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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
First  I have to apologize  for my back lag  of answering emails  and  forum posts. I am still trying to catch up  after being 3  days out  of order  due to a hip operation  and I slowly  try to catch up on patients, emails  and on here. So here not  as  an excuse  but as a  " time saver". I  got over the last  3 - 4  weeks  an incredible number of very nice  and positive e mails.
 Readers out there  seem  to  start to  get   some fun on what we do here  and in many cases  start to actually think in a  great way to  enhance  what we  do  and like to try to  get over as a message. So  to summarize  a  big group of  mails :
 MOXY  seems to have  an incredible  potential ( My add on NIRS ) . Problem  with the forum.  YOU ( Which is me )    run often away  with far  to much into  detailed  discussion and answers  with  some regular readers, who  are now as well  far ahead of  the majority of  new readers  and as  such   the new comber looses  connection  and   opportunities  to come back  with  very basic  questions  on MOXY
 My  simple answer to this is:  You are  all absolutely right. I am always getting back into the same stupid    habit  to try to show  all  and more  what is possible  and  often than  talk in " our " language  and therefor  loose  many great opportunities  to  invite  more people in our  small world  of  practical application and    physiological thinking.

 Okay  give me  another chance  and than many more  as I am sure I will get lost again. So please simply insist  and come back  and bug me.

 I like to use a  Case study here :
 Target readers:  Newcomers, personal coaches . PE teachers, Fitness center owners. Small interest groups  in any endurance sport. Sport  stores and more.
Goal: Show a very basic  nearly " classical " use  of MOXY. Many of the above group have all one  question and problem in common:
 How  can I use physiological testing ideas  for  my group or myself.
a) Invasive blood testing like lactate has  some legal problems and some  fear    for many people of  contamination, as well as there are more  and more   readers  questioning the   benefit  of  lactate testing in a group setting  or  even as a field test method
b) VO2  testing  is  interesting, somewhat  lab specific    and you often  can do one by one only. Still some possible contamination problem  with masks and all the limitation we  often discussed.
 Main problem  for sure is the price. A  decent  good VO2  equipment  is  somewhere  between 6'000 $  and up. And  it  can only be used  for the testing . So  the majority  off mails  clearly indicate, that MOXY  is   now  a very affordable  equipment of  the above  groups  and many  even  ask , whether it would make  sense  to  have  4  or more units.
 H ahaa I am biased. So my   best answer is  here. Start  with one  learn to see what you will do with it  and than you  still have 5'000 $  left  for  what ever you like to add later.

Basic case  we look at:
It is a  simple  step test done outdoors in running  with a GPS  guided  speed  control. There is many other I options    if you do not have a GPS    for speed control we can discuss later.
Test is  5 min step test . Start speed  3 mph . Speed increase very 5 min 1 mph  till subjective feeling  that is it. The run was done on a  relative  flat  road  around the neighbor hood.
 As usual  I  get  many  data's  and the only  part I use  is to not read  any comment  and just take the MOXY csv  file  to  look at this first. If  we have  HR  with it great  or  speed great. But I like to concentrate  just on  what we  get out of MOXY.

Moxy placement in this case:  MOXY  1  always dark  color.  Vastus lateralis left leg
                                            MOXY 2  always medium dark color Left  calf  muscle ( Gastrocnemius)
                                            MOXY 3 always  light color  on Deltoideus  left shoulder  pars   
                                            claviculare)

