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juergfeldmann

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 #1 
An  ongoing increase in  questions I get over  email is.
 Why   do you care  about tHb  so much  and  not  only using SmO2.
 Simple answer is that SmO2  is   %  of tHb  so  yes  SmO2  gives  us some  kind  of a trend that we  deliver  more O2  than needed , that we are in balance  or we use more currently than we  can  deliver. It is a great start  and a big step forward  to the classical  ideas, where we  had  to speculate   where we may  be in a  homeostasis  either based on  %  of  an old or relative  current  VO2 max test  or LT test  or FTP  or what ever sport test you use. Than you use  an indirect  based  feedback like HR  or  speed  or  Wattage  and hope the  result is  still holding up. Now  with NIRS  you at least  have an immediate live  feedback , where you are today  in today's  situation.  Use the  trend  as  many ask  for a magical SmO2  number.
Now   even  SmO2  %  number has its limitation.
  if used alone.
 60 %  SmO2    may mean  for 100 Hb  that 60  %  or 60 pieces  are loaded..
 Now  you  reduce blood flow  or  Hb  to  50  due  to vasoconstriction  and at the same  time you may reduce    intensity  so you use less O2   .
 so you  may see an increase of SmO2  to  70 % which means 35 pieces  are loaded  with O2. So  if you look  just SmO2  you get the wrong impression  as you seem to have more O2  available  when in fact  due to the vasoconstriction  you have less available and  the workout  may have to end  earlier.
 This is  easy  to time  or   try out in simple strength   workouts  by using a   compression  system like a  simple BP  cuff and reduce  inflow  by   cremating  compression enough  for free flow  but reduced  flow and you count  you biceps  curls.  Now  more and more accepted   institution look at this   regulations  of blood flow  and here  an abstract  from  a really great  group.
 This is great to see as it is much easier  for  us  after all this  years  to get somewhat taken  more seriously , when we look at   development  form classical ideas towards  some  integration of new  technology outside the science  community but in theoretical of closing the gap  between  science  and  practical applications.

 It is interesting how many  ask  for validation  and more  on new  ideas  when they are back up  by science.
 Ideas  like  there is no such thing like anaerobe  as pO2 is  protected.
 . lactate is    a buffer and  does not   only or  as  more  an exception than a rule gets  produced in hypoxia  but is produced  all the  time.
, High  energy  phosphate  like ATP  gets  deleted , when we  can see now in great  studies,  that it is protected  ion a needed base level  and many  more ideas we  try to defend   our ideas.
 Why  to cool  down   what is a lactate  tolerance  workout  and why do we have to tolerate lactate, VO2  max  an %  as a   use  of   equal  physiological load.  and much more  e we are used  to  defend  wit so called  science.

REGULATION OF INCREASED BLOOD FLOW

(HYPEREMIA) TO MUSCLES DURING EXERCISE: A

HIERARCHY OF COMPETING PHYSIOLOGICAL NEEDS

Michael J. Joyner and Darren P. Casey

Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota; and Department of Physical Therapy and

Rehabilitation Science, University of Iowa, Iowa City, Iowa

L Joyner MJ, Casey DP. Regulation of Increased Blood Flow (Hyperemia) to Muscles

During Exercise: A Hierarchy of Competing Physiological Needs. Physiol Rev 95: 549–

601, 2015; doi:10.1152/physrev.00035.2013.—This review focuses on how blood

flow to contracting skeletal muscles is regulated during exercise in humans. The idea is

that blood flow to the contracting muscles links oxygen in the atmosphere with the

contracting muscles where it is consumed. In this context, we take a top down approach and review

the basics of oxygen consumption at rest and during exercise in humans, how these values change

with training, and the systemic hemodynamic adaptations that support them. We highlight the very

high muscle blood flow responses to exercise discovered in the 1980s. We also discuss the

vasodilating factors in the contracting muscles responsible for these very high flows. Finally, the

competition between demand for blood flow by contracting muscles and maximum systemic

cardiac output is discussed as a potential challenge to blood pressure regulation during heavy large

muscle mass or whole body exercise in humans. At this time, no one dominant dilator mechanism

accounts for exercise hyperemia. Additionally, complex interactions between the sympathetic

nervous system and the microcirculation facilitate high levels of systemic oxygen extraction and

permit just enough sympathetic control of blood flow to contracting muscles to regulate blood

pressure during large muscle mass exercise in humans.

hourerg

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 #2 
Hello Juerg, great to be back paying attention to what you are cooking up.

