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juergfeldmann

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 #1 
I am far behind  and no  real excuse  as I have to  be more diligent  with my  time   investment for different projects. 4  groups  I like to  give some feedback's  as  they  all  make great points  and  sent great  information's.
All as  so often really  have  some connections as it is all  about physiological  thinking ideas.

Oleksy.
 Great  data  information of his effort.
Below  the summary  of his physiological feedback  just  from NIRS.

smo2  thb  all three circles.jpg 
 For people  really into  the physiological  feedback  look at the csv  file  as  most  are now  able  to make the interpretation thanks  to   a great time  commitment.

Summary  of my thoughts.
1. What limits  the performance.. That answer is  always easy,. It is the central    Governor. Need  and protection to survive.

So  fatigue  may start  in the head  and not where we like to search  for it.
Is it a theory  or  is there  at least some proof .

  1. How muscle fatigue originates in the head (as opposed to is all in the head).

    Posted on the ME Associations site,

    How muscle fatigue originates in the head, University of Zurich press release, 5 December 2011
    by Tony Britton on December 5, 2011
    From the University of Zurich media office, 5 December 2011

    Researchers from the University of Zurich have now studied in detail what sportsmen and women know from experience: The head plays a key role in tiring endurance performances. They have discovered a mechanism in the brain that triggers a reduction in muscle performance during tiring activities and ensures that ones own physiological limits are not exceeded. For the first time, the study demonstrates empirically that muscle fatigue and changes in the interaction between neuronal structures are linked.

    The extent to which we are able to activate our muscles voluntarily depends on motivation and will power or the physical condition and level of fatigue of the muscles, for instance. The latter particularly leads to noticeable and measurable performance impairments. For a long time, the research on muscle fatigue was largely confined to changes in the muscle itself. Now, a joint research project between the University of Zurich and ETH Zurich has shifted the focus to brain research. Headed by neuro-psychologist Kai Lutz from the University of Zurich in collaboration with Urs Boutellier from the Institute of Human Movement Sciences and Sport at ETH Zurich, the researchers discovered neuronal processes for the first time that are responsible for reducing muscle activity during muscle-fatiguing exercise. The third and final part of this series of experiments, which was conducted by Lea Hilty as part of her doctoral thesis, has now been published in the European Journal of Neuroscience.

    Muscles nerve impulses inhibit motoric area in the brain

    In the initial study, the researchers showed that nerve impulses from the muscle much like pain information inhibit the primary motoric area during a tiring, energy-demanding exercise. They were able to prove this using measurements in which study participants repeated thigh contractions until they could no longer attain the force required. If the same exercise was conducted under narcotization of the spinal chord (spinal anesthesia), thus interrupting the response from the muscle to the primary motoric area, the corresponding fatigue-related inhibition processes became significantly weaker than when the muscle information was intact.

    In a second step, using functional magnetic resonance imaging, the researchers were able to localize the brain regions that exhibit an increase in activity shortly before the interruption of a tiring, energy-demanding activity and are thus involved in signalizing the interruption: the thalamus and the insular cortex both areas which analyze information that indicates a threat to the organism, such as pain or hunger.

    Neuronal system has regulating effect on muscle performance

    The third study has now shown that the inhibitory influences on motoric activity are actually mediated via the insular cortex: In tests using a bicycle ergometer, the researchers determined that the communication between the insular cortex and the primary motoric area became more intensive as the fatigue progressed. This can be regarded as evidence that the neuronal system found not only informs the brain, but also actually has a regulating effect on motoric activity, says Lea Hilty, summing up the current result. And Kai Lutz points to the new research field that now opens up with these results: The findings are an important step in discovering the role the brain plays in muscle fatigue. Based on these studies, it wont just be possible to develop strategies to optimize muscular performance, but also specifically investigate reasons for reduced muscular performance in various diseases. Prolonged reduced physical performance is a symptom that is frequently observed in daily clinical practice. It can also appear as a side effect of certain medication. However, so-called chronic fatigue syndrome is often diagnosed without any apparent cause.

