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DanieleM

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 #16 
These are the intervals discussed in O2HHB-HHB view:

Etienne_HHB.png 
And confirms that O2HHB is not in balance as before.
 


Etiennebest

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Posts: 34
 #17 
Ok...let me try and wrap my head around this...
Below is a response to the further postings and also a summary of the things I think I should try to explore somehow. I'm doing this "in-line" and not reading ahead to see if there are additional answers...so things might change or seem inconsistent as I work through the reply.
If there are additional things I should explore, please let me know...

25/11
Juergf:

Possible  metaboreflex  at the end.
Breathing was VERY pronounced in the last two repeats...so the effect might have started to materialise during the second 275W set and be full blown by the end. 1min recovery probably insufficient to recover.
Possible cardiac compensation.
HR hit 141, very unusual for me in an indoor setting on a bike. So yes, quite possible that I finally got my heart to wake up at the end of the session.
Possible local limitation in delivery and utilization locally
Both? This should then make it easier for me to correct it since I do not have to put as much focus in not stressing too many compensators since there aren't that many?
Which one is for what or on what muscle.
Green is SmO2 on VL
Red is Smo2 on DA
Blue is Smo2 on Calf.
...that is no "fooling" anymore...
There is a distinct "uptick" in the HR between sets. In the first sets the HR response seems to stay consistent between sets, but during the sets that have been circled, the HR is not only increasing overall between sets but also steadily rising during sets to the point where it basically goes back to the previous maximum quite quickly. Am I looking at this correctly?
If you have a problem  increase  cerebral  Blood flow
I'm not sure if you're joking and mean we should think about the situation more or if you mean we should be considering the metaboreflex. Possibly both? [biggrin].
what   do you think  woudl we see  when we look at SV and SVR reaction options
SV would be up and SVR would be increasing or stable because of an increase in CO2?
My question...in the biased view. Is O2Hb increasing because my RF is up, because CO2 is causing vasodilation or because Thb is increasing overall?

27/11
Juergf:
...agree on how we could develop an action to see...
I'm all ears - if there is some part of the 5-1-5 you would like me to duplicate, or some other type of assessment you would like me to do to check a hypothesis then let me know.
1. SmO2 may drop or "hesitate to go up...
I do see a bit of a drop/hesitation in SmO2, but I'm not sure exactly what the graph should look like for this to be considered significant? The tHB seems a bit more pronounced.
2. Occlsuion.
Veneous occlusion release. What may we see with THb
I would expect to see a drop in Thb since the pooling is released, perhaps also an increase in SmO2 because O2 rich blood can now more easily enter the muscle (depends on the level of vasodilation).
Arterial occlusion release down to venous occlusion level how woudl tHB react than?
An initial increase and then leveling off (stabilisation) of the Thb level. SmO2 I would expect to increase?
3. ...end of the datas.
What caused the THb going
up.
I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.)
What caused SmO2 so it did not drop anymore?
THb is going up, so more oxygen getting to the muscle to balance it. I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.) Also work load is now more evenly distributed between VL and Bicep Femoris. PLUS increase in cadence means that there is less chance of occlusion happening?
Think SmO2 as % of tHb?
As per above, more Thb inflow. Could be that this is a new stable SmO2 "level"...that I might not be able to maintain for other reasons.
Now look where the work may have shifted to.
Better balance between bicep femoris and VL.
How would a body react in a survival mode
Non-involved muscles go first, then semi, then involved...RF is up, CO is up.
when he is not really stressed 
Keep going but react the bare minimum to get the job done?

27/11 (next post).
Juergf:
different reaction immediately after the load started
I see a sharp initial drop and then a sharp recovery followed by a more steady increase. Is this what you mean? Is this an indication of the venous occlusion I was referring to on the first graph (the occlusion, not the reason for it)?
Now
I'm not quite sure what I should be noticing on the blood volume trend graph and the one following. THb is up over all in the last set where I am really cranking it out. SmO2 is "level" vs. decreasing in the previous sets while Thb has the same upward trend?

27/11 (next post).
Juergf:
Does the drop in SmO2 really mean he was not anymore in O2 balance?
There seems to be an attempt to return to homeostasis at a lower SmO2.

DanieleM
And confirms that O2HHB is not in balance as before.

I think I agree with Daniele. CO is attempting to compensate, but there is a level of hypoxemia (is that the correct term) building up that it cannot compensate for through either vasodilation, RF, or CO.

