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juergfeldmann

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 #16 
I got 3  emails  with interpretations.
 2 of the mails are  from my high school students  with some interesting points.
Here the points . 
1.  Occlusion outflow limitation in all the  loads with a  nice one in the first load.
Discussion .
a) muscular weakness (  strengthen limitation ?)
b)   limitation in capillarisation ?
c) vasodilatation limiter ?

Question.
  what is the best  approach now  to  try to  improve this performance.

 What alternative  small assessments  can be done  to see , where we  would spent  the  best time  for the   hopefully most improvement.

Summary :
 First  step is  to make  a  NIRS interpretation based on  what we see.
 Find the  reason  for this limitation  after the interpretation.
 Now  you have the different options  of limitation  it is now up to the coaches    to make the  next  step how  to improve performance. Re assess see the result  and than readjust the   workout ideas if needed or keep going as you see  progress.   Now progress can be   either measured in actual performance if  we  can objectively  test performance or we see it in the NIRS respond.
juergfeldmann

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 #17 
This weeks task  for  our  high school student.
  Summary .
last week we looked at one leg  SmO2  and tHb  knowing, that it was an all out effort  for 10 - 15 seconds   followed by a  subjective  hard maintenance  work and 3  repeats  of this idea.
Below is the graph we discussed  and above the option on how we  could improve the performance of that leg.
thb smo2  VL  left good.jpg 
above again last weeks  puzzle  and we established   the different reactions we see.
 This than allows the coach  to   decide  which of the problems or weakness he may  try to focus on to improve the performance.
 So this week we tackle  the  other leg  see  below  and than look at the same  situation.  After that we will   go back  and see whether we can make a decision based on NIRS only which may be the   injured leg.

For the moment  we have a   50 /50  in our  small  group in town. With a  slightly lean towards the above graph as the  healthy leg  and below the  injured leg.

thb smo2  right  VL.jpg    The one line  is the  leaning indicator  for the above decision on  right versus left.
 So  this weeks  goal training  program ideas  for the  above graph.
 Than see how we  would  design a program , where we  have to legs  with this very  clear difference  and how we train them together  to  create  an even   situation for left and right.

Summary.
 At the end of the day it does not matter which is the strong  and which is the  injured leg. The training  idea is the same , how  to we improve performance of  both  to make them equal.
 it is the top athlete and the patient   The only   part which matters is the proper interpretation off the NIRS data's  and what they show is the  actual reason for the  graph. This than opens the different options  to tackle the current limitation of this performance. Have a great  day  and thanks  for the few e mails in this fun discussion. I will sent  to the  people  discuss this including Daniel   Ruud  and Jiris  the outcome of our small  discussion group  to show the thought behind  no matter whether    right  or wrong.

ryinc

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 #18 
My guess is left leg injured. It looks to be working harder in physiological terms for the same/simple wattage. Jiri, is the flat spot in top right of polar view of wattbike related to the more volatile thb pattern we see in one the legs?
juergfeldmann

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 #19 
Question?
 Based on what feedback  do you assume  the left  leg works harder ?
SmO2  trend  or tHb  reaction?

What  does tHb  may indicate in the two legs. ?
and  if it does what   may create one or the other  muscular  contraction reaction    and  why ?

Than  again if  we look individual  how   would you improve the  weakness.? This is our local weak discussion  we have here. Jiri thanks  and as you can see   1 assessment  feeds  us  with a  great 2 - 4 week  discussion and search  for answers  and creating more  questions. Lot's of  fun. So we do a  short term change in plan  as we will  look next month in the   reactions  concerning detraining  and  why  we have a  forced versus a voluntary  detraining or a  injury related   and a  just stop  training detraining   concept. We may tr throw one or the otehr   ideas back on here.
Have a great day.
ryinc

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 #20 
Jeurg, to answer your first question.

1. I would expect at that the given wattage, untrained leg would desaturate to a lower level because it is a harder wattage for it to push relative to max ability (i.e. sm02 is higher for right leg at same wattage). I considered that this could be the wrong way around to think about it. In other words level of desaturation might actually indicate leg is better trained, but decided first argument more likely.

2, the constant up and down tHb within load on the left leg is strange and not seen in right leg. Right leg just looks more "normal"

3. At hard load on injured leg might expect to see occlusion due to strength limitation (smo2 drops more and tHb increase) Neither leg clearly shows this but left looks closer to this pattern to me.

I would think strength in injured leg and co-ordination are the limiters. However that argument is more based on common sense the moxy interpretation.
juergfeldmann

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 #21 

thanks  for this really get  feedback. This is  what I  hope  from  forum discussions. Not the fear  whether we are right  or  wrong but the thinking process in itself.

a) I would expect at that the given wattage, untrained leg would desaturate to a lower level because it is a harder wattage for it to push relative to max ability (i.e. sm02 is higher for right leg at same wattage)

That is the   intriguing part in Jiri's puzzle.
As  he showed a  minimal difference in 48 / 52 power towards the left leg, but as Ruud pointed out this is  very minimal difference  and very often seen in left right leg comparison.  I was hoping it would be much of a bigger difference  so  we could argue,  yes the left legs  SmO2  drops more because it compensates  for the right leg  which than  could be the injured leg ?  We  can't  so ??

Questions ?

A  long term injured leg  may go through a  "de training"  stage. Depending on the lengths we will loose  first functional  abilities  before we see structural changes.
 Same is  when we  train just the opposite   first functional reactions  and if  proper stress is maintained  we hope  for structural  changes.

So  one of my thoughts was. . a)  did he lost in the injured leg  functionally the ability  to desaturate ( different functional reasons  why this happens [wink].

