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Development Team Member
Posts: 1,501
First again  thanks  for the  great feedback  and input.
 Allow me  to go  perhaps  step  by step  so it is not a dialogue  between  you  and me,  but hopefully we  can contribute  to some additional thoughts  for more  regular  and new  readers  here.
As you will  and all readers see :
 What I often get is the question:
 Can you not make it simple as a number  or formula.
Answer  sure we  can do this . We  can just  look at a  specific trend  in a  step test  and than assume ,where ever there is a  clear optical drop in SmO2  there is your critical  point  and depending on what we  like to sell, we name it  what is  easy to sell, like lactate threshold   or VO2  max  as  most people  phoning us  for testing  ask  for a VO2  max test or a lactate threshold  test. I than  try carefully to tell them , that this is great  for my bank account as it is easy to  do. The   software  spits the  " magical " point out  and the  software  makes the %  calculation  , you pay  and go  and the deal is done. ??

We all do this  and we  all sell it.
On this  forum  we try not to sell anything  but rather  open a  fair  discussion or  debate. Now in debates  when  absolutely perfect  we have  an opinion, we try to back it up  and if  good enough we may  have a positive debate  and add to each others  idea. That means including for us, that when the debate  shows, that the opposite  ideas  have a much better foundation, that we  are  willing to look at it  and in some  cases we may have to give up our  own  what we thought strong point.

 A  debate    is    as you   stand  naked here  and  you show  all what you have. the risk is that you have to give up  sometimes  and sometimes  you gain. This is  what we  like to do with MOXY. Not  a  desperate  defending on our ideas  and   equipment but a  fair  open  debate  in the hope  that  we  can give up our own EGO in many cases, where we  still lack  information.  So  not  a  shouting  match  but a  decent  debate on  what we like to  show   with NIRS. The  shouting debates  are in full swing here in Canada  for  election  and looking once in a  while  south than  they have the  same  "debates" no  space  for discussion but  senseless   story telling  with a  basket full of  empty promises.
 Hope we  do a  slightly better job here.

 Most regular readers , or  thinking readers who show up regular here  know by now , that we   have  more questions  than  answers  as  there is no such thing like a magical statistical number.
 I am absolutely convinced  that  earlier than later  some  companies or somebody will come  up  with this magical point  and will make lot's of money ( For  a while  at l least).

There was a  great article  in the early 1990  in the journal of Chest on  what I  describe  her. If you read it very  very carefully  than you see , what NIRS  may actually achieve , what the classical ideas where  at that time not able to achieve.

Chest. 1997 Mar;111(3):787-95.

Dangerous curves. A perspective on exercise, lactate, and the anaerobic threshold.

Myers J1, Ashley E.

Author information

  • 1Cardiology Division, Palo Alto Department of Veterans Affairs Medical Center, Stanford University, Calif, USA.


A number of general observations can be made from these recent studies. Lactate is a ubiquitous substance that is produced and removed from the body at all times, even at rest, both with and without the availability of oxygen. It is now recognized that lactate accumulates in the blood for several reasons, not just the fact that oxygen supply to the muscle is inadequate. Lactate production and removal is a continuous process; it is a change in the rate of one or the other that determines the blood lactate level. Rather than a specific threshold, there is most likely a period of time during which lactate production begins to exceed the body's capacity to remove it (through buffering or oxidation in other fibers). It may be appropriate to replace the term "anaerobic threshold" to a more functional description, since the muscles are never entirely anaerobic nor is there always a distinct threshold ("oxygen independent glycolysis" among others has been suggested) Lactate plays a major role as a metabolic substrate during exercise, is the preferred fuel for slow-twitch muscle fibers, and is a precursor for liver gluconeogenesis. The point at which lactate begins to accumulate in the blood, causing an increase in ventilation, is important to document clinically. Irrespective of the underlying mechanism or specific model that describes the process, the physiologic changes associated with lactate accumulation have significant import for cardiopulmonary performance. These include metabolic acidosis, impaired muscle contraction, hyperventilation, and altered oxygen kinetics, all of which contribute to an impaired capacity to perform work. Thus, any delay in the accumulation of blood lactate which can be attributed to an intervention (drug, exercise training, surgical, etc) may add important information concerning the efficacy of the intervention. A substantial body of evidence is available demonstrating that lactate accumulation occurs later (shifting to a higher percentage of Vo2max) after a period of endurance training. In athletes, the level of work that can be sustained prior to lactate accumulation, visually determined, is an accurate predictor of endurance performance. Presumably, these concepts have implications related to vocation/disability among patients with cardiovascular and pulmonary disease, but few such applied studies have been performed outside the laboratory. Blood lactate during exercise and its associated ventilatory changes maintain useful and interesting applications in both the clinical exercise laboratory and the sport sciences. However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science.

