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Thanks for the interesting webinar.

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Adding a graph of the SmO2, tHb, and other measures all together on a time scale which were taken during the HIT test would be informative. It is not in the presentation currently.

Furthermore I am wondering how long (i.e. that is just a decision just as 5 min on and 5 min off) the plateaus of on and off were taken? That is. I can do a sprint, recover and see SmO2 go up again. It goes up quickly but I can decide after (say) 20 seconds that it looks like a plateau or after say 30 seconds o it looks like a plateau. Ans did they choose that plateau as being the same level of plateau everytime did they let the plateau level vary? These are all important points which are not mentioned. And how long could the subject sprint for 350 watt? Any increase in TTE or???? My point of plateau on upper level also holds for the lower (desaturated level)

I can tell you that this decision can significanly alter the time you can hold on to the exercise. Also of course this influences the type of physiological stimulation!!!!

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Ruud i have been thinking about similar ideas as what you write above. I wonder if one of the metrics that will start to develop in this field is the gradient and change in gradient of Sm02. This could be used in future to help define the answers to the questions you are putting forward.

E.g. something like when the change in gradient of Sm02 is less than X% for at least Y seconds, then it is considered a "plateau"?

Steepness of gradient on load and recovery could be indicative too.

Just some ideas....


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Thanks for this good presentation. It certainly matches up with my uses for MOXY in my gym. How about "accessory" muscles rather than "non or less involved" muscles ?

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To Ruud's great points.
Absolutely agree and I like to show  hopefully later  some  of his  points  as  using SmO2  for interval or HIIT  alone is on pretty  shaky ground  to say the least.  Top SmO2 plateau  as well as bottom SmO2  plateau  tell you nothing really  other than  you  are in a  delivery  and utilization  balance. In fact to  really push  some  thoughts. A  dropping SmO2  or an increase in SmO2  really only means the  %  of  O2Hb  to  Hb  changed but it  really does not mean that we  use more or less O2 . This has to be   moved together  with  tHb.  and  as well  with  some  O2  demand.
If  I am already  " ranting"  the set up  for  looking  at   priority  or non priority muscle is  an example how we  can create a conclusion  by simply avoiding a  possible   information of  priority  and non priority muscles.
 For regular readers  following this  forum  carefully   they know, that we need an activity where the cardiac output  can not support the  huge amount of  blood vessels which may have a vasodilatation  during a    whole body workout. So like many great  researchers  showed , the Cardiac out put  can not maintain the  needed BP  and a s such the minimal  pO2 in the vital  systems  and as  such     CG  will create   vasoconstriction in   locomotor  muscles  which are non priority  for the motion. Typical  example we showed  are  swimming ,  rowing and cross-country  skiing. The  reaction is very  clear and easy  to see, between a  no priority  muscle who increases  activity  and a  non priority muscle who looses  blood supply  due to  protection of BP  and a limitation of  CO. In the demonstrated  cases  the  arm  initial  example to see blood shunt  was ,   as they mentioned,  for sure no intensity limitation for  a CO limitation. Even the second one in a  healthy person  will not  create a CO limitation due to duration as well as  due to   low   muscle mass involvement.
 In fact the limiter  will be very unlikely  CO  or delivery, but rather a  local muscle limitation and as  such non need to    shift blood  from less involved muscles  to the overloaded  locally fatigued  muscle groups.
The  interesting experiment shows, that   when CO is not  a limiter, than we  do not  see a shift of  blood or a  reduction ( vasoconstriction ) in blood  flow  in less priority muscles  as the  BP is well maintained  as   such  base pO2 in vital systems  as well.

 The only limitation is  the problem that the needed ATP    can  not anymore  be maintain or produced  so to protect the baseline ATP  the   Brain will reduce  motor unit  recruitment  down to a level  where O 2 supply  can maintain the needed ATP level  and as such we  will get a low  SmO2 pleatau  which is   on an individual low intensity  level which is an intensity who can be maintained  with the  available  O2  delivery  and utilization balance. Perhaps s more later