Things to try:
1. Change which leg goes into 6 O'clock position to see if there is a mechanical occlusion during the rest.
2. Try increasing the rest period to see what happens to the tHB in my DA.
3. Check mitochondrial density on VL (15 sec occlusion protocol on as described elsewhere?).
4. Have CO (specifically SV) measured at the local high performance centre.
5. I also had in mind an assessment to see what would happen if I decided to "boil the frog slowly". I.e. Do a very slow ramp test, maybe 2 hours, starting at the same very low wattage requirement with the end point at 300w and just see at what point my body realises that there is a "lion in front of the rabbit hole" and how it responds.
6. Do a session with variances in cadence to see whether there is a clear relationship between cadence and VL Thb.
ryinc

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Posts: 369
 #18 
We can get to this point later in the discussion on this thread as it , but here is the mark up of the point earlier made about cadence and VL Thb - is this correlation just coincidence? Image 1.jpg  Image 2.jpg    
Etiennebest

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Posts: 34
 #19 
That is pretty compelling Ryan. I'll add it to the list of things to look at.
juergfeldmann

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Posts: 1,501
 #20 
Thanks  so much  and  you can see we are getting there.
 Start  with Daniele.
Exactly  that  what  you have  to do. Look at  HHb  O2Hb  biased or   non biased  to see, whether the tHb increase  and the small SmO2  drop may indicate a  stable or  unstable   balance in  O2  delivery and demand.
 Look at his  graph  and look at my  end  tHb  SmO2  graph  and see, that the blast step  where we  have a  tHb  increase  and a flat  to slightly dropping  SmO2  really is a step  where he is  again in metabolic balance  due to the change in    cycling coordination.. The    issue here is , that tHB is a relative   feedback  so  you will learn individually  to see, how much  relative change in your body  will actually immediately  tell you  whether the drop in SmO2  and the  increase in tHB is  still dropping  SmO2  or balancing  form the increase.. Will see, whether I find  my  grade  10 - 12  class  section, where we  made some  simple example to show this off. Daniele  great work .
 By the way need your  address  again  to sent you the MOXY you earned. email me teh   shipping  contact   so I can sent  it off today  from here.
juergfeldmann

Development Team Member
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Posts: 1,501
 #21 
To Etienne  amazing    feedback.
 Please give me  time  for the evening as thsi is too good to  answer between  clients  here so will go step by step in a  different color  to give me y opinion  to open  for discussion. In some  answers  to  thoughts you will see, that I have   many own open  questions. so  thanks  so much.

 To  rinc , cadence  and tHb
 In  some sports  like  cycling but even more  amazing in rowing  tHb  and  stroke  rate  and in cycling  tHb  and cadence  have a direct impact.  This leads  to the ongoing discussion in  cycling  circles  on  low RPM  versus  high RPM  and many studies done argue , that low RPM is better.  Here my point.
 Delivery  and utilization locally never is addressed in most of this studies . The view is a systemic   feedback   from VO2  assessments  and sometimes  from  lactate.
 The interesting section is   compression and relaxation  and  time duration.
 In  all cases, where muscular strength and coordination is not an issue  we see in higher cadence a much nicer  tHB  reaction due to  short  compression and relaxation  shifts.
 When the same  cyclist  goes low RPM  we have a much longer compression  and a  less optimal  regular  flow. The feeling many   cyclist have, that there is a much  better feeling in te legs  by a  certain  optimal individual  RPM  which is  most often higher than  80  .
What we looked  is  at different  reactions  and  I will try to  find them again on individual  reaction of tHb..
 You can see in Etiennes case  again in his last  load  where he change  his  technique  his  . Look at his RPM  combined  with te relaxation. The question here is ,  how long he  would have been able to maintain this  or  whether it was  just a last load  effort  to mentally finish it off.
 Easy  to  try  out  do 4 - 7  sets  wit this load.  every second Ste  you  do the technique  you did  in the last  and every second you just push  12.00 - 6.00 . How long each set.  will you fail mentally  than go back to a  load in the 100 - 125  range  . How long . till SmO2  is the highest  you reach  and stay there  for   a  few minutes till you feel coordination  ready  to go  again.

 I will try to find some studies  we did  many years back in Mallorca  on RPM  and  how  to use  RPM  for specific  stimulation in delivery and utilization ideas.

This is  another  point  , where we  "hate " zoning  as I  can sue  RPM  to  work in a  very low intensity to create similar reactions as if  I go  very hard. just different use  of limiter and  compensator.

