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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
This is an ongoing source of  mails I am getting on this topic.
 Here once more the open question:
 Could it be that the "physical protocol" will force some specific physiological reaction due to the step length and as such may not give us the full  ability to see possible reactions.
Reason is the time lag of the actual physiological reaction  and or energy need and the possibility to actually deliver the energy on the one side and than on the other side the test system we use ( indirect) information like lactate and VO2) where the time of the result display may not be the same as the actual   activity .
 Example of lactate is the  easiest way to understand it  and it is discussed in length   many times on here already.
 MOXY means direct immediately info on O2 trends in the working and resting muscles.
.
I like to show you 2 test here from the same athlete. Both tests start by 100 watt and increase by 30 watt  on each step.
 One test is a 1 min step test and repeated 3  x in a row .
 The other is a 3 min step test done once.
 Yellow is tHb and purple is Hb Diff . or SmO2 trend.
. Red as usual O2Hb and blue HHb.
 You can see nicely , how the oxygenation  reaction or better the de-oxygenation reaction is really different.

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Here some additional thoughts to the"design" of a protocol, the interpretation and the outcome.

See the  by  now well know study on VO2 max on  a Kajaker and a runner in three different protocol set up. Dal Monte 1967
PIC 1 Question.
 Is the VO2 max  limiting performance ? 
or.
 Is the specific activity( Performance) the reason for a specific  limitation in VO2 ?

 So when we go with a similar question to respiration:
 Is a specific speed ( performance ) limiting the way you can breath or is the way you breath limiting your performance ?
 Here a small case study  Nick McLean ( Student form the UBC campus was looking at during his daily running workout.
 He uses a MOXY, lactate pro and  HR monitor with speed and HR.
 We may show more of his daily tasks with the goal to train  an open mind for his future  studies at a university. Here his second task.
 Remember the first task was a relative stable HR and change in RF  6 steps in 6 steps out  followed by 5/5  and 4/4 down to 1/1/
Now second task:
 Run out relative hard and settle in a speed, where you are able to  breath 6 steps in and 6 steps out.
 Than increase speed  so you are able to breath 5 in and 5 out.
 And so on till 1/1
 So the speed had to be adjusted so that the respiratory task could be full filled.
 Meaning, that if he run too fast and could not sustain the demand 4/4   for example he had to slow down till the speed allowed the forced respiration. 
 The question was to see, how HR and SmO2  and speed would react by a fixed RF.
 PIC 2 You can see the steps  from 6/6  down to 1/1 and  the SmO2 reaction accordingly.
 What we like to see is, whether we increase SmO2   have a plateau or decrease SmO2.
 Than we  will follow with  a 3 rd idea by running  10 min in the "plateau and same Respiration pattern and look speed and HR and than the first Respiration pattern, where we see a trend of dropping SmO2 value We argued  to do that in 4/4 and 2/2
 Yes old Hollmann / Hettinger students may remember that fun work done with  steps and respiration over 1/4 century back.
 So next time we will have Nick's info on the idea of running 4/4 2/2 10 min long  and repeat this 3 times each. Look at speed and lactate and HR and see, who " stable " or not the different values show up and what  may change by doing this type of workout.
 ?

Pic 3 Yellow  is tHb , red O2Hb , blue is HHb and purple is Hb Diff.
 You can see nicely how in some area O2Hb and HHb increase in the same time  as well as tHb or sometimes  one drops the other climbs.


Thirds task will be
 Than the next step is to take lactate at the 4/4 and 2/2 respiratory sets and see how the metabolic dynamic may change if there may be a change in SmO2 in the same sets.
 Here the result by looking at  SmO2

