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juergfeldmann

Development Team Member
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Posts: 1,501
 #1 

,I like to offer a physiological " cook book "  to  try to help the readers to easier understand on how we look  at physiological interpretations  and  based on this  how  to  understand  physiological guided  workouts.
Please  take it apart   or help  to add  with  questions and  suggestions or  where   I need  to clarify   some of the ideas.

Pictures  can replace  thousand  words.

1. The different  way of looking  at a  person ( athletes,  patients  or anybody )
ecgm 1.jpg


Ask yourself  what  classical testing ideas  you and I  may  use  or have used   are  in the above   picture.
What information  do we  get  form this ideas.
 How  do we apply the test result  when we  try to target a specific  system. Example:  You find  your LT  (  using one  of the +-25  different ideas  to find an LT. Lets'  take a  very common LT   idea.
The 1 mmol increase in lactate in 2  steps in a  row.
 How  do we know   in what  " zoning " or intensity  we  may overload  respiration  for example.

 2. If we translate the above ideas into a  race  or a  workout  we  may have the following picture.
ECGM 2 RACE.jpg 
I hopefully  get the  idea  over  with the above idea.
 You can win a race  but  you do not know  why. You may loose a race  but you   may  have an idea  why. It is all about the team  and how  they support each other.
Physiological example.
 Muscle weakness   may create an early  occlusion  direction  with a  outflow  restriction or  even a   complete  occlusion.
 This  create a  lower  return  of blood to the cardiac  system  and as  such  SV  will drop  due to lower pre load  and  to  try to maintain the needed CO  we  have to   increase  HR. Now  an increase in HR  will  change  CCT  ( cardiac  contraction time. CCT is the  multiplication.  of  HR  x  LVET  ( left ventricular  ejection  time ) LVET is   measured  in ms.
 From  hundreds  of  Physio flow test we did  we  got  a trend , where   better trained  a  athletes ( endurance  athletes  have  longer  LVET  than   less trained  athletes  or people. The  LVET  will drop  with increase in HR.
Untrained  person  example.   HR  150  LVET 200 ms  so  CCT =  30  sec.
Trained athletes                     HR  150  LVET 230 ms so CCT = 34.5  sec
CCT means the  time  during 1 min  where the cardiac muscle  itself  is getting limited  to non  O2  as  the cardiac  system is  getting blood during  diastolic    and not  during systolic  actions  ..
Hope  you see, where we  can go with this  situation.
 Longer  ejection time  more blood  for   locomotor  but less  for cardiac system. Risk  of   m  CG  reaction to protect the pO2  in the heart .  reaction see later.
 Second  example
 Respiratory   VE  l/min limitation. Your   push an intensity, where  the VE  needs to be 150 l/ min to maintain  H + balance  and to get rid  of  CO2  to achieve this. Your current  VE   peak is  120 L / min.
 So  you are short of  30 l  and will accumulate  CO2  rapidly. Reaction.  O2  diss curve shift  to  sustain the performance somewhat longer  (  fight an  flight )  and better utilization of   available O2   due to the  problem that in take  of O2  will be limited now. The  increase in CO2  will enhance  RF  but in a  weak respiratory system  may  drop TV.  / problem increase of  dead space  and so on. 

Question. Is  your favorite test system  giving you  any feedback on this potential performance limitation ? Your  or  our  body  has a  clear priority  list  to try  to stay  a life as long as possible.

ecgm Hirarchie O 2.jpg 


     This    pyramid  is the base    from the  fight  and flight  concept  (  survival)
ECGM  3  selye.jpg 

 
 


Easiest   example of this  concept  is the  survival  mode   in  cold  or  hot temperature

. ecgm  tempertaur.jpg 


If  we go  further to  the idea, that  cardiac  and respiratory  systems  are much more important to survive than your leg muscles , you can see, why ,  when we reach some critical intensities the  CG ( Brain ) may   redirect  energy  from less important body areas, like for example leg muscles , to  the  needed vital organs.

ecgm reaction  resp  card.jpg 

So the earliest  feedback , that wee  start  to " guide  up " loco motor   performance shows up in the  little or non-involved muscles if we have a vital system limitation. or will show up in the involved muscles  when we have a  loco motor  local limitation.