sMo2 runner  pic.jpg


So let's start  with the SmO2  information. SmO2 is given in % as an absolute number.
 It is the  %  of  Hb ( Mb ) loaded  with  oxygen.
Simple example. 100 Hb pieces.   and 65  of this Hb  ( Mb )  are loaded  with O2  so O2Hb ( loaded hemoglobin or  oxyhemoglobin   are loaded    and 35 HHb  deoxyhemoglobin   are not loaded  and SmO2  is  65 %. In  MOXY " language"  red  is used  for O2Hb,  blue is used  for HHb, green is used  for SmO2.
 Now  O2Hb  plus HHb   will give you  100  and it is the tHb ( total hemoglobin ) We use a brown color  for tHb.
 Basic interpretation
SmO2:
  An increase in SmO2 indicates  that we   deliver  more O2  to the test area  than we  for the current intensity actually  would need .
a flat SmO2 trace indicates, that  for the current situation we have in the test area a balanced situation, where  the amount of O2  delivered  equals the amount  of  utilized  Oxygen.
a dropping  SmO2  trace indicates  that  at that current situation in the test area  the   oxygen used  is higher than the amount  who  can  be or is  delivered.
 In other words    we have in this case a   " time "  situation  on how long we  can afford  to use  more than we  can deliver.?
 Okay your  turn. Let's  make  an interpretation  based on the above.
smo2  all three   all.jpg 
You  explain. every grid line ( 300 is 300 seconds  so approximately  5 min  change  off speed . first  0 - 300 is 3 mph  and than every   time  1 mph faster. So how many complete  steps  did he  do  ? Some interesting points.
 VL  and D ( delta  ) have  a relative similar trend  at least  the first 2 steps.
The  gastrocnemius (  calf ) seem to have a mind  on its own. Now in running the  running speed  can have an incredible influence on the calf  activity  as  in a very slow  speed  and here it is  3  mph  you run  very different , than  when you run 5  or  6 mph.
 Actually  really  can we  " run" 3 mph "  well for sure but interesting enough that  would be  for most of  us  fore foot running  even if  we  are heel striker  as it is  so slow  that you have some major  problem to   run over your heel if you are a heel striker.
Now   IF  this  would be the  case  here we would have a very  rapid  drop in SmO2   on the calf  but we  do not have that really . We see that drop  by  step 3. So  the question comes up , whether   in this case  step one  and 2  because of the slow pave  where actually done in walking so  very little  calf  activity   as we are clear heel striker. ?
Than by  step three  clear drop so  possible  as well from the speed  slow  jogging  and we  have a confirmation  form the vastus  lateralis  as he  has to work  harder now    when we  jog  than walk. Now  go  from calf to VL  to D  and try  where you would be able to see some relative clear  reactions inSmO2 trend.
 One more interesting point is the step 4  , where  at least the D   suggests , that there was a  moment of  a higher speed   followed by a possible correction of speed .?
 If  we have speed feedback   or even HR  we would have  the answer. So below  I  show you some suggestion  of " zoning"
 1. VL SmO2 trend
smo2  VL all plus  zoning.jpg 
Seems to be relative straight forward. We always  could discuss  HII ( High intensity ) I  chose  HII as he  was not able to finish the 5 min as it looks

 Now  same  idea  for  calf.
smo2 G all plus  zoning.jpg 
Some what not happy. Now this is  very subjective, but after all this years  of using NIRS  I never  be  happy with the calf muscle feedback . Sometimes  it seem to  work nicely  but  in many cases  the trend is not  optimal  like in this case. There  are  many reason  for this , so I do not use  MOXY on the calf.  The only possible reason  why people like it is , that it is  relative easy for placement. If people have   tights  on you can simply  push the lower part up  which is  for many people  more comfortable than  pushing your pants  down ( Smile )  most likely it is easier  to run with the pants  up than  with the pants  down. If you do not believe that try it out   ( But sent us the video )

So we  look at the third  MOXY placed on the front delta portion. So  this muscle is  actually involved in running, but much less  important  so least involved  muscle.



smo2 Delta all plus  zoning.jpg


Nearly the nicest trend.  Step 4  the questionable   drop and recovery  and steep  5 a small similar situation  as well. I added  with some rough look  at  the HR  the potential HR " zoning " to it.

Now that is it  Your basic ' Individual ZONING idea  based on SmO2 trend  and than using HR  or speed  ( performance  to guide the workouts. In most cases  we  may use the familiar  HR  as  HR monitors  are    all over    in any fitness   person. Nothing is  calculated  nothing is  %  it is all  feedback  from your body.
 Optimal  < Using HR  and  MOXY  and you  can daily have your   planned  optimal zone  based on live feedback  from HR  and SmO2    and sometimes  respiratory frequency.
 That is it.
 I will add  a next  thread  for the   advanced  use of this case study  and than  perhaps a third  for the  Pro user.


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Advanced use:
In the advanced  use  idea  we integrate  tHb  to it. tHb  as  an indication in many cases  on the blood flow  in the tested  area. 
Here the  overall view
ThB runner  pic.jpg 


tHb  can be influenced by different physiological reactions.
To make it again  simple.
 A  decrease in tHb  could be  named  vasoconstriction  or  reduction in blood flow. Vasoconstriction can have in  simple terms 2   reasons.
 1. Mechanical reason .  like muscle contraction  so we  compress the blood vessels  and we reduce blood flow  so tHb  drops (  similar like when we inflate a  BP cuff..
 So we have first a reduce  v blood flow  so  tHb  drops. If  we keep pumping up  we half suddenly a  pressure  , which   stops  outflow venous  occlusion or  at least reduces  outflow,  so  despite a  initial compression we now  may see  an increase in tHb as blood still moves in but less or nothing moves out..
 If  we let go  the  cuff or  muscle compression than we see  a drop  as we have  now  first a pooling outflow before we  are back to  " normal " flow. If  we  even increase more we  may reach  an in  and   anyway outflow pressure  and now  tHb is  flat. (  so it looks  like normal  but when we let go we see first a  drop  as again an outflow (  some exceptions ).
There is one  more easy  way to  see, whether it is a  complete occlusion or free flow. Look and think what you may expect  SmO2  would do under complete occlusion versus   free flow.
Now  lets go  again    from muscle to muscle  and you make the  interpretation.