It's going to take me some time to fully grasp how we interpret Moxy data but correct me if I'm wrong here in simple terms: tHb trend is going to be primarily dependent on what our heart is doing as well if our brain says to divert blood flow through vasoconstriction/dilation. SMO2 is going to be primarily dependent on our respiratory system and how well the sensed muscle is using the oxygen it is receiving? I would suspect then using SpO2 (finger, ear, etc.) in conjunction with the SMO2 readings, we could answer a lot of questions. Is that the case? Years ago, I tried to get SpO2 while rowing and erging and never succeeded. Do you have devices that can read through the noise and vibrations while exercising?
juergfeldmann

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 #3 
Thanks  for this  great nice  and simple  summary. I  always  try  and never succeed   so thanks  for this. It is my messy brain
 Answer  to  the first section. Yes   the summary on tHB  and  SmO2   and the combination  with SpO22  is  great  and   can be formulated like this  with always some add on  but  than  I get lost so  YES great..
 SpO2  sensors.
 They  are   all  motion sensitive  as well as you now  can see  depending on a free tHb  ( blood flow) To   accept  an SpO2  values  you like to have a  HR  belt on  and  if you have HR  and Pulsrate the same  you are relative confident you have a decent readings.
The ever growing market on optical pulse sensors shows , that technology is improving but as well that  HR is not  = PR . so optical   readings  are still pulse rate readings  and not as it is getting sold  HR  readings. We tested   different  equipment   and included  NIRS in the   forearm  muscles  for example  and as  soon we   have  a  severe  change in tHb  and  for sure  when we see a   trend towards  occlusion outflow restriction we see  some   problems  with  HR  = HR.

 In sports  with less extreme motion  influences  like  speed skating  or  even  biking or    veyr strong runners  but as well  rowing the bets SpO2  sensores  are the once  you can    fix  on an ear lobe  and have the feedback there
sandor

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 #4 
So in terms of SmO2 & tHB...

In 5 days of low intensity steady state workouts i see the following:
20 km per day, same time of day for each session

Mon SmO2 48     tHB 12.4
Tue  SmO2 48     tHB 12.4
Wed SmO2 48     tHB 12.9
Thur SmO2 48    tHB 12.4
Fri   SmO2 48     tHB 12.4


numbers are average for the whole session.

what is the cause in change of tHB?

perceived exertion was the same for all sessions.
heart rate varied widely, anywhere from low 120s to 150. high tHB session had much lower heart rates, and much lower pace in order to keep the SmO2 at the same level.


juergfeldmann

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 #5 
Interesting  numbers  .  I never use   average in  any sport  nor  do I use  SmO2  absolute numbers . The trend you see  we see very often  but   we often see the average doe not always  reflect the actual picture. That does not mean  that you have  an interest   task  at  hand.
 We   do not base the  intensity on a  SmO2  number  but it could be that the number  can be  similar over a period  of time.
 We  always  do a  "  calibration  " warm up in any sport  that is in the range of  10 - 15 min . This  can  be   in different ways  depending on what the coach  and what your assessment protocol gives  you as a hint in  what  the  limiter    may be  for the moment.
 So   the   " low  physiological intensity "  workout  is based on the   daily  trend in  SmO2  and thB. We look  for a   increase in SmO2  at the  calibration  load , than  try tor each a  flat  trend  SmO2  section  and  for a  short moment a  slightly  trend in dropping SmO2. Now  by doing that we  may much earlier see  that we have to chance   ideas of the workout. Each of the   warm up intensities    ends  with a 1  + min  break to see tHb  reaction  and SmO2 trend. So   physiological reactions  may  therefor show up  very early  as  a  drop in tHB  in the  one minute rest for example compared  to a normally increase in tHb. If  all goes  as usual  than  we   go    and back  off  form the intensity and go back  where we see again a short increase in SmO2  and than a stable SmO2  the rest of the  workout +-   and a  stable tHb  as well. It may  be  SmO2  stays  stable but tHb  may  drop. or other options.
 You may see in the one minute break  an insufficient  increase in SmO2  compared  to usual  and  at the same time a very high  tHB  reaction.
 Now  you have in this case a hint  that respiration may be not recovered . In the  first e ample cardiac   limitation   and so on.  Now  if  we are not sure than we simply  do a  short    section of a few  minutes, where we  additional challenge  respiration  or  cardiac  reactions  and we see whether it is one of the other  same as when you plan a  respiration  workout   during the load  or a  cardiac  stimulation in a low intensity. Depending on reaction we  change the training  idea or    finish the workout  and  go  to recover. Now  that does not mean that  this has to be done  It is  just what we  do  and not has to be the only  way  to use the information.