    Literature:

    Lea Hilty, Lutz Jncke, Roger Luechinger, Urs Boutellier, and Kai Lutz. Limitation of Physical Performance in a Muscle Fatiguing Handgrip Exercise Is Mediated by Thalamo-Insular Activity. Human Brain Mapping. December 10, 2010. doi: 10.1002/hbm.21177

    Lea Hilty, Kai Lutz, Konrad Maurer, Tobias Rodenkirch, Christina M. Spengler, Urs Boutellier, Lutz Jncke, and Markus Amann. Spinal opioid receptor-sensitive muscle afferents contribute to the fatigue-induced increase in intracortical inhibition in healthy humans. Experimental Physiology. February 11, 2011. doi: 10.1113/expphysiol.2010.056226

    Lea Hilty, Nicolas Langer, Roberto Pascual-Marqui, Urs Boutellier, and Kai Lutz. Fatigue-induced increase in intracortical communication between mid ?anterior insular and motor cortex during cycling exercise. European Journal of Neuroscience. November 21, 2011. doi: 10.1111/j.1460-9568.2011.07909.x
    .
Now  in  the above data  collection you have three  circles.
 If  you take the time  and look at closer you may  find  some directions.
 It appears  that in all three areas   he was running into a  delivery limitation.. The first  circle  is of  no  surprise  as usual  the   next 2  circles  show the same reason fro delivery limitation.
 
a)  he   lost his performance  due to a delivery limitation  which  " killed " his overall  performance by about  20 +-  min  and he had  no chance  to recover from it.


Question. What  can  cause a delivery limitation.?  Now  as we  now  know it is a delivery limitation the coach  can  work specifically with it.
 There are  often three   clear options and  than some additional   version to  work on.
 1. Short term  option.
 If  it is  in the midst of a racing  season in sport  we may like to  look at a short  term functional  option  to  see,whether we  can  change the delivery limitation   to  create a  better   performance  for an upcoming important  race  or event.
How  : ? you simply  create  the delivery limitation and than look live  on the screen with NIRS   whether you can solve the problem  with some  cycling specific    options.
The result  may be  that it actually works  and you ahve a short term solution  for this  problem or limitation.

or It may  show up , that  you can not functionally overcome the delivery limitation  as it is a  structural limitation and you have to improve  the structure  of this  athlete.

Now   there are different  options of a structural  limitation for delivery.
 3  most common once  is :
 A ) too low  cardiac out put  ( better a  to  small SV ) Important here is to avoid  an improvement  of  HR    at  the cost of  SV. Keep that in mind.
b)  capillarisation limitation  in the locomotor  group or   strengths limitation
c) respiratory limitation  eitehr  as  actual metaboreflex  or  as a  actual VE limitation  so CO2  accumulation  C is  in this  case  of lower priority  to  assess  based on  what we see in the last  circle  at the end of the  effort. Why ?how  would a VE limitation look like?
Metaborelfex? . well possible as a combination of the  muscular  limitation, but  the SmO2/tHb  trend  indicates  more likely not.

So  closer look for the coach on A  and B.
 Now  decision  time  for middle term or long   term   gala setting in structural changes.
Meaning: we have a  next  season goal setting we have to reach   .
 We  have a  4  year  olympic    cycle or what ever  to reach

or much more important is  a health  reason of a  patient . So functional ideas  are  worth less   and only middle  or  a long term structural changes  are a goal

Example :  post ACL  repair of  a  downhill skier. ( middle  term  for next   winter not  this one)
COPD  client  who like to try to get of oxygen  for walks.
Perosn  with Lymes  disease  who  tries  top go back  to performance sport   instead of  actually getting  healthy  if possible.
So  the key in all cases is  to look at the structural needs  before we  look at actual performance improvement.

In our  above  case  or in any case, where we have a  delivery limitation. The  question than is   how I may  tackle  this  challenge.
 Do I  work on intermuscular  coordination ( Seboo )   or on intramuscular  coordination  when I  try to solve the delivery over the locomotion systems.
  How  do I do  that.
 - Look  first   whether the cardiac  system actually   is able  to allow  a  higher intermuscular coordination or whether  the CO is really the main structural  problem.
Why is this important.

If  your  CO  is  the actual limitation and you add  a great intermuscular training to develop more  demand  for O2  but you simply  can not deliver, you create  " sleeping giant  even more "  and  your  will have no   benefit  in the long term. You may   in a  short effort  , where CO  is not  a main   problem, create a   progress  so in sports where  this is the key it may be  a good  idea
 In  a  sport with  loads longer  than  30 -  60  seconds  you may  loose.

This is  what very often happen,  as we may simply add more  km  and hours  to a  training plan  and  higher intensity.
 So  we may  nicely improve   utilization  with some   HIIT (  but we may MISS)  the  limiter   after  a while, as     better utilization may create a higher demand of  CO2  release , but the VE  was never improved  with the workout  you did based ion performance alone.
 Or  you may in fact improve  your  coordination  and your mitochondria density  nicely, but you never  improved  the CO   so you create a  sleeping giant.

Than the  question  fo relative  strength. Do  you  can afford  to gain muscular  weight  or  do you better improve  CO .