 The red   section  tells  you what I mean , looking  for " acidosis "  so O2  diss curve  shift influence  of  SmO2.
Impaired muscle contraction looking  at tHb  reactions
 Hyper ventilation looking again on tHb  reaction  and SmO2  due to O2  disscurve shift.
altered  oxygen kinetics  due to  all what we  talk about  when we talk about limiter  and compensator

.However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science.

   Perhaps not  anymore  or  at least  not as much as it did in the past  thanks to combination of cardiac , respiratory,  muscle contraction  and other feed backs,  which can show up sometimes very clear  sometimes   more hidden in  NIRS data collection.

So let's stick here  with our  own critical interpretations  with sometimes  more than  one  option  to work on , but than we  can go  and try  and test  and see live, whether the idea  is a good one  or whether we  have to reassess  once more.
 So in this way  we go through your   many great points  below. So  do not  be surprised  if more  questions show up  than  we had   before we started this.

Point A.
 have re-read through the posts a few times now and I feel like I have a much better understanding now about the theory of looking  at the cardiac limiters/compensators,

 I  think  the concept  is  clear  but just to be sure.
. We  do NOT look  for  just a  cardiac limitation or  compensation, This is  one  possible  limitation  of many.
 Here  some   pictures  from the ide a of feed back loops  and  we  may for  sure  forgot  some.


A as  I can recall critical  voice  form  UK   from a  cycling coach   gave some great hints in that direction. He argued  with  right, that  we can not  blame the limitation just ion cardiac  respiratory  or muscular  reasoning.
 Absolutely  true  and you can see that there  are many more feedback loops. Interesting  enough the same reader  ask to make it much easier  so  SmO2  goes up it means this  and down it means that. Well  you see, where we have our  own contradictions  and that is good. We  can start easy but   have to accept , that there may be much  more option  which have to be discussed.

 So  therefor let's  go  back  with this in mind  to the  easier model

limiter compensator  Day 1..jpg 

Now  I use this here  due to :
  I am somewhat stuck on the differentiation between muscle limiters as in your isometric biceps example. Are these different limiters or are these just description of the 'phases' during muscle limitation?

Absolutely  great point.
We  will have many great feedbacks  here.

 We  can always look at it  from different directions. Let's see whether I  can get that  clear  through.

In your   feedback  Isometric  muscle contraction.
LIMITER: a)  could be the  delivery system really  and not the muscle contraction, as the contraction is so string, that it overrules  the  pressure  from the delivery system.
b) in fact  when looking  form a  muscle contraction quality point o f view, than a  perfect  arterial occlusion  would be a  perfect  good muscle contraction  so strong , that you close up in and outflow.
 tHb will be stable.
 The bad    story  from this stable tHb  is , that it means  either no flow  ( occlusion )  so  blood volume does not change  due to no inflow  and no outflow. or perfect flow !!!!
 Where do we see   what is what :
  NO  flow   means   that no matter  what you do   like nothing  ( occlusion test )  or  a hard load    SmO2  will drop. In case of nothing  no activity it will drop  slow , in case of   high intensity activity if will drop fast.

Unfortunately that could be the case  as  ell when we have flow    in cases, where delivery is  lower  than  utilization. So we have to look at either   when we let go the load  and hope  for an occlusion outflow. There is one  rare  but possible situation, where the re is  minimal  or  no clear out  flow ???
 What situation is this.???

 Now  when we look a  " general  " reaction than  when we look  at   art occlusion created  by  actual  very intense  contraction the SmO2  drop is very rapid   compared  with a  drop in SmO2  due to  lower delivery than utilization.
 We  are talking in the range  of  10 - 15  seconds    to end the load   versus  minutes  to end the load.
So  are there different LIMITERS :  Yes    and you  can see  how we look at this question.
Again  form a different point of view  in the isometric  contraction of the biceps.
question : delivery limitation , when looking  from a  point, where we hope we  can  go for a  while, so  when  we create an occlusion than  we  have not  enough vasodilatation  to overcome the compression, so it  could be a cardiac limitation.
 But  if  we have a great cardiac  system  and we still see an occlusion trend or  a  very strong    compression  trend , than  we  could have a  muscular strength limitation . So  an increase in absolute strength  ( max  strength w) would  reduce the %  of  maximal  contraction  force  by a given load  and  the cardiac  out put   may have  better chance to  actually keep blood vessels open.
 Rhomert  and  other  we  showed  somewhere but here  just as a  rep.

blut geafeass und muskel contraction.jpg 

Very old  overhead from a presentation I gave in Spian  ice  ages  back  ( wow I am getting old )