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Third task.
 So our next small task for our student was to :
a) show how relative lactate values can look depending on handling problems , when taking samples.
b) Assess the reactions of SmO2 compared to "feeling". Meaning the reaction SmO2 may show, when you think you go hard and possibly " anaerobic"
Goal :
1. Feeling does not tell you , whether you "run out " of O2 or whether you overload with " lactate acid."
It is just a subjective situation telling you , that somewhere in the total system something does not work optimal anymore.
The fun part is to see, how feeling fits together with physiological information.
Example: How does it feel, when Stroke volume drops ?
How does it feel when you start to get hypocapnic or hypercapnic and how can I see that to confirm my feeling.
It is all about BIO markers which will give you a bio feedback.
The goal is to understand the " feeling " and signs your physiological systems sent to your CG ( central governor) and if you have this information , how in training and perhaps in a race can use that for a better personal performance.
We have the great info from our friends from Norway on upper body and lower body SmO2 trends. So the next step is to see, how we may be able to try to " activate" the existing and available O2 in their upper body so it can be used for performance , if that is needed.

So the task here was.
Based on the SmO2 trend from the first case study we decided to go for a run with 2 respiratory tasks.
a) 4 steps in 4 steps put and 2 steps in 2 steps out
 The question was:
 How will SmO2 react with each repetition of the runs.
 10 min 4/4  10 min 2/2  and this repeated 23 x in a row.
 Would at the end in the last 4/4 and 2/2 the feeling be the same when doing the same speed and how  will the SmO2 trend look like.
 The picture shows you  the 3  sets of 4/4 and 2/2  The"pace" was given by the forced respiratory pattern he had to follow.
 Interestingly enough the  speed was incredible close to  3 x the same as you can see.
 Different is the story with the HR.
 And most interesting is that the " hardest" felt load  showed the most O2  in the muscle.
 BUT : It was not bio available.
. Key question.
 How do we have to train to make  available O2 in the muscles bio available. Why   in some athletes we see a great ability to use available  O2  and in others the opposite.
Which one is or has the better " anaerobic " power and which one has the better  aerobic  power ? What causes this difference and if I train one ability  do I loose the other or can I have both abilities and use what ever I need  under certain situations?