Important  for sports  like  rock  climbing , or   light  weight rowers  or boxing or any sports where we have weight  classes.

So    you   again first  may have to rule out, that  the CO  is not  close  to its limitation before  you add mitochondrial  improvement  and   inter muscular  coordination.


This   you do  with some simple  cardiac overload exercises  or  data collections.  Or  you   can  go back and  check  your old  VO2  test  with your  coach  as  often we  can see some trends  there.

Many VO2 users  in this  forum so  they may be ready  to  kick in their   knowledge  on how they use  the VO2  test  for this information.

SEBOO

That moves  us over  to seboo's  great data sharing.
 We  do NOT have  enough to be sure but we have a trend.
 See the   first  2  datas where we  had some difference in tHb reactions  and than look at his  last  FTP  feedback.

In the  first glimpse  he shows  a intermuscular  weakness with a  total overload  and overuse  in his sport with the VL  at least. He  can push great but the delivery  limitation  shown in his  VL  will never allow  him  to do some  sudden sprints  or attacks  as  the " gas  tank" is close  to empty (  SmO2 levels.)


Now  you look at  FTP  end  and the  " fatigues  "  assessment  and you see a trend  that his  cardiac  system  may be  close to a limitation  and or  may  be used often as a  compensator.

If  it is a limiter  than intermuscular  coordination   improvement will back fire  over longer    time loads.
 If  it is a early compensator   than  it is important to train the  intermuscular  coordination without  always  asking  for help  from CO  so we do not overload the commentator  and make  a  limiter out of  him. 

Below  a  live  example  from a top athlete, ( Interval sport )who exactly  works  on that task. He has to learn to deoxygenate  for example  with or  without CO involvement.

leg 2.jpg 
Above  you see   after  calibration of  today's physiological  reaction (  first  20 min )   11  deoxygenation loads. He  could  have  actually  stopped  after  6 .
 What you see if  you look at  tHb and HR  that he had  to try  to  create a deoxygenetion load  a  deoxygenation with minimal  CO involvement every second  time (  See HR )  and   minimal   loss of blood flow.


Now below  another  example  great numbers  from an athlete who has a great control over this options  already . As well 20 min calibration and  the same task.


leg 1.jpg

As a summary  and a   discussion point  to Seboo's   information in what  NIRS/ MOXY  can do.
 I  strongly believe it is a live  feedback tools ( not a test  tool )  to  achieve the specific  individual goals  you set  for a  patient or  client.

Do  you like to  deliver   blood form  the actual  main delivery systems  or  do you like to shift blood  form one are  to another  , do you like to stimulate a local  area  or  doe you like to stimulate the  whole  team team ( systemic.).
 Below  a  repeat graph  set  we had  already on the forum a  few  times   as a   review.

This basic  research was  done in California  in the five  star  training center in Yucca Valley under the help  of Mary Ann Kelly.

localleg only  O2  utilization.jpg 
Above an exampel of a live  training , where the goal was to only locally overload.  workout on a bike.   Below  a   workout  whit the goal  to shift  blood from  upper body  to lower body . You can see    that as  son leg  workout  stops  and no load on arms  at all we see the SmO2   change in legs up in arms  down.
No  no integration of  arms  and we are   sure as no SEMG  activity  and actually no activity  at  all  as soon the SmO2  of legs  reaches  the critical level. so arms  not even doing anything on handle bars

hard load  wiht O2  shift.jpg 

No  third  graph below .
A  systemic  deoxygenation  with  one muscle  in  the activity involved  and the  upper body muscle  no activity  at all  as the idea was  to create a systemic  deoxygenation.

respiratory  O2  reaction systemic.jpg 

Last  for   the moment.
 the running  example. The VO2  feedback  we got  combined  with the NIRS  we have    may suggest a different limitation  than what    seems to be  first the case.  The answer   hopefully comes  form VO2 users  and readers on this forum . 

Important.
  Nirs  the  way we  use it is a   live feedback  for individual planned   and targeted   goals  and not  a test equipment.
 We   really should not make  an assessment  and than use  the results    for a few weeks. We  really use  NIRS a   live feedback to make the assessment now  today  and    with the  individual goal in mind.

Is  that  crazy ?
  Perhaps not, as this is a serious   discussion behind  the scene , as  ideas like LT  and VO2   start to   slightly loos attraction and may  fall apart as we progress in physiological live   feedback  equipment.