 I will show  you  as well a personal  ZONING  I  do.
 I name it SMS

S  for  smart
 M  for  mindfull  and  S  for  survival.
 Most regular readers will find , where the S  shifts  to M  and than  to  S  back. in a 5 /1/5  Tip assessment. 
In  Zone  S  for  smart   you can train any  target  you have   from a physiological point  individually.

In  Zone M  for mindful  you  train your limiter  and have to watch  whet he you like to integrate  or not a compensator.
In  zone S  for survival  you  do exactly that , you loose  any  control on what  you like to target  as you simple  push  ever body to its limit. You not  just loose  stimulation goal  control but you as well loose  control on what the  workout  really  creates  at the   end of  adaptation.  as you have no  clue  what  caused  what reaction.
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #22 

I  try to add some additional  feedback  in red below in each section

Ok...let me try and wrap my head around this...
Below is a response to the further postings and also a summary of the things I think I should try to explore somehow. I'm doing this "in-line" and not reading ahead to see if there are additional answers...so things might change or seem inconsistent as I work through the reply.
If there are additional things I should explore, please let me know...

25/11
Juergf:

Possible  metaboreflex  at the end.
Breathing was VERY pronounced in the last two repeats...so the effect might have started to materialise during the second 275W set and be full blown by the end. 1min recovery probably insufficient to recover.
Great feedback  and observation.
Here some d additional  thoughts on this feeling.
In  many cases in high intensity we  start to " fight"   to r try to get rid of CO2  as it is the fastest  way to  try at least to keep H + in a  certain balance. As long we  can keep H + in balance  it seems that the homeostasis extracellular  allows us  to  keep going  somewhat longer  and as  such  lactate will increase  in the blood as well as it is a  additional buffer  help  .
For  skeptics  and LT believer. Here what you try as a small  practical  session.
 Bike  and go to MAX LAss . So you may be  200 watt  and 3.4 +- lactate  when you  are in a  steady state. Now go  for as long as you  can with hyperventilation, meaning  fast and very deep breathing so you get rid  of CO2. Than  check lactate again. Than  go a few minutes  normocapnic before you  do the opposite breathe  hypercapnic so  retain CO2.
Than  take lactate. For  NIRS user  looking ot find a  SmO2 break point   connection  with a LT  theory do the same  and  look what you get  and than  try to explain   what happened  .

Now back to Etienne specific.
a) actual respiratory weakness, meaning you simply  have a limited VE  (  l/min"  ability   to move air  due to different reasons. Now one interesting reason we never actually look at it is  not the size  of the lungs, it is the size of the "cage" (  rib cage) combined with the  thoracic  mobility
In  sports  like  cycling this is  very common. due to the position.
kyphosis of a cyclist.jpg 

Creating  a  so called Sternosymphysale posture with all negative  reactions in  muscular dysbalance  and muscular  dysharmonie. Key  word  ITB, patella  pain to name  some common  one.
 The  result is 
COGWHEE.JPGSo even the many coaches    and exercise physiologist  who  believe  respiration is never a limitation.
 Respiration    done in a certain way  will mobilize  costovertebral joints  as well as  thoracic inter vertebral joints. 

MOXY  reactions in case of a  VE limited  respiratory ability.
 Result is a  increase in CO2.
 SmO2  reaction . sharp  drop  after it seems it    was stable  or  minimal drop.
tHB reaction. Recovery  section , " hesitation of increase in SmO2  or limited  max  increase compared  to the previous  rest period  , where  the athlete  was still normocapnic. ( O2  disscurve  right )
 tHb   overshoot  due to  additional  vasodilatation   from high CO2
Attention: This is the cook book.
In case  you as well reach a  caraid  limitation  the reaction  will be different depending on the  priority of " survival:
 Think   what  may change.
b) in case of an  actual metaboreflex.
 Meaning the   extremity muscle  steel blood  form vital systems.
 
tHb reaction, Vasoconstriction,. unsure  whether it will show up  systemically as  the non involved muscle  may  take little  O2  already..  If  we play  with teh O2  diss curve  we will see it systemically but metaboreflex    can   in some cases really react  just  locally  so lower extremity only in runners. Both in  rowers  or  cross country skiers.

So go back  and look  what we see.
 So  somewhat later  I will be back

Possible cardiac
compensation.