 So  a less low SmO2  could be  an indication of this loss. This  would than indicate the right leg. But you are right   in case of  same load    would we  expect  a lower SmO2  from the weaker  muscle.

Now   we may have to  try perhaps  to  think different.  What creates use  of O2  and where is  O2 optimally   utilized.  If  we assume it could be in the mitochondria  than the question comes in on what  type of  muscle fibers  do we loose   during  injury  and inactivity  FTF  or STF  and from the  FTF the  FTF  a  type ?  Together  with the loss of mitochondria  we have a  loss of  capillary density . Respective. before we loose   mitochondria  we loose   capillary density  and   before we  gain mitochondria  we  create  capillaries.

Side note. Go back to  Daniele's  3  overlaps  , look the discussion   than  make some thoughts n  what  actually may happens  next  if  the change we see is  what we believe it is ?

 Now  back  to  the discussion. If  we  think he may have lost  functional deoxygenation, SmO2  will drop less  and if  we  push further to assume  it was a long enough injury  he may have started to loose  mitochondria intensity  and STF  and  possibly  activity of  FTF oxydative    fibers.
 If  that  may be the case we  loose  SmO2  utilization ability  and we loose   delivery  as well local.  But 2  But's
  a ) we loose as well muscle contraction quality so less explosive  contraction ability.
BUT as we  may as well loose  capillarisation we would  loose  earlier  blood flow ability  so yes  we  would expect an occlusion in a  weaker leg.  Now  I    was looking from a  quality  of  muscle  contraction a she had to start all out.
 The left leg  shows a  nice   venous occlusion trend  with an out flow  which  makes the tHb  somewhat restless. The  right leg shows a  muscle compression out  flow  with a  flow   when  easing on  inflow or back flow.

So a loss of blood vessels would  allow  an easier   occlusion by the same CO and both legs  have the same CO effect.

But a loss of  recruitment  ability  would weaken  the sudden   contraction force. so less aggressive contraction would lead to an outflow only versus a good leg  explosive  would lead to a venous occlusion trend.

After every load  and we have three loads  the  CO  most likely  will be higher  as a reaction so more  force  for vasodilatation  after  each   load. If we lost  capillaries  than we would see a minimal to  low  increase in tHb over the three loads.
 In fact a weaker muscle may  keep a higher SEMG tension so  tHb  my in fact be the same or even drop despite and increase in CO  vasodilatation.

When we look e see the left  tHb going up and up  with each load. This  could indicate a reaction  after  occlusion stimulation  or  an increase in HR
 ( CO  after each load.

 The HR  during this loads will be not  reacting very much    for sure not during the all out  so we have a delivery limitation and minimal vasodilatation help  from CO. The HR  will lag behind  and with it CO   and will peak   somewhere   at the end of the load.

 This sounds  all interesting but why o we have a very similar performance.( wattage )
What we see in detraining often is, that people often loose their  STF  or oxydative ability  and drop back to  "genetic" ratio.

They loose very little on actual strength    for short term loads like in this case.
 They loose  contraction quality  so SEMG peaks are lower so less  force  in a sudden time frame  so  less  often do we see an occlusion trend  just a compression trend.
 Than they loose  utilization  ability  so less drop in SmO2. Than they loose   blood vessels    delivery option  so less often do we see an increase in tHb  with the increase in CO.
 Now  all this is base on observation and some theories  
 but  we still have to  look at individual cases and I may be  very wrong in Jiri's  case.
 If  it is in fact the left leg  which is the injured leg  we have to  do some additional  assessments.
 one  way is to make a  5/1/5  and see in the longer loads  what may have happened  with the O2  utilization ability and the tHb as we progressively  load  and   allow a proper delivery help . Where as in this example we  shut out the delivery section due to the all out  and my  confuse the outcome of the puzzle.

 Just some thought on an interesting case.

 

Jiri Dostal

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Posts: 51
 #22 
So, here is the solution...

... the injured leg was.... the RIGHT LEG.  

Here are few hints and thoughts:

  • Polar graph from Wattbike. Yes- the ratio 48/52 is normal. However look back at the picture ( wattbike polar graph) attached to one of my previous posts. What do you see there? A clear diference between left and right side. The right side clearly lacks the upper part of the curve... which is in fact represent 4-5h in the "cycling clock". This is a typical assymetry you see on the injured or otherwise affected legs. This also gives a hint, that wattage itseld says very little. Moreover you need to understand what that "wattage" means - peak force?  Average force? Median force? What is the refresh rate? What is the averaging rate? Etc...many questions, but very little information without knowing answers to them...

  • Moxy data. I have seen several cases of the detrained or injued or otherwise affected legs. Here are few hints just based on my personal observation. Please note, this is not a scientific approach, it is rather experience based thoughts, and I would love to hear your critical feedback
-THb -  affected legs usually have signs of higher compression patterns vs. non injured legs. I can just speculate why, but there will be most likely many factors. In our case, there is a clear difference between LL with "freeflow" durin all tests, and RL with compression- arterial occlusion and decompression pattern

-SmO2 - inactive leg as lower ability to desaturate despite of fact, that it has the same workload ( double checked by Wattbike polar graph and data outup) as the non injured leg.... so the energy has to come from O2 independent metabolism. In our case it is very nicely seen in Biased charts. 

Once again, no science, just an observation so far. However very interesting, and stimulating me to think much deeper.

Good night to everyone

Jiri



juergfeldmann

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Posts: 1,501
 #23 

Thanks  for this  fun  puzzle Jiri. There   may be a little bit science in may approach  where I was looking just on NIRS feedback without  the wattage. Or  perhaps  I had a  50 / 50  chance ? Please if you have time read my swenglish  explanation carefully  and come back  with feedbacks  and additional questions

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