James G Hopker 1*and Louis Passfield 1

 

Prescribing training involves the manipulation of intensity, duration and frequency of the sessions to improve cycling performance. As sports scientists our ideal is to help provide an objective scientific basis for this training prescription. But whilst we have developed an intimate knowledge of training adaptations and their regulating molecular signals (Stepto et al., 2009), we do not appear to be moving closer to providing a scientific basis from which to design effective training programmes (Borreson and Lambert, 2009).

 Below we post 3 questions for future training related research studies to consider.

 1) Are training studies using appropriate indices for specifying training intensity?

 2) Should training studies take more account of individual variation?

 3) Are training studies examining the right question?

 

There appears to be increasing agreement that the response to a standardised training programme can be remarkably diverse (Mann et al., 2014).

 This has lead some to examine these training “responders” and “non-responders” and its genetic basis (Ehlert et al. 2013).
Surprisingly, the alternative hypothesis that training has not been standardised appropriately appears to have been little considered (Mann et al. 2014).

From this perspective the issue becomes not whether a cyclist is a responder or a non-responder, but rather what is his or her optimal training intensity.

For example, it has long been established that cyclists’ time to exhaustion at the same relative intensity can vary hugely. Coyle et al. (1988) found that at 88% VO2max cyclists’ time to exhaustion varied from 12 min to 75 min.
However, the method for prescribing training in most studies remains standardised as a percentage of maximum.

Consequently, it seems unsurprising that the training response differs between two cyclists training at a standardised intensity that yields such a diverse response to even a single bout of exercise.

Even where the ability to sustain a standardised training intensity is more carefully controlled, the underlying assumption that this is linked to a training response remains unproven.


 

sebo2000

Development Team Member
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Posts: 227
 #2 

Juerg,

Thanks for posting those examples with O2 shuttle from non-priority muscles to working muscles, it confirms my question about hamstrings to VL O2 shift during rest after hard sprint. When I was looking at SmO2 after sprint, Moxy attached to hamstring it looked like curve shift, Hamstrings SmO2 was dropping rapidly but VL was increasing.

Your examples are priceless please keep them coming.

 What you see if  you look at  tHb and HR  that he had  to try  to  create a deoxygenetion load  a  deoxygenation with minimal  CO involvement every second  time (  See HR )  and   minimal   loss of blood flow.

 How is he doing this? Is it static muscle contraction every second time?

 

 

In the Oleksyn case:

First It seems he has his W’ not setup properly (if it is even possible to set it up properly….)  

His W’ doesn’t go to 0, but only to 10” when I blow up at 10 is when I race without warmup or when my W’ is not setup properly.

I think Oleksy exploded not in 25 min, but much earlier between 15-20min, if he would just ease up during that SmO2 dip between 15-20m he would probably have no problem to continue without blowup. Considering fairly stable tHb while SmO2 was at all time low, it seems he could have problem with respiratory system at high loads. Was there any warm-up done? I would love to see any data from before this race. In 35min he also works hard in high 300W's but his SmO2 looks much better, maybe because he is already properly warmed up?

Olexy.JPG 


juergfeldmann

Development Team Member
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Posts: 1,501
 #3 
Perhaps  some  readers may like to know  what W  bal actually  suppose  to tell u s.
 ?

How is he doing this? Is it static muscle contraction every second time?

No  not  at all it is    always  during actual muscle activity   for what ever sport  you do.
sebo2000

Development Team Member
Registered:
Posts: 227
 #4 
W prime stands for a physical amount of anaerobic energy every individual has available to them above Critical Power.

More of that "magic number" here:

http://cyclingcenterdallas.com/blog/2015/09/14/what-is-w-prime-and-how-can-it-make-me-a-stronger-cyclist

As much as I like the idea, it is just theoretical "magic" that has very little to do with reality. Here is why:

I can set my W' based on 1 hour TT effort quite precisely, I will bonk after 1 hour. Then I can do literally 10 high intensity sprints and my W prime will be negative indicating it is not set properly... because it can not be negative...

Then I will adjust my W prime based on those sprints, and I will never be close to draining my tank over one hour TT.....

Our physiological system is way to dynamic for W prime to be meaningful. I have set my W prime based on training on the trainer, and first outside crit tanked that number to -35%!!! Then it was good for some time 2-3 weeks, Provincial road race just smashed it again to -15% I was never able to hit 0 after that adjustment in 2016 season.

You could use it as kinda "warning" before bonking, but you need to keep in mind it is dynamic, so you would have to leave some room in case you have bad day... 

Another strange "phenomena" if your FTP is 300W and you go for an hour at 298W your W prime will not move (since you are below CP), despite the fact you might be totally dead, but W prime shows you are fresh at 0...




How is he doing this? Is it static muscle contraction every second time?