HR hit 141, very unusual for me in an indoor setting on a bike. So yes, quite possible that I finally got my heart to wake up at the end of the session.
Possible local limitation in delivery and utilization locally
Both? This should then make it easier for me to correct it since I do not have to put as much focus in not stressing too many compensators since there aren't that many?
Which one is for what or on what muscle.
Green is SmO2 on VL
Red is Smo2 on DA
Blue is Smo2 on Calf.
...that is no "fooling" anymore...
There is a distinct "uptick" in the HR between sets. In the first sets the HR response seems to stay consistent between sets, but during the sets that have been circled, the HR is not only increasing overall between sets but also steadily rising during sets to the point where it basically goes back to the previous maximum quite quickly. Am I looking at this correctly?
If you have a problem  increase  cerebral  Blood flow
I'm not sure if you're joking and mean we should think about the situation more or if you mean we should be considering the metaboreflex. Possibly both? [biggrin].
what   do you think  woudl we see  when we look at SV and SVR reaction options
SV would be up and SVR would be increasing or stable because of an increase in CO2?
My question...in the biased view. Is O2Hb increasing because my RF is up, because CO2 is causing vasodilation or because Thb is increasing overall?

27/11
Juergf:
...agree on how we could develop an action to see...
I'm all ears - if there is some part of the 5-1-5 you would like me to duplicate, or some other type of assessment you would like me to do to check a hypothesis then let me know.
1. SmO2 may drop or "hesitate to go up...
I do see a bit of a drop/hesitation in SmO2, but I'm not sure exactly what the graph should look like for this to be considered significant? The tHB seems a bit more pronounced.
2. Occlsuion.
Veneous occlusion release. What may we see with THb
I would expect to see a drop in Thb since the pooling is released, perhaps also an increase in SmO2 because O2 rich blood can now more easily enter the muscle (depends on the level of vasodilation).
Arterial occlusion release down to venous occlusion level how woudl tHB react than?
An initial increase and then leveling off (stabilisation) of the Thb level. SmO2 I would expect to increase?
3. ...end of the datas.
What caused the THb going
up.
I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.)
What caused SmO2 so it did not drop anymore?
THb is going up, so more oxygen getting to the muscle to balance it. I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.) Also work load is now more evenly distributed between VL and Bicep Femoris. PLUS increase in cadence means that there is less chance of occlusion happening?
Think SmO2 as % of tHb?
As per above, more Thb inflow. Could be that this is a new stable SmO2 "level"...that I might not be able to maintain for other reasons.
Now look where the work may have shifted to.
Better balance between bicep femoris and VL.
How would a body react in a survival mode
Non-involved muscles go first, then semi, then involved...RF is up, CO is up.
when he is not really stressed 
Keep going but react the bare minimum to get the job done?

27/11 (next post).
Juergf:
different reaction immediately after the load started
I see a sharp initial drop and then a sharp recovery followed by a more steady increase. Is this what you mean? Is this an indication of the venous occlusion I was referring to on the first graph (the occlusion, not the reason for it)?
Now
I'm not quite sure what I should be noticing on the blood volume trend graph and the one following. THb is up over all in the last set where I am really cranking it out. SmO2 is "level" vs. decreasing in the previous sets while Thb has the same upward trend?

27/11 (next post).
Juergf:
Does the drop in SmO2 really mean he was not anymore in O2 balance?
There seems to be an attempt to return to homeostasis at a lower SmO2.

DanieleM
And confirms that O2HHB is not in balance as before.

I think I agree with Daniele. CO is attempting to compensate, but there is a level of hypoxemia (is that the correct term) building up that it cannot compensate for through either vasodilation, RF, or CO.

Things to try:
1. Change which leg goes into 6 O'clock position to see if there is a mechanical occlusion during the rest.
2. Try increasing the rest period to see what happens to the tHB in my DA.
3. Check mitochondrial density on VL (15 sec occlusion protocol on as described elsewhere?).
4. Have CO (specifically SV) measured at the local high performance centre.
5. I also had in mind an assessment to see what would happen if I decided to "boil the frog slowly". I.e. Do a very slow ramp test, maybe 2 hours, starting at the same very low wattage requirement with the end point at 300w and just see at what point my body realises that there is a "lion in front of the rabbit hole" and how it responds.
6. Do a session with variances in cadence to see whether there is a clear relationship between cadence and VL Thb.