 This  than may look like this .
ecgm  fiunctionla  structrural.jpg 


Example of a THb  functional reaction. Vasoconstriction   ( Drop in tHb )  to protect BP  due to a cardiac  limitation.
 Functional  SmO2  reaction.  Drop in  SmO2  due to a  respiratory limitation during a   game . Holding breath  like in wrestling )

Example  structural  change in tHb. (  Andrews    hint )  increase in tHb  at 1 min rests  or end of a  step test  far above  resting tHb. (  most often due to  a  much  bigger   vascularisation in this athletes muscles
 Example structural  change in SmO2  reaction. Very low  SmO2  plateau in certain muscles  but sustainable performance. Indication of a very   optimal  utilisation ( mitochondria density.) in this muscles.
 See Ruud and Daniele's VL  reaction compared  to their RF  reaction.
  This leads us  to the ext.  step.
 Each team member   ( heart ,  respiration and muscles   itself has some additionally team members.

ECGM  4  tram in the  team.jpg 

They  are  all interlinked  with each other.
 
 Example . A  higher TV in respiration will change  the HR  and the  SV   of the cardiac system.
 This  ultimately will show up in a difference in SmO2  and tHb  trends.  A better  intermuscular coordination will show up as a different  SmO2  reaction in a main  contributor.
 Example  Ruud and Daniele.
 Their  VL  is the main contributor in cycling.  To keep the VL as efficient  as possible in a  high intensity  they  will try to add additional help   fur  example by  activating RF. Now this only  works  if  delivery systems  are  strong enough  as an additional  sue of O2  due to an additional  muscle  help  will  create  higher O2  demand  and if this is not achievable  from delivery   ( heart )  or the additional CO2  production overrules  the   limited VE  from respiration, the  performance  increase  can not take place.
  This is   one  reason why in top athletes VO2  peak (  max )  does not increase  and some times  actually  drops ( Racliffe) but  actual performance in their sport improves.
 A  limitation  of  vital delivery system will not allow a further O2  use  from super trained  locomotor  muscles (  Sleeping giant )
 A   beginner  where   delivery is not problem  will  have it easy to  increase VO2  peak  as he simply adds to a  weak  coordination  even more muscles  to keep balance  and what ever  he needs to keep going. Exercise physiologist  from top  endurance teams  all see that ( no  further VO2  improvement.)  if the substitute  additional  O2  than  VO2  can go  up as well as performance. 
Result   delivery is a limitation, solution  prop  up  delivery . How ?   simple find a substance  who allows  a higher delivery.
 EPO , plasma expander a.s.o  all what we see.
 Did  you ever asked  your team  doctor or  coach   how  you could increase your respiratory system  to improve   CO2  output. Or in other words  you have a  VE  l/Min  tested in a  VO2  peak test of  150  but you like to be able  to   move 250 L ?  Is the practical  approach  to improve personal training  ( stimulation ) planning completely lost in statistical zoning  calculations  and  absolute  test ideas  based on performance.   do we  gap the ideas  form a lab  with the option  for coaches.

 
ECGM 3  wrong path.jpg 


Summary : Short overview  on how  we approach   thoughts , when looking  at physiological feed backs.


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #2 
Thanks  for the interesting responses  and one  questions people had in common. 
How  does  NIRS  fit into  VO2  and lactate ?

 We  may be able to  ask the question  different. How  does VO2  and lactate  fit into NIRS.
Here a  super  basic  explanation I use  for my   students in the  high school.

nirs  and vo2   ice hcokey.jpg


In other words , they  have  all a  connection as they all deal  with energy  situations   during rest  and performance. All have one goal  for coaches ,
 Finding the  critical intensity , where  utilization and delivery    just may loose  a balanced situation.
 So   using VO2    is one indirect method  to do it  with some  as  often discussed  disadvantage   to  apply it in the field  or during a race. But it is a great  equipment  allowing us  to   create a great feedback  and  when   combining  with NIRS it is getting  even  more fun to use.  There is a reason  why one of the top VO2  equipment companies . COSMED  Italy   added  direct  SmO2  and tHb   feedback  to their   new VO2  equipment by  combing  feedback  form MOXY    to their  VO2  data.
 
So lets look first  VO2  and  MOXY / NIRS. Now we discussed this before .
 VO2  = CO  x  a - v  O2  difference. as a very basic  formula.

 The   content of this  idea  is somewhat  more complex.

but let's start   simple first.

Remember the black  athlete.
 Than  what we hope to get as message/  the team in the athletes.
 Here a  picture  of the main team members in a  different way.

vo2  AND ECGM.jpg

Each member  can be assessed  with some  different points  and you can see  NIRS is  nearly  in all  available  with  as usual some  restriction  and some needed  combinations  .