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To  the  point of  non involved  and involved  muscles.
 The name  showed up in studeis  done in Japan  and  other great places   in the   early 2000 .  . Dr. Bellar  has  absolutely right  not  a good name and a very poor  decision  from my side  to take it over  without thinking.
 Andri  has a much better option  as he  suggested  priority and non priority  muscles  and we use  this in our research  and coaching  circles   now   really     all the time when we design training plans.
 The priority is  a  great     word , who  shows the picture , whether the   body really needs  this muscles    to survive.  You can   run  or bike easy  without  upper body   in case CO is   reaching a limitation so  priority to  run away is  in legs  and   the   option to  divert  blood to the legs    makes  sense  in this  case. Again remember  Shift  or vasoconstriction in the discussed idea only will take place  when there is a CO limitation  .In a HIIT there is NOT a shift  during   the load,in the recovery time as  priority  muscles will reload   before we can afford  reloading non priority muscles. This in case in the rest period  the delivery is limited. We showed many examples in this  direction in the forum. Cases, where  the  ; load  really stopped  so no way  the  no priority  muscle  was  now increasing activity  but we see  the  drop in this  muscles  as we see an increase in  SmO2 in the priority muscles.  To  ryincs  idea n the slope. We  id  about  10 year back this as  an initial idea on TSI %  and slope  as we have an incredible  sophisticated  software. We  failed   but that does not mean it may  go  so great if  people work  again on this. Our  conclusion was. SmO2  or TSI  alone  is  not an optimal feedback   and has to be connected d with tHb  and in some cases  with  HR  and RF  to  stay on simple  bio markers. This after we made it  very complicated  with Physio flow , VO2  blood sampling  SEMG  and more. So  fun to see, hen  slowly some  institution move again to  the  steps  we did  and we see, where they have similar  questions  and  problems  as we have and where they make conclusions  we did    to just  find out  we  where wrong. Fun times  as MOXY is more and more accepted.  The  interpretation is the first step. And we work  since a while actual physiological  training    so this will come up  for sure in the next  5  -  10 years.
Here a reminder.
If  we know  the history we  may avoid  many  steps   which where already done from smart people  reinvent the wheel ) and  can move forward  faster.

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To the point on vasoconstriction.  There is evidence that increased sympathetic outflow during exercise exerts a pressure causing the body to balance blood pressure and cardiac output.   Studies on adrenergic blockade have shown this during exercise, though some animal studies where the sympathetic nerves have been severed do not show comparable results.  However, alpha adrenergic receptor mediated vasoconstriction has been demonstrated to be attenuated by very modest changes in local environment pH.  Based upon the conclusions of some of the best minds in this field ( see Buckwalter and Clifford's review in Ex Sport Sci Review 2001) it is apparent that muscular contractions have a variety of way to attenuate sympathetic vasoconstriction.  

Therefore if the muscle is "non priority" but still has increased metabolism during the exercise it is likely to produce a local environment capable of attenuating sympathetic vasoconstriction.  We have seen that sEMG increases in these "non priority" muscles during cycling, signaling increased contractile activity.  

I guess to summarize my thoughts:  

1) It is not in dispute that sympathetic outflow increases during intense exercise and has the potential to cause vasoconstriction

2) There is evidence that many factors associated with muscle contraction can attenuate this increase

3) In a human with only Moxy it will be very difficult to study the interplay between Sympathetic vasoconstriction/attenuation via activation

My question:  Since we all agree that using Moxy we can see changes in these non priority muscles can we use this information to tell the coach/trainer something valuable.  I.E. does it really matter the underlying cause, if the coach knows that it signals a change in mechanics.  Again just my thoughts I don't claim to have all the answers in regard to this topics... 

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Posts: 1,501
Thanks  for the  nice feedback
 Here  where  it  may be interesting  to  add some more thoughts  over the next little  while.

My question:  Since we all agree that using Moxy we can see changes in these non priority muscles can we use this information to tell the coach/trainer something valuable.  I.E. does it really matter the underlying cause, if the coach knows that it signals a change in mechanics.  Again just my thoughts I don't claim to have all the answers in regard to this topics... 
a) The  initial    question  for us  was many years back,  how we  can combine and possibly see  interactions   with  cardiac information's  by collecting  SV, HR, EF %  SVR  LVET  and so on , than combine this  with respiratory feedbacks   like  FeO2 %  and  CO2  reactions  as well  as how this gas exchange  information is influenced  by TV  and RF  and therefor  possible change  O2 dissociation curve. Than integrating  NIRS  and   in NIRS using initially a  3    depth feedback   with Portamon  to understand possible shift of   Blood   from  the  surface to the muscle of  vica verca . ( we showed some of this   case studies in the forum a  while back   and   many years back in  the Fact- Canada  forum.  Than    the old    version of adding SEMG  as an additional  idea  to see,, whether  we simply start using   more muscle  for an overall performance or  not. And  as we  where  really keen in blood  values we  test  factroes  like ammonia  , lactate   Bicarbonate  and more.
 One  section we  very early on had  problems  was  that  Physio  flow ,NIRS   and SEMG gave us instant  live feedback's , where blood tests  and VO2  mask  test  where indirect  feedback's.
 So  as   all can imagine, there was immediately the open questions  on the individual time lag  in blood values  and  VO2  values  , So  the fun part than was  to play around  with  manipulation  of VO2   values  like TV  and RF manipulation including adding  O2  or reducing O2.
  The  result s  for us  where  somewhat intriguing as we  very  fast   had  the  question n thee actual  values  of  VO2  and Blood  values in the filed  due to the time lag question. This pushed  us to use  RF  and TV  as a  immediate feedback  and than looked  at influencing of cardiac parameters  and NIRS parameters.
 We  did  hundreds of test over many years  and had the privilege  to  have    people like Frank Bour    visiting us  as to help as well his dad.