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #23 
  next   section  with some feedback  and  thoughts

Possible cardiac
compensation.
There are  some interesting observations  when we look at your TIP  HR trends.

hr.jpg 


1. You c an see that after  the initial  HR increase  from a  low 50 +-  to 75 we have a minimal increase  till step 5.

10 beats over this 4  steps, where after this  you have to increase  +- 10 beats  for each step. What is interesting as well is , that in the one minute recovery  you drop basically  back to " resting " HR. Some  would call that no EPOC or no need  to keep  CO  due to stimulation  from the 5 min  before.
 There  are  two main reactions in people.
1. Reaction over HR to increase  CO. This is  a fast functional reaction  and often triggered over some hormonal releases as well. So the first  HR increase  may just reflect this reaction.
But than  some react   over  SV  so little  to no HR  response  but increase in CO over  SV. Now    we can argue, that there is  minimal  to  no  increase in   preload  in this stage  due to minimal increase in blood flow return  due to small muscle pump in this low intensity as well as  small contribution of  respiration as    a help  for  return  of blood.
 But there is  an additional gear in the system  to help. It is  contractility of the heart  and will show up    due to a higher  EF %  ( ejection fraction  % ) EF  % is  in simple terms  the  amount  of  blood  thrown out     when we  take EDV  (  end diastolic  volume  or the  amount of blood after filling,  and the  amount in %  of blood left over  ESV  end systolic volume   , which is the  SV So 100 ml  EDV   30 ml ESV =  70 ml SV  or  70 %  EF.
The  changes  between  SV  and HR  reactions often  can cause  some trouble  to maintain  BP  and here  again  nature  has a solution  and one  we can see systemically  is  called  systemic vascular resistance.  Below you see at the  start phase of this client an  "Internal  fight "  for BP  and you look carefully you see  where the SVR  reacts.

eva G.jpg 

look  at  right  1702   corner  as this is the SVR.

Now from the  5  th  step you  added  HR  by +- 10 beats  per step indicating, that besides a  help   from SV you added  some help  for CO  as well from HR.
 We used  many many years back a  simple  direction  or people using just HR  and performance  for testing Below is a  simple summary  where we  can get some indication  whether we react  with HR  or SV  at the  start and  at the end  of a  step test . See whether it makes  sense. horizontal axis  is HR  and ventricle  axis is performance.
LLL  and ULL.jpg 

Now you add  to all of this, what some   educational  books   not accept yet, the individual reaction of  SV. I learned  at school , that  SV  will go up  and the plateau.  Once we started  using Physioflow  we had  to correct this cook book  to : Any thing is possible   So  below the options  of  CO  reactions   and the contribution  from SV.

different   trends in sv in step test - Copy.jpg 

Summary of this section.
Your  low resting HR  indicates, that you have a big  SV  even at rest. Your  10 beats +-  increase  at  step  5  indicates, that you need  help  for CO  over HR, which  could indicate a  leveling of   in SV  contribution. Your linear   HR  reaction till to the end   indicates a  possible stable  SV    from the  5  th  step on. This are all theoretical speculation . The answer is in a  Physio flow assessment.


HR hit 141, very unusual for me in an indoor setting on a bike. So yes, quite possible that I finally got my heart to wake up at the end of the session.

What is  your  HR in running or   rowing  for example ?
.

Possible local limitation in delivery and utilization locally
Both? This should then make it easier for me to correct it since I do not have to put as much focus in not stressing too many compensators since there aren't that many?
haha   I like  this  attitude. Here a  critical  feedback.

First. Yes  if  local  muscular  limitations like  vascularsisation and mitochondria  density  are  the limiter, than  you can nearly train anything and you make  progress. That is the dream coming up    every years  first of  January. You  get most  people with this limitation  and they will see huge improvement over the first 6 0 8 weeks no matter  what the personal  trainer will do  as they  create a functional  survival  response  from doing nothing  to  do  anything. The   lucky part is , that 75 - 80 %  of this people  will quite in the next  few  weeks  anyway  and   nobody ever  got the feeling , that the training  program  was pretty much a  survival   exercise   for 2 month

Now  more serious:  if you have  no  or  only a small compensator , yes it is  easier  to work out but much harder to know , which system you may have overloaded  as all work hard in every workout. So recovery control is crucial.  I   believe  that you have  a  great compensator  with your cardiac system  and   you have to  look for smart workouts  to not   bring this guy  every time  to   work  . So lots;  for   workouts  to try to avoid  cardiac compensation.

