even reach  100 %  VO2 max  in a 140 %  wattage of  VO2  max ). No matter    about  that.
 But  why woudl  you do this short  burst of  sprints, when you anyway knwo it will rebound the performance b back to your  Zone 1 ?  To use  Ryans  question
 i am not quite sure i understand what the advantage of this workout would be, since it seems to trigger HR response just delayed..

To Kotinos  point. Again  with any  ( ANY  ) muscles  we  run into   a  functional respond  and  depending on how  I create the   functional respond  this may turn into a   structural adaptation. Nice  examples  are  change in muscle  fibers metabolic  reactions. (  Key  words   functional or structural  scoliosis  in extremity muscles.
 Cardiac  hyper trophy  depending on cardiac stimulation, Diaphragm change   to manly STF    fibers in  COPD  and so on. Thai are all structural; changes  initially triggered  by a functional adaptation.

So  the question is not just on  recovery  timing   and how  much but the  never ending  question on  what actually fatigues   what ever fatigue  may be.

 The  question  whether  the   full   half  or  3/4  recovery has an influence  on  outcome is  a   easy one. Yes absolutely  huge differences in   end result  and  is it is one   which most likely  makes the  biggest difference in success  of  rehabilitation  case  whether it is  a  post  ACL  program or a  post  cardiac   problem, a post  rotator  cuff rehab  or a   post pneumonia   therapy reaction. Now  this  is   as well true in sport  where we   may not have a clear  problem  but a  clear goal to improve  it just never is addressed in this  way. Mitochondrial density  increase is one of  the  nice  examples.
 The start  to  get this into a physiological guided  program is to  recognize  and  see the reaction by proper NIRS interpretation and that's  where we  try to help you on this forum. And I hope it works  otherways  take it  apart again and again.
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #9 
What is lost by recovering fully?
 We could change the question to a positive  way  instead on  what is lost  to  what  can be gained.
One  example is   where discuss this   a few times. look the start  of a 5/1/  assessment  and the reaction. or look the difference in 2   sprints   in looking the first  and second  sprint.
 To create the same reaction gain  as we have  at the start of a  5/1/5  or  the same as we have in an  initial sprint  you have to  do  what ?

1. Slowly, or
2. Emergently.

Good points  and  fits   somewhat into the idea  of  functional reaction ( emergency )  and structural adaptation    slowly. Look at  Walter  Canon  and his  fight an flight suggestions.


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #10 
Ryan
  I hope you are getting your TUE forms for your goats signed, haha.


Ryan h ah  they   wold  fail any  drug testing as they are  too spoiled with carrots  and Banana  and cabbage   so  I think  they are  fat   and not  muscular. But here a fun   article  from my  old school days time  as this  idea in sport was alrready  used.

 

naesthesia. 1977 Jun;32(6):544-53.

Red cell 2,3-diphosphoglycerate and oxygen affinity.

MacDonald R.

Abstract

The ease with which haemoglobin releases oxygen to the tissues is controlled by erythrocytic 2,3-diphosphoglycerate (2,3-DPG) such that an increase in the concentration of 2,3-DPG decreases oxygen affinity and vice versa. This review article describes the synthesis and breakdown of 2,3-DPG in the Embden-Meyerof pathway in red cells and briefly explains the molecular basis for its effect on oxygen affinity. Interaction of the effects of pH, Pco2, temperature and 2,3-DPG on the oxyhaemoglobin dissociation curve are discussed. The role of 2,3-DPG in the intraerythrocytic adaptation to various types of hypoxaemia is described. The increased oxygen affinity of blood stored in acid-citrate-dextrose (ACD) solution has been shown to be due to the decrease in the concentration of 2,3-DPG which occurs during storage. Methods of maintaining the concentration of 2,3-DPG in stored blood are described. The clinical implication of transfusion of elderly people, anaemic or pregnant patients with ACD stored blood to anaesthetically and surgically acceptable haemoglobin concentrations are discussed. Hypophosphataemia in association with parenteral feeding reduces 2,3-DPG concentration and so increases oxygen affinity. Since post-operative use of intravenous fluids such as dextrose or dextrose/saline also lead to hypophosphataemia, the addition of inorganic phosphorus to routine post-operative intravenous fluid may be advisable. Disorders of acid-base balance effect oxygen affinity not only by the direct effect of pH on the oxyhaemoglobin dissociation curve but by its control of 2,3-DPG metabolism. Management of acid-base disorders and pre-operative aklalinization of patients with sickle cell disease whould take account of this. It is known that anaesthesia alters the position of the oxyhaemoglobin dissociation curve, but it is thought that this is independent of any effects which anaesthetic agents may have on 2,3-DPG concentration. In vitro manipulation of 2,3-DPG concentration with steroids has already been carried out. Elucidation of the role of 2,3-DPG in the control of oxygen affinity may ultimately lead to iatrogenic manipulation of oxygen affinity in vivo.