Lower  HR    is due to the lower  intensity  for sure  so less CO  demand  and   lower intensity means  as well lower muscular  contraction  so   CO  wins  easier over  compression   of the muscles  so tHb  is higher.  The  fact  that SmO2 trend  was  similar  by a  lower intensity  would for  could suggest a  lower SmO2 in case of  same  load.
 So lower SmO2  at the same load  suggest  a higher utilization  due to  a  lower   delivery for  example
If  cardiac  than tHb  would not have reacted  . it could respiration    or   we can think  through more  . Interesting  topic  to keep discussion to show  how they  all hang  together.
sandor

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 #6 
in terms of the average SmO2 i quoted, 48 was my target, varied between 46 - 53 while rowing. when i am doing low steady state, rest periods peaking to 70.

i know i am working backwards, or different, in my day to day training than others here, but i am trying to determine intensity levels via Moxy as a sole measurement (well, two measurements SmO2 & THB) on the water i feel Moxy may be the most sensitive & accurate real time assessment i have.  

pace & heart rate are too variable & lactate isn't realtime - on days like yesterday, with a quartering tail wind & high water flow speeds, pace can change 0.5 m/s in 500 meters, with no change in physical effort.


this is part of the reason i started (and continue) to get lactate measurements with the Moxy data - because i know that 48 SmO2 for 90 minutes produces 1.7 mmol for me currently. The interesting thing is that this holds true regardless of tHB or heart rate. 

so yes, n=1, so it is anecdotal, but my working idea is that the tHB trend is perhaps showing higher due to deeper recovery. i can get the oxygen there, but the muscles aren't in a condition to use it, hence lower pace for the same SmO2 (& same blood lactate)

is this completely off base? it matches my 2 weeks of testing on the erg, where my base steady state training was based on watts @ lactate (1.8 mmol) 
first few days after a rest day & everything would be steady Moxy:watts:lactate, then as the week wore on, i realized that watts had to be lowered to keep the same SmO2, and lactate level (this was new to me, as i had never done this many lactate tests in such a short time period) 




so, in short, could the increased tHB in certain sessions be associated with on going deeper recovery of the targeted muscles?
if so, there could be many ramifications...
juergfeldmann

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 #7 

sandor
 hmm problems here with  sending  lets  try  this  way long  respond s but  can not load it will try different later

 

juergfeldmann

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 #8 
I seem to have  problems here to upload  jpg  and  copies so  it may be me but  can c  somebody   try if it is the   page  Thanks

It  tells  me this page  can't  be display

juergfeldmann

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 #9 

Sandor

is this completely off base? it matches my 2 weeks of testing on the erg

Not  at all  as nothing is off base on here. It in fact may be  brilliant  and it is  what MOXY is an individual tracing of  physiological  individual feedback.
 So  BIG thanks  to you  and  hat off  for the   incredible  feedback  and  openness  to  off this  for discussion.  Just because I  work on  all of this   since  30 years does not mean  at all that  I am the  chef  or  top cook  it    actually means  , that I may be  sometimes  " nose  blind "  to , as  we all are towards  new  directions and ideas.  So let's  follow this   further though and I will add in a   separate  set  some ideas  I on  rowing  from my point of  view  and we  can mix  and match  and  take apart   where we  have questions  and added  new ideas and  try out. You are brilliant  thanks so much.

i feel Moxy may be the most sensitive & accurate real time assessment i have.  


As you  and most  may guess  I have  little   doubt  about that.
  So let s'  keep loud  thinking on here.

 The most interesting section is the  day  with the higher  than  average  tHb  reaction.  So  the base question is always v, what influences  tHb.
 a)  is it a mechanical  reaction  so   in rowing  that  could be   muscle contraction force  so intra muscular  contraction on the one  side in VL   or    but as well an intermuscular  contraction  change.

a1. Intra muscular   contraction change. This  would be  easy to support with SEMG . what it means is, that you recruit   less motor units than  on the other days. Now  here the  split  question. If you  recruit less motor units  you will have less   strength  so speed  will be lower.
 Now  you could recruit less motor units  and still go the same  speed  because  you compensate  in  with other  muscels. ( intermuscular coordination.)
 we will get  back to this  in  more details  as we progress.
  Now we know  form yoir greta feedback  , that you  felt  slower  by the same SmO2  but a higher  tHb.
.
Or the opposite speculation b y the same speed as on the other days   we may have seen  same thB  as  same  muscle  contraction   but   most likely a  lower SmO2 ? ( Speculation.)
  That would or  could indicate  that by the  same speed on this  day you had a  not   as optimal delivery  so you had  to  increase or  where  forced  to increase utilization.
 So  questions : What  creates a  drop in SmO2.