 Vastus lateralis. Now I added  SmO2  to it so it is  easier  to  make  some conclusions.
thb  smo2 VL all.jpg 


Nice isn't it  and that's' all out of the small unit. Tell yourself  honest. What can you read   even remote  close  to what we see here  form a VO2  max test or  a  Maximal HR test or even worse  a   formula  of   age related  to potential  Max  HR ??
  Now  next is  calf muscle
  thb  smo2  G  all.jpg 

And last the delta  information
thb  smo2   Delta  all.jpg 


Now  you can see  in the delta  that there was  a clear  change in speed in step 4

Now  I like to finish the advanced  section with the explanation , why in many cases  a simple  mount of the moxy  on the arm  is the fastest  best way  to do. Push the sleeve  up and mount it there. I have  for myself  a   shirt  with a build in    section so I can simply push the  shirt in. No PR  for the shirt company here. Smile . For  cyclists  you simply build it into the cycling shorts

 Here the  explanation  why it   works.We  had it many times  and we  backed it up  with some great  studies  form different   section of  medicine.


o2  horarchie  SmO2 runner.jpg



o2  horarchie   all musce;les  runnerjpg.jpg 


So much  for the advanced  readers. Now lets  see in the next thread  whether we can challenge the  pros   in our  reader group.


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Pro interpretation
 Bad  wording   our Pro's  do not need  an interpretation, they simply need some additional pictures  to the once  we had  before.
 Okay here we  go. I  would  argue , that this person has a good delivery  system  and has a limitation in  vascularisation, and as  such  mitochondria density. Now remember. we normally use a 5/1/5  and in that idea the one  minute rest  to  try to find the limiter  and compensator  as it repeats  it every 4 5 min. What  repeat's its elf. The  nice situation, where  we suddenly completely stop[   O2  demand  form working muscles  but we  keep up  for a  certain lag time the delivery  for this O2  demand. Than we start suddenly  and now  we have  a huge  demand  but  not  anymore  a great delivery  which again   has a lag  time  befog it picks  up.
 Now in a  5 min step test we have both situations  once ??
Now look  at  advanced   pictures  and use  SmO2 tHb  from  VL  or  even  from   calf  muscle.
 Than  we can  add   more  and here   is a biased  feedback  form all there muscles . You make the interpretation.
Biased  runner  pic.jpg


VL  biased
Bias VL  all.jpg 


Calf  biased
Bias Gastro  all.jpg 


Delta biased
Bias  Delta  all.jpg


 Biased  means here. That we look O2Hb  and HHb trend  as it develops over the test   by assuming  that  both  are  equal  at thee start  so  0. This  show s us nicely  whether  and what  happens  during the test on relative change in O2     in each step.

 Now you add HR  and performance  and  in many cases  easy RF  to it  and you have a physiological test  with a physiological feedback  clearly into much  more  depth  than anything we use  or used in the past  for a fraction of   equipment   easy to use  for any body   and  anywhere  and in any sport.

danz

Development Team Member
Registered:
Posts: 4
 #4 
Hi Juerg,

Thank you from all the "beginners" out there.  I have some questions regarding the analysis.  I'll start with the first graph and then move on.

So the SmO2 graphs and zoning for each of the muscles.  I understand how the basic zonings are figured out based on basic trends...rising SmO2-ARI, stable SmO2-STEI, dropping SmO2-FEI and then the HII maybe a tough one on this...

Now for vascularization development, I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable...why not at the highest intensity of the STEI zone?...is it the high O2 content within the muscle that triggers the stimulus for capillarization...then how about mitochondrial density?...why not the highest intensity of STEI zone therefore putting a stress on enzymatic activity, mitochondrial activity?

Now the dropping FEI zone would indicate an increased demand for O2 but decrease in ability to supply it (via cardiac or respiratory or maybe the delivery men?)...however can this dropping Sm02 be a result of poor capillarization?mitochondrial density?...how can we tell the difference between the supplying part being a limiter vs. the using parts (enzymatic or mito)

Okay, maybe too many questions for the beginner part...one more thought:

the speed check in step four...my interpretation based on looking at the tHb would be that the subject started the step too fast, hence the drop in tHb in the deltoid (blood moved away from least involved muscle) and then once the speed was correct it went back up...