So in short  the same question as  Dr. Bellar  has :
 can we use this information to tell the coach/trainer something valuable.

This  question motivated  us  to buy  anything out there  where we could combine    with the goal  to see  whether  any  idea  would  be  usable  to  move back to the grass root   so patients  can work with it with a minimal   money investment  and an optimal feedback.

I.E. does it really matter the underlying cause,

This  was the  other  most important  question
Why. If  I have a  cardiac  patient  with a leaking  aortic  valve,  how intense  can I   push him  to maintain current  ability  without  speeding up the   problem.
If  I have a  COPD   patient
How   hard  can I  push his  walks  to not  create  a  secondary  right ventricular problem  due to the  COPD  limitation or a  overload of his kidneys.
 Or  what is  the best  respiratory  workout  to balance the  chronic  overload d of  his  respiratory mussels. Or  how    do I maintain  or improve   muscular   situations in a severe  leg  accident, where I can not load  the  bone structures  for  3   + month.
 Sure many coaches will argue   that they  do not have this cases.
 I  would argue  you have  you simply just  do not see it that  clear.
 So starting  with people we knew  their  limiter  clearly  we  worked  our  way up  to  so called  healthy people  to see, whether we  would be able to see similar  trends.
 Than using the individual approach we have  with clear limiter patients  and use  this training  and stimulation ideas on  actual  healthy people.

This created  the idea of Limiter  and compensator  and the   feedback , that if  we do not know the limiter  we may overload the compensator.
  Again COPD  limiter  respiration  compensator cardiac  right ventricle-    sudden problem in  the compensator.
 Fast forward.
 Athlete  with a respiratory limitation ( not  metaboreflex)  so he  will compensate  with  2.3 DPG  and  all what shifts  O2  disscurve to the right.
 Picture  great utilization, but  poor  delivery. Result  nothing he simply may  reach his performance limitation,   so   some possible answer you reached  you genetic limitation, when in fact  I as a coach  reached my limitation to understand a possible  plateau in his current performance.

 does it really matter the underlying cause,

I believe  strongly yes,  and that what motivated  me   over he  last  35 +- years  to fins   ways  to  solve some of this intriguing  problems.
 Can we  do it  with NIRS.
 Much more than  I  thought  when   we started out combing  all of the above feedback's.
 The end result  starts  at the   least important  body  part  which is a non priority  muscle  as  the  body can most    afford  to  reduce   performance there  for survival reasons.

So  yes  what is the underlying cause.
 Is  it a  leg limitation  so I  try as I can afford  to integrate arms  to   push  the  same or  short tear a higher performance. As  nicely presented in the webinar.
 Or  is it a cardiac limitation  so CO  reaches a   limitation ( sleeping giant  / Marshall)  and  we  simply  can not afford  to open    or deliver blood  to all the  muscles  who could  help in a  higher performance.

So vasoconstriction due  to mechanical muscle  compression SEMG  up  or  sympathetic  vasoconstriction to maintain BP ?
Depending  which one will  most likely  change  the stimulation approach.

Or  other example.
 Long   endurance   load   and  now we see a  change in SmO2  and tHB  after a  certain  time.
 Now  it is nice  to  know  what causes  the drop.

 a) local muscular limitation, 
b) respiration  fatigue
 c)  cardiac limitation.  Now  the  easy us e of NIRS  combined  with  HR  and in some  cases  with RF  can  give a  nice  indication what is most likely the reason  for the  change in the NIRS  data's in a  priority or in a  non priority   muscle .
 Summary . Initially  we  found this  difference  by using all the toys  we had  and finally  started to see, that in most  cases (I not all ) we  actually only  need  MOXY  or  NIRS    and have the answer. So we can go live in the field  and correct if we like  the reaction or  keep the  compensator  overloading if this is the goal.

 I will show  possibly on here  some cases  where we  use this and how   as we work  daily  in this  direction.
 In 60 min I will do a specific  workout  in BFR  with a  severe   injury case and I will  ask whether I can show in the evening the live feedback  how we  control with NIRS  the load  , the rest  and the length of the  workout.
 Thanks' again  for the feedback.
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