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #11 
Here another example, where I like to make the case, that  using SmO2  alone   is  okay   when we start using  NIRS  but   we loose  a lot of options  or even may make  wrong  conclusions on the  training  outcome   compared  to  when we  would add more feedback's  and for sure as  we have them any way  adding tHb  trends  to it.

 Here the example  below.

thb smo2 three otption.jpg


N
ow  try  to ignore  the tHb trace and you can see that desaturation levels  all drop  down to 20 - 25 % and the  resaturation levels all climb back up  to 75 - 80 %. If  we think positive and say  wee  have a 5 %  inaccuracy  than we  can say it is pretty close  to  the same levels. The idea was  to create  this   SmO2   relative stable amplitude but  creating very different muscular reactions. Now   this was  one example  the high school students  used  to explain  what  the  tHb reaction  could mean   from a  muscle contraction   point of  view  and why the different   loads  may end with different physiological  reactions and therefor results. ,because  we may trigger different functional reactions  and  depending on how we  follow up  different structural adaptations. The first  part was  for the student  to   highlight  some   reactions. below  the    outcome of this  than you work  for yourself  on interpretations.

thb smo2 three otption with colour.jpg 
.To  end this    part I like to  show  two pictures I showed a  few  times  and it starts  perhaps to make  more sense. The pictures  or the context of it  is  pretty much  40 years  old in my university script  and it was motivated    by my favorite  Teacher  . Prof . G  Schoenholzer, the   father  of  high altitude    training    starting back  to the 1928  Olympic  winter games in St,. Moritz  and  ending  partially  with the  1968  Olympics in mexico. He was  far  ahead of  his time  and one part I see now  40 years later   he is still ahead of much  what we  do.  The  specif  lecture  on functional  and structural  reactions was the highlight  of his physiological view , that  physiological reactions  can be predicted  or  calculated as they happen  as the  systems  will decide  on the  timing  of physiological reactions and adaptation which  are highly individual. The   periodisation which was   or  sometime still isl big  ,  starting with the Russian ideas  over the  eat German ideas, was  for him needed   to calculate  pharmacological   timing much rather than  what would make  physiological sense.
. So   Walter Canon's  fight  and flight is a  perfect example of a functional reaction options.

canon.jpg 

Now  if  you look the  few key points you can see why I   immediately jumped  and bought any  equipment  which  gave some options  to actually seee the   fight  and flight reactions live.

a) CO  =  Physio flow  feedback   I was looking for . HR , SV, EDV, EF % , LVET, SVR  and this all live  and in the field.
b) blood flow  and oxygenation,  NIRS technology   ( portamon  and  MOXY) Live  and for the  field
+  NIRS  finger pulse oxymeter
c )  VE =  any VO2  equipment like K42B  at that time  as it  was portable  and   usable in the field  as well I was looking  for. CO2. FeO2  %  RF, TV, VO2  and all the possible    combinations.  plus   NIRS  CO2  capno meter.
d) Vasodilatation  and  vasoconstriction.   NIRS  equipment
e  [wink] muscle activity  SEMG portable   and live.
  End result  now .  moving back  to just one  small  equipment or better 2  of  them  the  MOXY  and we  can   very often get  conclusions   what the other once  would show  due to the  hierarchy  of  O2  supply    and demand.

 This  than  helps  to see  when  we may move  form a functional  reaction to an structural change  or adaptation.

 Here  the graph 

F  and S.jpg

Previous Topic | Next Topic
Print
Reply

Quick Navigation:

Easily create a Forum Website with Website Toolbox.

HTML hit counter - Quick-counter.net