Here  when we look at NIRS just   in combination  with  systems  and VO2  alone.
 Picture is out  of Holmbergs  great cross-country  presentation.
MOXY AND VO2.jpg 


 Now  as mentioned  it is somewhat more  complicated  and let's look at a different view.  So  VO2 - CO  x  a- v O2  diff.

vo2  over all.jpg

I  showed this  slide   for  sure before but  perhaps after all this  time it may start to make some sense  and it is a  summary  on what we used  prior  to  just moving down to MOXY only.  But as well it shows , that we  sometimes may make  conclusion  with MOXY  , which we  may have to review  and than  we go back and  combine  all the tools  we have.   It  shows  as well that VO2  is  an end result  of a very  big team all creating  demand  for  O2.  That  explains  why  two people with the same  VO2  max  ( peak ) result may  have a very different performance outcome.
 Most  discussed  example is  Paul Tergat  and  Lance Armstrong  before  NY  marathon  with both  85  +-  VO2  peak   both running the same race  and   having nearly  60 min time difference  at the end of the race.

VO2  is a great  equipment  which when  we look it at that outside the box can give a great additional feedback  and  confirmation  to when we use MOXY. As  soon I have time I will show  some   rowing VO2  MOXY  test result  and how  they  go nicely  with each other when combined.
 So here when we  just look the  idea  with  the   view  of delivery  ) CO  and  VE  and  utilization a-v O2  difference.

vo2 delivery  anf ur tilation.jpg 

One problem  we  had  with  VO2  is time lag  and therefor  we   made some  different conclusions. As  VO2  did not reacted in the  first  30 +  seconds  we assumed  there was  no O2 used. So  there was a deficit  create  and  the rest is history. NIRS  and  even better technology  showed  us  that we   did not had the  full picture  yet.

This is  what we learned.
class VO2.jpg

Now  you add  to the  historical  testing ideas lactate  sampling, where we  have as well an  unknown  lag time  for a  summary of possible lactate in the systemic  circulation with no  idea, when and where it  got used  as buffer  or   predicted  and  not needed.  And you end up  with a  very logical   but not up to date  idea  of  anaerobic  alacticid. Due  to  lag time  of  sampling  reaction and lag time  of  VO2  sampling  reaction.

So a similar load in NIRS  showed up like the below picture.
moxy VO2.jpg
   and  when we now overlap this  you can see , where we  have some confusion  if  we  do not  allow to  objectively look at all the  sampling ideas.

overlap VO2.jpg 


Now  this confusion is  even  bigger  when  it comes  to combined  lactate and NIRS.
 Historic   reminder.
 Any  current LT idea  or lactate discussion  was originally based on the assumption  , that lactate is a bed   and ugly substance and the resin of many  bad  reactions after a  hard  workout  or  race.
 So we had  to learn to tolerate this    substance and had  to get rid  of it as  fast as possible in between  intervals'  or  after   training and races.
 Cool down   is  one of the reason  we did  it, getting rid  of lactic  acid.

Today  we  would love to actually I inject  lactate  so we  can go longer and  faster  when pushing it  to the opposite  spectrum . ( see g  BROOKS INTERVIEW.)


So there is this   idea,  that lactate trend  and SmO2  trend  move together.
 Example   In a three minute  classical step test    we see an increase in lactate  and a  drop in  SmO2 . So  search  for a break pint  and than you have   the LT  and as you will have a BP in the NIRS  curve   than you have LT  by using just NIRS.
 Now  we  will have again  go back to history  and see  that lactate  can change its   trend  by different step length and different    situations like  diets and so on. I  like to  get back to this in a  great data collection from a  6 min double  dip  lactate sampling idea  combined  with MOXY  in the  MLSS section later. 

Here just some questions:

a)  you  do with the same athlete a  wingate  test and a 3 min VO2 max test.
a 1 )  is the max  or peak VO2  value the  same in both tests ?
a2) is the lactate value  at the end of the test  taken the same in both tests.
a 3  ) is the  drop in SmO2  and tHB  the same  at the end of both tests.

b )  in which test  is the end test lactate higher  wingate  or VO2  max.
b1)  In which test is the  SmO2   lowest level lower  ?

In the wingate test   we see a fast drop in SmO2 ,   cane we see a fast increasein lactate.?
 . On the other side  what happens  when we  end the wingate  test  and SmO2  goes up ,  which  direction is lactate  going ?

So  does a  drop in SmO2   can show  an increase of  lactate   or  could it be that the increase of lactate  shows  up  as we see  an increase in SmO2. ?
  c) how  do we know , that the lactate we can measure in the finger is  from the muscle  we applied   the NIRS.  And many more critical questions we should be able to ask, when we allow  us to ask the same  critical questions  when using  NIRS.


Kirill

Development Team Member
Registered:
Posts: 91
 #3 
i dont see pics

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