So  as you can see  we  can take limitation  form tow or more areas.
 If  we have a occlusion trend  than it can eb muscular  maximal strength weakness  for example  or it  could be  cardiac  output  weakness but they feed each other . A  reduction in blood flow  due to muscular  compression educes  back flow   for a good preload  and as  such  the SV  will drop  and as  such  CO. How  can we  look at this.
A ) HR  If  HR  can go up we  can maintain CO  ( HR  x SV ) .  or   possibly better  with the 5/1/5  idea. I If the  CO is  great, than  at rest  we see a  great overshoot of tHb  as it opens all  compressed blood vessels  due to no existing contraction  at rest.
 If  we  have  no overshoot  just base line than we  may have a vascularisation limitation or  a CO limitation ( or  as in some cases an athlete who dories not relax
Now  additionally we  can look at trends in less involved muscles . So a cardiac limitation wil,  show up  as a  drop in tHB  at rest in  minimal involved muscles   as  the e weak CO  can not maintain the BP..

 We  will back here many more times.
  Summary. Yes different limiters but look at what you lie  to  achieve  and what question you have.
 Isometric  biceps    and good or bad  to have an occlusion . Here is  where you add  performance.
 Same contraction strength a few weeks  late r and no occlusion  than you know  you made  progress as you now have a delivery ability and will be able  to maintain the same grip strength over a much longer time.
 Yes in some cases  it sounds  crazy .
 Example  motocross  or  MTB  downhill forearm pump  or  rock climbing.
 More  strength  more  contraction .
 Yes  but  by the same  strength  in the grip less   occlusion if the h maximal strength is  higher.  Hope it makes sense
 Next up  we  go further down in your  feedback  but ask  back here  so we not get  lost.



Development Team Member
Posts: 1,501
Part 2   of  some additional add on  or  better  trying to  explain it  hope fully better. Here the section  I  try to address
"  I can see that as the subject starts the contraction the increase in tHb indicates a pooling due to the overwhelming peripheral resistance from the muscles which I connect to a venous occlusion. However I don’t quite understand your other terminology. Are you saying that during the first rep the compression of the muscle forced the blood that was in the muscle out, creating a drop in tHb .
I think we are looking here  at the  biceps  contraction.

biceps closer look.jpg

I hope  it is this  section you had  your  feedback  and questions on " terminology"
 Let's see  whether I can add some more feedback  as your  explanation with the garden hose as  mentioned is  exactly  what we  try  to use.
1. Time 860 green  down arrow green line This is  his  first  biceps  contraction.. We see  very often , that the first  contraction  is  of  a  different " quality " than the follow up  contractions.
 Same  with SEMG  and that's  why we  are relative confident  we  can  explain  what happens.
 The SEMG  activity in the  first  contraction  has  very often a   lower  amplitude  than the follow up  contractions.
The same interesting  picture  in  NIRS  with a  much easier to identify initial  drop in tHb  than the following  contractions. Our  explanation is  a  not   optimal intramuscular  contraction  the first time around  and than  the second  time a much better one. Meaning the first time  it  took  some  time  before we  had  a the full  availed  muscle contraction  which  than is  strong enough to initially  stop  out  flow  but still has  inflow.
 ( venous  occlusion trend  or   outflow restriction.) To use the   garden hose  example.
 The first    reaction is a  push or pressure on the garden hos e which reduce  blood flow  due to the compression.  tHb  drops.  Now  we have  and I will explain this in our   hurdler  topic ,  a situation that:
 a)  we  maintain this  contraction force  of  o so much pressure  we may see  no a  stable tHb   if   we have a balance between the compression  form the muscle contraction  and the pressure  from  the cardiac  out put.  So  in  a  start of  an activity we  will see   first a  drop in tHb  due to this  contraction compression  and  due to the fact , that cardiac  out put is  very low  and it will take  some time  to increase HR  and   with that  CO.
 Below a  very close look  on a  running test  in the start phase
col warm up start thb.jpg 
You  can see  out of a  "cold " start  the initial drop in tHb  as a  compression outflow by  0.
 Than approximately  30 +-  seconds  later you see  an increase  of tHb.
 In contrast to the biceps   example, where the increase is  due to  compression    of the muscle  contraction, which  increased  above the venous  BP  level  and therefor  slowed  down  reduced  or completely  closed  the out  flow option. ( inflow  still works  as it needs a  higher  compression on the arterial systems  ( better hose  quality ) than on the " cheaper  " hose  w quality of the venous    blood vessels.