In a little bit I'll come back with questions regarding the "advanced" interpretations...tHb stuff and occlusions...


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #5 
Thanks  Dan ,
 Here a  try  to give some feedback  and some   even may be  actual answers  .
  Sorry but I  write  a lot  ans sometimes it may be smart sometimes  more    confusing.
 so here your  question where I need some help:

I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable

I   am nor  sure but I  can't remember  nor    would I have the courage top  give  an answer on how  coaches  out there   with much more experience  suppose to train  vascularisation and mitochondria  density.
 This  is up to the  coaches  to  do that. We  simply  supply  a  tool  so  coaches  can see  what is limiter and what is compensator.  In the past they did not had this  now  they  know  after a test  what  has to be improved  and now  they can   create a training plan based on this  directions  and goals  rather than on %  of something.. But again  can you  show  me  what the heck I may have written in a  pdf  or   on the forum. on how to stimulate  mitochondria density and capillarisation. 


   2.  Now the dropping FEI zone would indicate an increased demand for O2 but decrease in ability to supply it (via cardiac or respiratory or maybe the delivery men?)...

I am not  sure  whether   we  can  do this that simple  and that is the risk  when  going too basic. So here  my take.
 A  dropping SmO2  .where we  use  to  make  the  ideas,  that this is in FEI,  can have different reasons.
a) Same  O2  demand  but less supply than before  so SmO2  drops.. Could be seen in  tHb reaction. So  same  CO    perhaps even same HR  and Same SV  but more  muscle compression. Or  Same  CO  but lower  SV  and  higher HR  and more muscle compression  and  many more options.

b) Higher O2  demand  and higher  O2  delivery, but the demand  is higher  than the even increased  delivery  can handle  so SmO2  is dropping as well as well.

c) your  suggestion  as a decrease in delivery  and  an increase in demand  so SmO2  drops.

 d)  same delivery  but higher  demand  so SmO2  drops.   

This  options  will help you do  get more feedback on limiter  and  compensator.
  So that would lead  to  some  thoughts on your  last part 

 however can this dropping Sm02 be a result of poor capillarization?mitochondrial density.

poor  capillarisation  could be a part  of   poor delivery  ability or  as  capillarisation is a part of the delivery system .
 SmO2  is a part of the  energy delivery idea  so O2   %  of the tHb.. Whether we  have a great  loaded Hb  depends  mainly  on the exchange  area in the lungs to the blood. Once it is in the blood it  will be somehow  delivered.
 . If  we have a great CO  and  a good  respiration  (  CO2  balanced   than we  have a good loaded  blood  SpO2. Now  the delivery   is no  dependent  on the   blood vessels  and  as such  on the    ability to utilize  it  in the mitochondria..
So  a poor    capillarisation  and  a low  mitochondria density  would    not change the  amount  of O2  I have loaded  , in fact it may be  that I  have a great CO  and optimal loading,   and I load  so much ,  that I   not  or barely will see a  dent in the utilization if there is  a  poor  mitochondria density.
. That is the reason why we  have in many cases  a  very interesting situation.  A  top endurance athlete  and  I  work for the moment with a  100 - 150 mile runner,  barely shows  a drop in SmO2  and he  can go  long  and  long   relative  fast  long meaning over  10  plus  hours  and fast meaning 5 min / km  and faster  for that duration.
  His  deliver   when we test him is incredible    and his    ability  to move on FFA  and using O2  as well  but  he  is  in complete balance   after " warm up  where  he is  " fully moving O2  and   his  is balanced  in his race speed.  Interestingly enough  barely can handle  changes in speed   otherwise ,  he runs into trouble.

 On the other side  we have very healthy  but  very untrained  people. Their  delivery system is not great but healthy  an good enough to delver far  more than they  can utilize  or turn  around. So  same picture    as we  see an increase in SmO2  an than minimal  sometimes no  drop in SmO2   even in an all out    intensity.


 Like  poor CO  is a part of  poor   or lets put it more positive  not optimal delivery. Sop the  question is,  whether  when I have   a low  mitochondria  density , whether  SmO2  drops really  as I simply  turn  around  what i  get delivered.  As  O2  only  can drop  or  possibly only can drop  if it is used  it seems to me  it depends  on mitochondria  activity  and  as well density.
. So low  density  no  drop of  O2  as  it is  not  utilized.
 Hmm does that  makes  sense.
.The other interesting part is    as well that  mitochondria density is directly  connected  with capillarisation. The ability  to use O2    can be dependent  on the mitochondrial  activity.
 So to create in simple terms  more  mitochondria   I have  to   develop  first more blood vessels.
 