Which one is for what or on what muscle.
Green is SmO2 on VL
Red is Smo2 on DA
Blue is Smo2 on Calf.

r D b VL g C.jpg 

Red is  DA
Blue is VL  and 
green is  calf

 
...that is no "fooling" anymore...
There is a distinct "uptick" in the HR between sets. In the first sets the HR response seems to stay consistent between sets, but during the sets that have been circled, the HR is not only increasing overall between sets but also steadily rising during sets to the point where it basically goes back to the previous maximum quite quickly. Am I looking at this correctly?
Yes interesting is  that in most  steps  after the 4 th  you increase HR  even   or  despite the same load indicating, that  in the same load  you need to compensate  to maintain the O2  demand as good as possible Now  you as well compensate  with  tHb.
thb  smo2  rend loads.jpg 
 After   the initial  drop  of tHb  due to muscular compression we see a great  increase in tHb  as  an attempt  to  supply  more blood  ( vasodilatation.)  different  mechanism  who create vasodilatation as  often discussed. Main risk  of  vasodilatation is  not to be able to maintain BP. In your case   no issue  as cardiac  ability  seems  to easy handle this situation. In fact  in the last step  you can see a nice increase in tHb due  to your change in load on the VL.  Now   watch careful the tHB trend  at rest peak  and SmO2  trend at rest peak. What  could this indicate ?

If you have a problem  increase  cerebral  Blood flow
I'm not sure if you're joking and mean we should think about the situation more or if you mean we should be considering the metaboreflex. Possibly both? [biggrin].
hmm  I never joke  . life is  far too serious   ( Smile ). Here the answer  as it is  perhaps a  joke ?


brain and normal breathing.jpg 


what   do you think  woudl we see  when we look at SV and SVR reaction options
SV would be up and SVR would be increasing or stable because of an increase in CO2?
Look at the physio flow pic  in this section
Think about   what SVR  job is ? So  fight between BP ( vasoconstriction ) and  vasodilatation effect of  CO2.

My question...in the biased view. Is O2Hb increasing because my RF is up, because CO2 is causing vasodilation or because Thb is increasing overall?

Look  for a possible answer outside  bias  and go to base lien ideas of tHb and SmO2  in the above picture

27/11
Juergf:
...agree on how we could develop an action to see...
I'm all ears - if there is some part of the 5-1-5 you would like me to duplicate, or some other type of assessment you would like me to do to check a hypothesis then let me know.
As all  ideas have  its limitations  we often look after  an initial hint on limiter and compensator   on options  to addd some additional  ideas to a  workout  or  a  assessment idea.
Here   small  inside view  . This is as south African ultarmarathon runner. He  has  a so many of the  great endurance athletes a cardiac  limitation  as the incredible hours  of  runs  create a huge  problem   and he  developed the " sleeping giant" An incredible  capillary  bed and a huge  mitochondrial density.   Than he  added in  some races   beet  juice  and   it  did not worked  out  as planned .
 Why ?
 So here after a  long  run  and than we had  to asses daily  to  show him how long it takes  to recover his  overloaded  cardiac system  and learn , that you can run yourself  to  death.

   tired  smo2  thb  close.jpg 

Above  after   run. below  11 days later  finally  back to his  " normal "    reactions.

recovered  smo2  thb  close.jpg 

Allow  me  to get a break here  and than we  will tackle the next session.

1. SmO2 may drop or "hesitate to go up...
I do see a bit of a drop/hesitation in SmO2, but I'm not sure exactly what the graph should look like for this to be considered significant? The tHB seems a bit more pronounced.
2. Occlsuion.
Veneous occlusion release. What may we see with THb
I would expect to see a drop in Thb since the pooling is released, perhaps also an increase in SmO2 because O2 rich blood can now more easily enter the muscle (depends on the level of vasodilation).
Arterial occlusion release down to venous occlusion level how woudl tHB react than?
An initial increase and then leveling off (stabilisation) of the Thb level. SmO2 I would expect to increase?
3. ...end of the datas.
What caused the THb going
up.
I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.)
What caused SmO2 so it did not drop anymore?
THb is going up, so more oxygen getting to the muscle to balance it. I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.) Also work load is now more evenly distributed between VL and Bicep Femoris. PLUS increase in cadence means that there is less chance of occlusion happening?
Think SmO2 as % of tHb?
As per above, more Thb inflow. Could be that this is a new stable SmO2 "level"...that I might not be able to maintain for other reasons.
Now look where the work may have shifted to.
Better balance between bicep femoris and VL.
How would a body react in a survival mode
Non-involved muscles go first, then semi, then involved...RF is up, CO is up.
when he is not really stressed 
Keep going but react the bare minimum to get the job done?