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #4 
Some thoughts to daily case studies we do and the  trend in SmO2.
1. When ever we overload  a specific vital system ( respiratory , cardiac system ) than we can see the following day a higher SmO2 by a given performance  in a simple step test , where we compare performance versus the bio marker of our choice. Some may remember  from many years back  the FaCT software from Herb, where we had something called performance line. Than we would overlap the performance line from a baseline test with the new updated test result and would look at the change of the 2 performance lines.
 At that time our Bio marker was HR.
 Some would use the same idea but would choose to take lactate and the trend of the lactate curve as an indication of performance change.
 The problematic with lactate was, that nutrition,   plus as we know now fatigue of some vital organs would dramatically change and manipulate the lactate curve.
 The " classical " idea , that a right shift indicates an improvement of aerobic performance was sometimes true but in some cases a low for a high carb loading a fatigued respiratory system or cardiac system could move the classical lactate curve in  both directions left or right , and any conclusion was build more on speculation than of actual information.
 Now the whole idea of using a performance line or performance information  is getting a whole new value.
 By using SmO2 combined with HR and RF and performance, we have a fully new information option to verify , whether a vital physiological system is not recovered yet or whether the local muscular system may need some recovery time.
 The careful reader may have observed, that in some case studies we showed the SmO2 does not drop anymore  down to the same level as " fatigue " may come into play. One may consider , that  some physiological reactions ( perhaps protective reactions )  limit or at least diminish the ability to use oxygen , which is in the tested muscle are for energy production. Therefore despite the  presence of oxygen the local muscular system will have to find O2 independent energy suppliers to maintain the ATP demand on the one side but as well to maintain  a possible needed minimal level of ATP and pO2.
So the interesting question now is ( as well brought up by our Norwegian group ) how or what can be done to actually try to get to the O2 which is clearly in the working muscles, but it can't be used, or in other words it is there but not  BIO available ..
a) is it structural limitation ( type of muscle fibers ? Capillarisation limitation , mitochondrial situation and more. ( like  local muscle strength.
b) is it a functional limitation>  O2 Diss curve positioning for example.
Here what we play around with.
 a) structural limitation can be  tested by doing a full IPAHD assessment and as well looking at T1 T3 levels for vascularisation reactions. To stimulate this we combine MOXY and Portamon and play with temperature changes ( ice and Heat)
 Here what we see. If we apply heat on the tested area we see an increase in T1 on the Portamon and a decrease in SmO2   and with ice we see the opposite , a decrease of T1  and an increase in SmO2  on MOXY.. In athletes with a huge capillarsiation bed or a speculative huge capillarisation bed this trends are very clear. In people  with suspected  minimal capilarisation have very minimal changes with this  assessment.
Now with temperature we know for sure the effect on vasodilatation and vasoconstriction. With respiratory manipulation we know often just from reading literature, that there is a vasodilatation and vasoconstriction effect  when either moving into hypercapnia or hypocapnia.
 The major problem is the sustainability of this  hyper or hypocapniac level over a long enough time to actually have the reaction.
 Hypocapnia can be easy done just by normal hyperventilation at a given intensity and it can be sustain on a stable level easy over 10 - 15 min and or longer, if the athlete is respiratory trained.
 So by working out hypocapnic we actually can see and influenced  the SmO2 values and therefor have the ability to set a very new or at least now visible stimulus.
This happens for sure daily in many workouts but till as of now we never really knew , which athlete actually did this type of training as it was never controlled nor did we ever cared about it.
 Hypocapnic workouts tend to create a vasoconstriction in the extremity muscles and  shift the O2 diss curve to the left. This will create a very unique stimulation . As the O2 Diss curve is on the left side we see a very nice and high SmO2   ( unreal seen ) as  it looks as if  we have lot's of SmO2 available. Well we have a lot of O2 in place but it is NOT bio available and as such we have a high SmO2 but we may in fact work hypoxic in the muscle due to the lack of BIO availability.
 Dream , crazy idea or reality ?
 If   and if this may be the case, than we would see, that at a give workout, where we move from a hypercapnic  respiration to a hypocapnic respiration  the metabolic  demand will shift from available O2  to less available O2  and therefore by a given speed the lactate, if the step is long enough will increase together with an increase in SmO2. Once we shift back to hypercapnia the SmO2 will drop and the lactate as well.This is a perfect example , that a drop in SmO2  not always will indicate an increase in lactate.
 Unfortunately  all existing studies I found will indicate , that this will be the case. A drop in the SmO2  curve in a 3 min test will be compared to an increase in lactate.
 I could not find one single study as of yet. where  the authors  collected as well the respiratory information ( RF , TV EtCO2 and so on ) to  combine the trend in SmO2 with the lactate information and than take into consideration the lag of the lactate information compared to the immediate SmO2 information.
 plus therefor the need to have at least a 5 min step length ( we use 10 min step length and double dip result when assessing lactate.
 Have fun to digest this ideas and please come back and take it apart so we can learn together.





Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #5 
Here a test sent to me a few days ago.
 I like to show you just the lactate trends.
 The protocol is our IPAHD protocol.
 This  client gave on his  base information a FTP of 319 watt.
 Based on this info we design a IPAHD.
 Step 1. 150 watt 5 min / 1 min rest / 5 min 150
 2 step 200/1/200
3rd 250/1/250
4th 300/1/300
and with a 319 FTP watt we expected  at least one 350 5 min load.
FTP would be the wattage average you are able to push over 1 h  TT.
So the graph 1 means first 5 min 2 means second 5 min same wattage 3 new wattage 4 repeat the new wattage and so on.
 The graph shows you the lactate trend and it is on of  most IPAHD lactate trend information, where you can see, that if we would have done 3  or 5 min step length and move up to the next load the lactate curve would every time look very different.
 Taking any absolute value , or any tangent or angel against the lactate curve or better lactate values is an interesting concept with many mathematical and statistical options, but as a tool of using it as a way of designing any intensity is at least questionable.
 What is fun to see is, that if the step length are long enough and we interrupt the homeostasis with a break in the  same step load we actually can see, where the body is metabolically still able to try to maintain a homeostasis and where it  goes out of control.
 Now you combine this information with MOXY ( NIRS ) info as well as with cardiac and respiratory info and you have for each of the system an information , where and when  the system can't maintain the homeostasis anymore.
 Give it some thought and come back with  ideas , questions and information.

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