 But I can   improve  mitochondrial  utilization  without more mitochondria    and than I can  turn  more  energy , around as well.
 
That is the  every  15 years new  discussion between HIT  and LSD.
 A  very high intensity training    and much research shows that over  6 - 8  weeks  is more successful in using O2  than   a  LSD  for  6 - 8 weeks.

 So the conclusion we  than learn is  HIT is better than LSD  and it is used  as a great   fitness PR  for centers.
 Go short and hard  an you   will have the same  end result as  when you go long or  slow  actually even better as you  do not  " waste " time. Than  EPOC moves in it  an you  have a  very    Gospel like   group  of people running for that.

 LSD  over  6 - 8  weeks shows    limited  changes      as  it  is  an intensity, where a lot of  structural changes  take place  like for example   vascularisation  or  numbers  of mitochondria.
. There are  ample of    research done  showing this
BUT  you have to  look at   studies  over  3  -5   and more years.  If you go all  out HIT  and this is the only  traininig your do  you see   great and  fast improvement for  6  - 8  Weeks.  Do the same  for  16 -  18 weeks  and than  for  3  - 4 years  and  compared  with the once  who  do   a lot  of LSD  (    and  see, how they stake  up  now.


Problme :  I  can not  find , so please help.  A HIT  research. where they  did  the HIT over a  3 -4  years  duration and than compared  with the LSD idea. On the other side  we have  even longer studies  on LSD  from cross counrty skiing  and  rowing, where  in this sports  80 +0-  %  of the time invested  is done in a LSD  or they use   lactate    as a no show  for their LSD  as it is  still produced  but  it is turned  around and does not show up in the finger  or ear.  If    and just  IF  we  can do  a  20 min HIT  and than go  and win a  50 km  cross country  skii or a   Tour  de france, may  allow to ask the question, why all this pros  train so much  and so long  and  so  slow. Will try to fond ome  stduie s who show tweh ratio of    LSD  to  HIT  in   endurance
sport.


This    discussion may answer  Dan's  first  question on  STEI  and   intensity  versus  high SmO2.
 What is  your goal :
 Functional versus  structural ?
 Here a little bit more  to start.


Structural and functional adaptations of the cardiovascular system by training.

Huonker M, Halle M, Keul J.

Source

Department of Rehabilitation, Prevention and Sports Medicine, Freiburg University Hospital, Germany.

Abstract

Muscular training induces structural and functional adaptations within the cardiovascular system which vary according to type, intensity and duration of muscular exertion. Dynamic muscular training for more than 5 h a week involving more than 1/6th of the skeletal muscle mass causes an increase in parasympathetic tone and an eccentric myocardial hypertrophy. The dimensions of all cardiac chambers enlarge up to 20% and the cardiac muscle mass may increase by 70%-80%. Static muscular training does not induce any change in the parasympathetic heart regulation, nor does it lead to any disproportional increase in cardiac muscle mass relative to skeletal muscle mass. However, a tendency towards a concentric myocardial hypertrophy can be observed. The effects of regular muscular training on the arteries are the subject of current scientific investigation. To explain the acute and chronic adaptations of the arterial vasculature to exercise, a "shear stress" hypothesis has been proposed. During dynamic muscular exercise the regional arterial blood flow is enhanced. This leads to an acute increase in intraluminal shear forces, which stimulates the vascular endothelium with a reactive flow-dependent regional vasodilation mediated by endothelial-derived relaxing factors (EDRF, EDNO). Chronic enhancement of shear forces induces endothelial cell-mediated alterations in gene expression (endothelin, growth factors, regulators of fibrinolysis) and chronic structural adaptations of the vascular wall (cytoskeletal redistribution, cell shape change). Recent duplex sonographic studies in humans have revealed a significant lumen increase of muscular type arteries induced by dynamic, predominantly aerobic muscular training, but not by static muscular training. These structural adaptations are confined to those arteries supplying exercising muscle groups, whereas functional adaptations with an improvement of regional compliance are found in all arteries.

 

and some  more    I put  together

Functional vs Structural changes through training

 

This blog is about making athletes think about their training, why do certain things and what happens when we try to adapt training programmes to our physiology instead of following the normal cookie cutter approach of just doing. Understanding what functional and structural changes are helps with this understanding of why we see certain changes through training. There is no official definition and these ideas come from FaCT so I have made my own version of the definition here plus given a few examples so you can get a idea of what functional and structural training is.