No  not  at all it is    always  during actual muscle activity   for what ever sport  you do.


Could you share what activity\sport was done during that interval?







 

juergfeldmann

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Registered:
Posts: 1,501
 #5 
Cross country  skiing on roller  skis on a road  with  the    laptop in  the  back back so we  could use peripedal. The reason why SmO2    top and bottom is not perfect  like in a  live feedback  was,  because the  athlete used  his body feeling  so when to go  again and when  to stop the load  to get  this  for the upcoming  race season.  Below  a  picture   form two guys in great Briton. Marcel   and Duncan  from Abu Dhabi  now back in Canada.
 The where even much better. They used VO2,  NIRS  and physio  flow   all at the same time in  the field. 
 Wold's   unique  and only done case study  ever many many
years back . Great guys.
  On the  dash board of the car  you see Duncan looking at  real live   hemodynamic  feedback of Marcels   HR  and Stroke volume  and therefor  Cardiac  out put  as well below  not  seen on the pic   EF %  and Systemic  vascular  Resistance  and  most likely  LVET  ( left ventricular  ejection fraction. ) 
 Now  SVR  and tHb  go  often very  close  together  with HR  and SV.

Marcel real.jpg


T
his  just  to illustrate  that w e sometimes  have to  smile when we read  articles  who claim   that they   will be at the fore front.
 Nobody is on the forefront  as we   steady keep  improving  as there is no  end  result her just a  ongoing  critical reevaluation on what we  do  and  where we   try to improve.  Just because it is  not published  does not mean it is not  done or existing. 

Oleksiy

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Posts: 8
 #6 
Thank you very much for reviewing my case. Here's may be a few more datapoints:

I use to have:
  Peak Cardiac Output: 28,1 l/min
  Peak heart rate: 185 b/min
  Peak stroke volume: ca. 150 ml

Those number are a little outdated, but i'd like to believe my level of fitness didn't deteriorate since. 

The W' setting should be more or less about right, a week after (Nov 26) on another event i did deep down to -3.2

Warm up was a bit of a problem 5 min easy spinning, all I had:

Screen Shot 2016-12-25 at 11.00.49 PM.png 

Sorry for late reply. And have a good holidays!

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #7 
Sorry  but  with this grpahs  I can not  do a lot  in fact they may look fascinating like many NIRS datas we  can see this  days  but  are minimal  in value  to discuss.
 The same  for me is true  when I   get emails  sending  me lactate curves  or even individual lactate numbers  and so on.
 The same would be true if I  get a  SmO2  number  lets  say  73  sent  with the question  whether that is good or bad. A  single  lactate number  or a  single  Sm,O2  number or  as suhc a  W  bal  has little  practical values as  the systems  are  dynamic . They  would have to be steady readjusted.
  So  what is the best  information we  can get to understand  what 3.4 mmol lactate means  now  , or what  73  SmO2  values  means now  or a   climbing or  dropping W  bal trend.

Well having a live feedback ion what is happening now. So  steady lactate  vales as  they have a lag time   so it is not possible , 
BUT we  ca have stead live feedback on SmO2  and tHb numbers  and adjust according
It s really interesting  but over  the   now close  to 100 years  our dream as coaches  or in exercise physiology  is  or was to find out, where we have sufficient  or  more than needed  energy  available , than  sneak into  the  intensity (  Ramp or  step tests ) where we  see a  problem showing up,  but we   just can balance  energy supply  and demand  ( like the idea of  Lac steady state or MAX lass )  and than  find the "critical " or  " magical " point  where  the  energy supply  can not  follow  anymore  the  energy  utilization and we  see an  end to the   performance coming earlier or  later..

So  very smart people developed  some incredible tools and  formulas  to try to  get as  close as possible to the real  world of  steady  and dynamic  changes  when we  work out, knowing , theta the best way  would be to see it live steady  instead  of having a  one day test and than hope ,that we  are as close as possible   for the next  few weeks.
. Now  we have  a  tool  where  we have a much closer and steady live feedback  and  what do we do. We have  groups and companies  forcing a  technology, which can show  live , with minimal time lag,what is going on ,back into a  great,  but outdated  idea  of an indirect  heavy time lag  including  systems like VO2  and lactate. 
 Why would we do this and why  the huge  resistance  from many  to  at least give it a closer  open critical look  by adding the same critical  questions back to what we  do   or did. Again I will do that with a Swiss company  where we ave lactate , VO2  and NIRS  datas  not  to   critic one as being better than  the other, but being different  and  it would  be just fair  for all of the system to ask them same  question we now  with  NIRS ideas.

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