27/11 (next post).
Juergf:
different reaction immediately after the load started
I see a sharp initial drop and then a sharp recovery followed by a more steady increase. Is this what you mean? Is this an indication of the venous occlusion I was referring to on the first graph (the occlusion, not the reason for it)?
Now
I'm not quite sure what I should be noticing on the blood volume trend graph and the one following. THb is up over all in the last set where I am really cranking it out. SmO2 is "level" vs. decreasing in the previous sets while Thb has the same upward trend?

27/11 (next post).
Juergf:
Does the drop in SmO2 really mean he was not anymore in O2 balance?
There seems to be an attempt to return to homeostasis at a lower SmO2.

DanieleM
And confirms that O2HHB is not in balance as before.

I think I agree with Daniele. CO is attempting to compensate, but there is a level of hypoxemia (is that the correct term) building up that it cannot compensate for through either vasodilation, RF, or CO.

Things to try:
1. Change which leg goes into 6 O'clock position to see if there is a mechanical occlusion during the rest.
2. Try increasing the rest period to see what happens to the tHB in my DA.
3. Check mitochondrial density on VL (15 sec occlusion protocol on as described elsewhere?).
4. Have CO (specifically SV) measured at the local high performance centre.
5. I also had in mind an assessment to see what would happen if I decided to "boil the frog slowly". I.e. Do a very slow ramp test, maybe 2 hours, starting at the same very low wattage requirement with the end point at 300w and just see at what point my body realises that there is a "lion in front of the rabbit hole" and how it responds.
6. Do a session with variances in cadence to see whether there is a clear relationship between cadence and VL Thb.
 

Etiennebest

Development Team Member
Registered:
Posts: 34
 #24 
What is  your  HR in running or   rowing  for example ?

Three data points (5km TT Run):
Older, Pre Ironman SA:
April 2015: MAX HR 159bpm / AVG 148 (4:55/km pace).

Recent:
August 2015: MAX HR 152bpm /AVG HR 137 (5:36/km start of season pace).
October 2015: MAX HR 146bpm / AVG 138 (5:05/km early season pace).




juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #25 
Okay back  for   another section on  Etienne's  great  points


1. SmO2 may drop or "hesitate to go up...

I do see a bit of a drop/hesitation in SmO2, but I'm not sure exactly what the graph should look like for this to be considered significant? The tHB seems a bit more pronounced.
I have to  check  that  one more closely or help  me  with the exact  section we are talking about . Thanks

2. Occlsuion.
Veneous occlusion release. What may we see with THb
I would expect to see a drop in Thb since the pooling is released, perhaps also an increase in SmO2 because O2 rich blood can now more easily enter the muscle (depends on the level of vasodilation).
One of the  problems  with  reactions after occlusion is  really the  "timing"  or better  duration  of the occlusion . If we  are lucky o have a decent length of  a venous occlusion  with a  decent  CO than e  have a   nice pooling  of blood  and therefor  the  release  of the occlusion shows up  with a nice tHb drop. Shorter time in lower intensity  do  not show a   perfect picture. This is  again where  it is not easy to make a cookbook  but  additional feedbacks  will help. So  higher  HR   could indicate a higher CO  so  possible  easier to  se a occlusion reaction. SmO2  can go anywhere, as it depends   on the  release  of the occlusion  so  how  extreme you reduce  more units,  do you release  extreme  or just enough  to see  an outflow. Now  you as an athlete  can see that bets as yo do it. That is a weakness  when we  only look  graphs but the strength on athletes  who understand   on what you look for live. Feeling feedback  and knowledge  may be a  good recipe.

Arterial occlusion release down to venous occlusion level how would tHB react than?
An initial increase and then leveling off (stabilisation) of the Thb level. SmO2 I would expect to increase?
An arterial occlusion means we  have no inflow  and no  outflow  so tHb is the   blood volume in the tested area. . When we release some of the  occlusion pressure than e  will open up the inflow  but  may  still keep outflow  closed  so we  really have the same as  when we  have a  simple  outflow occlusion.

SmO2  reactions. In general the SmO2  trend  will follow  as usual. If the activity  which creates the occlusion  has an intensity, where more  O2 is used than delivered  SmO2 drops and vica versa. This  reaction  can be used for example in bike fitting to see, whether the occlusion trend was due  to mechanical pressure or due to  actual activity related  occlusion  for muscle compression.