 

Don't confuse the definitions of functional training (or functional strength training) which Wiki writes it as, training the body for activities of daily life, which in short is transferring the strengths from one movement with resistance to a sport or activity.

 

Functional change definition: This is normally a short term result of training and is where the initial changes in the body is seen. Functional changes are often temporary and is gained and lost quickly.

 

Structural change definition: This is a long term change in the body that results from starting as a functional change and through months and sometimes years of specific training to develop that specific system may see the development of a structural change which supports the human body.

 

So when the two definition are combined then functional and structural training implies to the development of the human body through specific training which will normally start with functional change, and through specific stresses and adaptions lead to a structural change which will improve athletic performance. The development of the structure of the body which broadly speaking will include the respiratory system, cardiac system, muscular system, hormones, blood system etc.

 

Here are some simple examples: A professional cyclist who has been cycling for years, has a higher amount of mitochondria growth and capillarization compared to a amateur. Using the same trained cyclist, his muscles have developed from being a amateur cyclist being functionally good to adjusting the muscle fibres structurally so that they can better perform the required activity.

 

Athletes thus in general have a higher ability to utilise oxygen and pump a higher volume of blood which is developed through training.

 

You say so what, this is obvious. Here are some more examples to think through: A novice cross country skier will have problems initially learning to ski and use a huge amount of energy learning to balance, after a few days he has learned to balance and found the needed coordination and he will be skiing faster simply by having made a functional change. Now you did some tests as he started skiing and a few weeks later the skier has shown an improvement and you think, great he is fitter, but most likely due to the improved balance and coordination the skier is able to use more muscle to ski faster, which may show a higher VO2, instead of using muscle to balance. The Skier will initially very quickly develop the utilisation ability through capillarization and mitochondria density and the before mentioned improved balance and co-ordination. This is often the big improvements seen in research studies which last only a few weeks versus trained athletes where changes are small as there is very little room for functional changes. To make structural changes which will strengthen the athletes respiratory system, improve cardiac output and stroke volume may take months or even years.

 

Another type of example: A athlete goes to altitude or sleeps in a altitude tent and is able to raise his blood values, now he goes back to a lower altitude to compete and if he is a responder to altitude, he/her body is simply utilising the extra oxygen available to the body. To make a real altitude adaption takes many years of IHT and altitude training where the body learns to adapt, and to better utilize and deliver.

 

Some individuals can improve Stroke Volume (SV) through certain training protocols or even exercise which can be due to a plasma volume increase. This again is a very functional change which is temporary. Repeating this functional training over several weeks, sometimes months should (if the correct stimulus is used with the correct timing to stress the limitation) see a structural change in End Diastolic Volume (EDV) as a change in heart size, thus a higher volume ability to pump blood (stroke volume) and a lower heart rate (CO=SVxHR).

 

So in any system that you are training you need to think, is it development or just utilisation, i.e. capillarization or capillary utilisation, SV through plasma expansion or SV through EDV improvement, mitochondria density or mitochondria enzyme reaction. Is the sudden improvement weather related, (hot=warmer tarmac=different reactions on bicycle/skate wheels resistance.) or is it true structural adaptation. Another improvement which has not even been mentioned is on the mental side. Once you have done lets say a performance test, you know how it feels, so next time in most cases without any physical improvement you know how to pace it better. Changes in nutrition can make functional changes to blood (e.g. beet root) certain supplements which may buffer H+. Respiratory training with specific devices will initially show great improvements as coordination and general conditioning improves (similar to the idea with the skier) but long term diaphragm strength and transfer of training to sport specific activity may take months.

 

The key to train structure, you need to find what is the limitation which is creating the weak link in athletic performance.  

If  I   make a  short summary in a picture   than it looks like this  below.
F  and S.jpg 

 






Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #6 
Second  case study  running 5 min step test sent to us. This was  done on a treadmill   same protocol as the outside one.


danz

Development Team Member
Registered:
Posts: 4
 #7 
Thank you Juerg...as you can see beginner can get fairly crazy pretty quickly[eek][wink]...after I posted my response of questions I reread what I had written (again) and realized I was asking questions that "sort of" pertained to the analysis but not really...so I wall try to stay on interpreting the information and figuring out the limiter...

Basically, we can perhaps come up with rough zoning ideas with SmO2 only but it isn't until we add the tHb that we can start to sort out the why?

And was the interpretation of the speed check correct? (please give me that one)...

So once we add tHb, we can start to toy around with the idea of figuring out the compensator and limiter...especially with a second or third moxy in place and maybe more info (HR, resp)?