 So in a  venous occlusion  it   increases  due to out flow   restriction. See  graph  from the   Artinis group. ( Portamon)
veneous occlusion.jpg 

Now just  to  avoid  confusion ( hope fully ) the picture  is a  static  example  so  artificial occlusion  idea.
 BUT  even here we  will have  a small drop in tHB  before  we see an increase  due to the  cuff. Look carefully  as we have an initial  small compression.
 Green is Thb  in this case.
 Now  what is different as well is  that when we  move  so  lot's  of activity we  have the same tHb reaction but not  as in this  example a  increase in O2 Hb  and HHb in this nice  way as we  may  use  more O2  than  O2  is delivered. so somewhat  or often different  reaction  in the way that  HHb ( blue goes  much more up  and O2Hb  red  goes much more  down. Very individual reaction  due to the nature , that a  muscular created  occlusion trend is not that predictable  than a  lab  created   cuff  occlusion study.  Now in the small tHb  start  load picture (  courtesy  of Mary Ann Kelly case study ) the  situation is  an initial  compression outflow. After  30 seconds  the cardiac  system  and the respiratory  system  kick  in more effective  and the HR  as a simple bio marker  will increase. This leads  to a higher  blood pressure  and as  such the question is , whether the blood  pressure  reaches  and even  balance  force  like the contraction pressure or  whether it will be  higher or  lower.
 Higher  BP  will start to over rule the muscle compression pressure  and tHb will increase as  we see.
 Lower BP  will  not   allow a higher blood flow in  fact we  may see an increase now  due  to occlusion ( pooling ) effect. Unfortunately it looks initially the same.
 If  cardiac out put  overrules    we  see  2  possible  additional indication.
 1. More blood    which is oxygenated  so  O2 Hb goes up  and  SmO2  can do  go up.

col thb smo2 r leg.jpg 

Above you see the full running 5/1/5  assessment  and the thb  we had  just the start phase  again  and  now  with the SmO2  trend.

Now you see the "dilemma"  again  . If  we  go with ATP  Cr.P  glucose and  anaerobic    alacticid  ideas  we have  a hard  time  to accept the reaction of the NIRS  trend. If  we  go  with somewhat  newer  and interesting  research  than  we have the following  fight  in front of us.

No such thing like anaerobe

 This  are  two  sections   form our  MOXY introduction seminar in Boulder Colorado  where we had the  pleasure  as well to have Frank Bour  and his  genius  Physio flow as a presenter  with us.

pp start  thb  no warm up.jpg 

pp start  smo2  no warm up.jpg 

 I hope  this  makes  some sense.
 So back to  the original  explanation biceps  now  in short.  1.  Sometimes  initial  tHb  drop as a  contraction compression out  flow.
2. If  very strong  contraction we see a  increase in tHB  as  a pooling  due  to venous occlusion  trend.
 If  very  rapid  extreme  contraction this  increase my  be very short  and will go over into a  flat tHb   meaning we reached  an arterial occlusion  so  no  inflow no outflow  so no change in blood flow or  volume.
 Than  when  the athlete hesitates  or looses  some  contraction force  he  may create a  venous occlusion and  has  again inflow  and he  may go up  again.
 If  he  hesitates  and releases  more  pressure we  may have  short    occlusion outflow  and thB  drops . If  we  motivate   again he may increase force again  and  may reach once  more  a venous occlusion  force  and tHb  goes  up  as you can see in the last  contraction , before he  gives  up  and than tHb  drops  as  an occlusion  outflow.

 Now this interactions between  compression  and   cardiac  pressure  but as well vasodilatation  and vasoconstriction   stimulation due  for  example CO2  levels  will  dramatically  influence the duration  an athlete  can  maintain a  critical load.  ( question  off  blood flow  or  restriction  due to changing physiological reactions.)Now  what makes it  even more interesting is that this balance between this  reactions can change  from day to day  depending on your  stimulation you may have done  the day before.
 Example. You did a  very specific  respiratory  workout    with  a high VE  of 250 l / min  but you kept  the  cardiac out put  on  slightly   above resting level  as you had a cardiac stimulation  2  days before  so rest  day  for the cardiac  system  but  full load  for your respiratory  system. So next  day the respiratory system is NOT recovered  so very easy a problem  with  CO2  release. By the way the HRV  will   create  some   big  questions as it is not included in this  possibility  despite the fact that HRV  is heavily influenced  by the respiratory system .
 The  blood vessel reaction will be  very different  and the duration on a critical speed  will be  very different.
 This is  the   amazing  and interesting  discussion on many    forums  on  the ability to predict  or better hope to predict   CP  duration  based on  formulas  and  mathematical  ideas. The  assumptions  are  so  open on what today  may be  reacting as  a limiter that it is  for me  fascinating to see , with  what security  and absolute  certainty  this  groups  are  able to predict performance. Does it work in reality ? 

Will be  back in the hurdler  topic  on the  tHb  reaction n some different details.

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