3. ...end of the datas.
What caused the THb going
up.
I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.)
Yes I think the fact, that you  concentrated on your  360 +- pedalstroke  and  stopped  just  pushing 12 - 6   change the muscle contraction force and you released somewhat and tHb increases. SmO2  hesitates  so  we see what we see including an additional  increase in tHb  due to the CO2   situation  we pointed  out.
What caused SmO2 so it did not drop anymore?
THb is going up, so more oxygen getting to the muscle to balance it. I see some of what was mentioned in 1. Hesitation in SmO2, definite THB overshoot at the end of the set (easy to see if compared to the previous set.) Also work load is now more evenly distributed between VL and Bicep Femoris. PLUS increase in cadence means that there is less chance of occlusion happening?
Yes
Think SmO2 as % of tHb?
As per above, more Thb inflow. Could be that this is a new stable SmO2 "level"...that I might not be able to maintain for other reasons.
Yes  the weakness is , that we d not  have an actual amount  when we look at tHb  so we have to look as Daniele showed nicely  at HHb  and O2Hb reactions.
Now look where the work may have shifted to.
Better balance between bicep femoris and VL.
Possible  , I would leave it more general  that you most likely created a better intermuscular coordination with what ever muscle can add to a pedal stroke.
How would a body react in a survival mode
Non-involved muscles go first, then semi, then involved...RF is up, CO is up.
Yes  and  when we look available  bio marker   than RF  and HR  would be some we could look at.
when he is not really stressed 
Keep going but react the bare minimum to get the job done?
Pretty  daily human reaction isn't  it.


27/11 (next post).
Juergf:
different reaction immediately after the load started
I see a sharp initial drop and then a sharp recovery followed by a more steady increase. Is this what you mean? Is this an indication of the venous occlusion I was referring to on the first graph (the occlusion, not the reason for it)?

Yes  that is the reaction To be sure  we have a difference between   compression  ( sharp  drop )  and  decompression fast sharp initial increase before  gradual increase in tHb and a potential occlusion  reaction  you   have to use a SEMG.
 Or  if you have a great power meter  you an see , whether your wattage overshoots in the  initial start to get the system going.
In most cases  it is a compression/decompression and in your case  most likely as well as you can see this reaction more in the lower intensity where you overshoot contraction force  and than readjust to the actual needed amount  of contraction strength .As  higher intensity as less overshoot reaction so  just compression and than  increase  due to   different vasodilation reactions.
.
Now
I'm not quite sure what I should be noticing on the blood volume trend graph and the one following. THb is up over all in the last set where I am really cranking it out. SmO2 is "level" vs. decreasing in the previous sets while Thb has the same upward trend?
Yes:  SmO2  flat as you changed to a better intermuscular contraction. tHb overshoot as you  changed to a better intermuscular  contraction so more muscle involved  so less  muscle contraction, higher  CO  so  more vasodilatation  so tHb  geo sup easier. If  respiration  is in trouble  we as well will see that  as well in  other  muscles  now  more involved  O2  diss curve shift  possible  so  in calf  we  would see a drop in SmO2 sharp if you involved this one as well. but as well in  noninvolved muscles.
27/11 (next post).
Juergf:
Does the drop in SmO2 really mean he was not anymore in O2 balance?
There seems to be an attempt to return to homeostasis at a lower SmO2.

DanieleM
And confirms that O2HHB is not in balance as before.

I think I agree with Daniele. CO is attempting to compensate, but there is a level of hypoxemia (is that the correct term) building up that it cannot compensate for through either vasodilation, RF, or CO.
Yes nice  pic  from Daniele
Things to try:
1. Change which leg goes into 6 O'clock position to see if there is a mechanical occlusion during the rest.
Yes

2. Try increasing the rest period to see what happens to the tHB in my DA.
Yes
Check mitochondrial density on VL (15 sec occlusion protocol on as described elsewhere?).
Good luck

4. Have CO (specifically SV) measured at the local high performance centre.
Yes  and good luck  as well
5. I also had in mind an assessment to see what would happen if I decided to "boil the frog slowly". I.e. Do a very slow ramp test, maybe 2 hours, starting at the same very low wattage requirement with the end point at 300w and just see at what point my body realises that there is a "lion in front of the rabbit hole" and how it responds.
Could be  fun, a good workout and interesting

6. Do a session with variances in cadence to see whether there is a clear relationship between cadence and VL Thb.
Absolutely as this I  super individual
 

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