Can you define a couple of terms for me to make sure we are on the same page...at the start of the advanced interpretation, you discuss vasoconstriction...and you state that it can be cause by two things, 1 being mechanical and then you don't mention the other...my questions are in bold trying to piece together what is happening at the start of each new step or at high intensity

A  decrease in tHb  could be  named  vasoconstriction  or  reduction in blood flow. Vasoconstriction can have in  simple terms 2   reasons.
 1. Mechanical reason .  like muscle contraction  so we  compress the blood vessels  and we reduce blood flow  so tHb  drops (  similar like when we inflate a  BP cuff..
 So we have first a reduce  v blood flow  so  tHb  drops. Is this due to arterial occlusion when muscle first contracts or high contraction force? If  we keep pumping up How because we have a reduction in blood flow?  we half suddenly a  pressure  , which   stops  outflow venous  occlusion or  at least reduces  outflow,  so  despite a  initial compression we now  may see  an increase in tHb as blood still moves in but less or nothing moves out..So now in this situation we have an increase in tHb because we have a venous occlusion but not an arterial occlusion?  which come first?
 If  we let go  the  cuff or  muscle compression than we see  a drop  as we have  now  first a pooling outflow before we  are back to  " normal " flow. If  we  even increase more we  may reach  an in  and   anyway outflow pressure  and now  tHb is  flat. (  so it looks  like normal  but when we let go we see first a  drop  as again an outflow (  some exceptions ).
There is one  more easy  way to  see, whether it is a  complete occlusion or free flow. Look and think what you may expect  SmO2  would do under complete occlusion versus   free flow.My guess is that it would drop, no blood moving in or out but O2 being used

Thanks and more to come...
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #8 
Dan. Thanks  for  insisting.  I  often miss answers  or points  so  ye s  come always back. So let's see  where i got  lost  as usual.  a ) 

And was the interpretation of the speed check correct? (please give me that one)...
 
and  the original summary ? 
 Now for vascularization development, I read on the forum or in the pdf's that training at the highest point of SmO2 would be valuable...why not at the highest intensity of the STEI zone?...is it the high O2 content within the muscle that triggers the stimulus for capillarization...then how about mitochondrial density?...why not the highest intensity of STEI zone therefore putting a stress on enzymatic activity, mitochondrial activity?

The  answer is  often not that clear  even  when  we often get  straight forward   intensities  for this.
 I believe  we have to look at the different situations  who ask  for  limitations  and compensations. Vascularisation  can perhaps  even be called  angiogenesis or  new  build ups of blood vessels.
 The actual reasons or  triggers to this  steps  is not  well know but  we have different theories. For  mechanical  forces  over  chemical reactions  and  more.
 Than there is the   big big  discussion   whether the " recruitment" of    blood vessels is really as we  all learn  or learned. Here the old idea in a picture   we often as well show in presentations. Whne I  checked d  my last presentation  I had to ask my self, is this really up to date  or  is it just a nice  way  to avoid  questions on this  topic  as it  looks  so logic. Here  what i mean.
old  ideas on capillarisation.jpg 


This is  what I  normally used   as  a part of the  physiological reactions. It was  simple clear  and made  some sense  and I  like all of us  had  to  believe, what the researcher  would come up  with. I   over all this years  never got challenged  on this one  even If  I had  top Ph. D  guys in the   courses. I hate  that as I am  sure  we  always have to challenge in one or the other way, when there are  some open  questions.
 So I was digging around  as the idea  was just too nice  to be  completely  true. No  Problem . I  do not have an answer anymore.
 Here  why.





new idea.jpg 
And here the  new  picture  I use  together with the old one ?

new  ideas on capillarisation.jpg 

Than we add  functional  and structural  challenge  and reactions  and we  have even more open  questions.
 So my  answer  for myself  is:  I have no clue  anymore.
 So  what I do I  assess  with what I have  and if it is one MOXY  I use one moxy  if   I have  other additional tools  great I  can add them  as well.
 Now   when the assessment suggest a  capillarisation limitation I  try different approaches.
 a)  I make a short term plasma  volume  expansion workout  and  see, whether I have a different reaction the next  day  due to the short term functional increase in CO  .
 A  capillarsiation limitation  can show up as a  basic  calibration  tHb   value  of    let's  say 12. than  during a  workout  or assessment  when I suddenly stop the load   but keep CO  up , I can see, whether I easy overshoot  today 12  tHb  value  as a sign of an increase in blood flow in the tested  area. A  limitation in capillarisation will often show a minimal increase  after  I get rid  of  muscle compression as  most of the vessels are alread   open or  circulated.
 Hope this makes  sense.
 
Next up
  you discuss vasoconstriction...and you state that it can be cause by two things, 1 being mechanical and then you don't mention the other.
 
H aha see that is  me  start out nicely  and forget the end:
1.Mechanical.    and here I mean different  mechanical or  outside  pressure.
   Physiological mechanical is  most often the  actual muscle contraction compression. It  shows  up in tHb  as a  drop in  the trace. If  after the initial  muscle compression like you  start running or  rowing or  any activity the  now  " balance"  muscle activity is  slightly lower in  strength or motor unit recruitment you than have a decompression to  the now  actual blood flow.

load 2.jpg 
Above  an example  who could show that initial  drop followed  by  a  decompression    reaction  in tHb.
  If . the   muscle contraction force  is    strong or   may get  even stronger, than you  will see  an increase in tHb as well after the initial drop,  but now  it is  NOT a decompression but a  start  or  a  complete    venous occlusion or   outflow  restriction  and tHb goes up. Again if you keep increasing your force you may see a  stop in tHB increase as you reach  an  arterial  or  complete  occlusion.
 Now you will have  a  different  situation, as you let go and you have  an  outflow  from the pooled blood.. See below a  biceps    contraction   picture.
 Important.  If you read  studies  on occlusions it is not a  physiological occlusion but it is an  artificial occlusion over a cuff.
 If  this is done  perfect  you will have no  outflow of tHb  but instantly a  venous or  arterial occlusion

biceps closer look.jpg 

Now  other mechanical    compression  can be  from clothing. That's  why we  do not like bandage  or  circular    options to mount a NIRS.  Compression stockings is  an other  mechanical  compression  so  we do not like to use  compression sleeves  for  NIRS  assessment.
 Another mechanical reason is positioning. Like how a player  in an  off ice  section sits  or stands  on the bench.
 Or  how a rower  in the start situation hold his legs  or    when you change  from an  upper handle  bar  position to an aero position and so on.  Even in a bike test  6  or  12 0 clock position of your leg   ( try it out. )
 Now    besides mechanical  tHb  reactions we  have physiological  tHb reactions.
 The most  common  two are:
 Vasodilatation due to increase in CO  or  CO2   and  vasoconstriction due to  reflex  reactions like BP  correction. Here  an old      paper  but  a very nice  one

blood pressure.jpg 

sleeping giant.jpg    

sleeping giant blood flow 2.jpg 


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #9 

Okay  next  section  on Dan's   part :
 So now in this situation we have an increase in tHb because we have a venous occlusion but not an arterial occlusion? which come first 
  Think as in blood pressure  you have  an upper  and lower  BP.  so  when you  reach the lower   BP  resistance  you   have no outflow  anymore  and you can feel that in your arm  as you reached venous  BP  , than  once you reach  arterial pressure  ( upper pressure ) you stop inflow  as well so you  have no  flow anymore. So venous  before  arterial.    

2. My guess is that it would drop, no blood moving in or out but O2 being used
This is Dan's  great  feedback on  what happens in an  arterial occlusion with SmO2  to a free flow    on SmO2.

Now  here a  fun  home experiment.

  The " classical " idea is, that when you do  a  one or  2  rep   muscle activity like lets' say a bicep s curl. That  for this one or 2  reps  you do not use O2  or  in other  terms it is  completely  anaerobic  alacticid.
  Now  if that is  true   we do not need O2  for that   ???
 So make an occlusion  with a  band  on your  upper arm  just above  biceps  and  have a MOXY on your biceps  or  forearm or both. Now  simply wait  as you have no inflow  anymore  but your cells  or  who ever still will use O2. So you will see SmO2  dropping  slowly  but surely  and you do nothing.
 Now  once your each    perhaps  not even  zero  but 10  start doing your  1  or  2  rep  weight  with biceps  and tell us   on here how  you did  it  , where you  able to do it  and   if you do any other loads  can you do it  as long it is  " anaerobe  so up to  perhaps 6  loads. .


 Remember the discussion o HIT  and ts  surprisingly good result  on  O2    usage    compared  with LSD.
 Well HIT is highly aerobic  and uses  per time  unit  much more O2  than LSD . So it is not what we learned   , anaerobic  alacticid,  but highly aerobic  and high lacticid  . So no wonder  we have a similar  functional reaction but even much better than  doing an LSD  workout. We  train functionally  a  much more e and more intense  O2  usage  and recovery  of CrP  where we need  O2  as well. SmO2  can be used  as a  indirect feedback on  your CrP  recovery. STF  fibers  have a much faster SmO2  recovery  than FTF  fibers. We  come back later on  that one  as well.  The  question:
 How  did we  find out the difference in recovery of STF  and FTF  without using a biopsy .?

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