Less delivery over  cardiac  out put  . So  we may see by the same   performance  a higher HR  as we may have a lower SV.  Lower  SV  or in general SV is  influenced  by  plasma  volume. Higher  plasma  volume  lower HR  and higher SV.
 If test is a clear  situation  you can check RH in the p morning as your  RH  will be lower  as well due to the higher SV.
 CO  5 L/ min.  RH  50  so  SV =  100 ml  So  45  HR  5 L  CO  =  SV ?

Now in this case  HRV   will be higher  as well.

2.  Lower SmO2  by the same  load  or  lower load  to maintain SmO2  can as well be caused as a delivery problem  from the respiratory system.
 Example.
 You may  have the  same  RF  as you may have a  great pattern in rowing  how  we  and when you breath , but  TV  can change  without  really feeling it.
 So  lower  TV  same  RF  means   higher dead space volume    to be moved   so less O2  in filtration but as well less CO2  out put. You shift    towards  the right in O2  diss curve  and therefor  have it easier  to release SmO2  so by the same load due to a respiration not optimal  day  you  will see a   further  drop.

 Now  HRV is  heavily   influenced  by  rrespiration  reactiosn, which  thrrouws  all the nice  ideas, that we  can sue  HRV  for  feedback on cardiac  reactions soemwehat out the window.
 That's  why we   check in resting .  RHR  and HRV  as well as  RRR  ( resting respiratory  rate  and   CO2   ( ETt CO2 )

Now  we  think lower delivery  when we  assume that by these ame  load  you  would have  had a  lower SmO2  than on all other days   so  more utilization  due a  delivery  problem ?

 Now  as you  correct   to  a base line SmO2  you try to archive , the speed  was less ,  less  muscle compression ?  but  perhaps  as well O2 needed  for less   speed ???
 The tHb  was higher  due  to   perhaps less   muscle compression  which  was less motor unit recruitment  which  would mean less O2   needed  or utilized. ?
 If  we have the same  SmO2  by a higher  tHb  we  actually have more  O2  than  same  SmO2  by a  lower tHb !!
 SmO2  is a  %  of  loaded  O2Hb    from the tHb.
 So 100 tHb  and  50 SmO2  means  50 Hb loaded.
 Now  150 tHb  and  50  % SmO22  means 75 Hb loaded  I  forgot  but  did  we had  a HR    for the off  day  or not  compared  to other  days.

 Now  here a first feedback to the  5/1/5  on the water.

First let's  look an overall  view

juergfeldmann

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 #10 
Okay seems we  are back on  screen  let's  see graphs I will be back on  his  5/1/5   so here just an  early hint  for me.
 His  " critical    "intensity is   between the time 600 and  1200 or his  third  load.  Possibly already somewhat to high  for a  STEI intensity . Will explain  how I  look  at it   today evening.  My  view  but  any bodies  view is   welcome.
thb  smo2 all.jpg  .
 Here some more  ideas
bias  all.jpg

sandor

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 #11 
Quote:
 The tHb  was higher  due  to   perhaps less   muscle compression  which  was less motor unit recruitment  which  would mean less O2   needed  or utilized. ?
 If  we have the same  SmO2  by a higher  tHb  we  actually have more  O2  than  same  SmO2  by a  lower tHb !!


this is the kind of thing i am wondering.

now i will watch for days with altered tHB, try to maintain SmO2 & test lactate. one interesting thing is that my SmO2 would not recover like the other days. typically i get 25 minutes steady state, then need to turn around. 1' rest usually raises SmO2 to the upper 60s, i start to row & it peaks to mid-70s & then i settle it in to 48. on the high tHB day, i could barely peak SmO2 in the low 60s.


heart rates (avg for the workout)
142
146
122 (high tHB)
135
137

i really want to do a 5-1-5 or 4-1 or something similar in the the range of the first two load levels of my 5-1-5. i think this is the area i want to see more details of (between 600 & 1200). i am figuring 5 or six levels of load, with ten watt spacing. just need to wait for a day that the river & weather cooperate [smile]

Ruud_G

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 #12 
High tHb day, low HR, SmO2 same, lot of (more) CO2 vasodilatation (high tHb) => in rest period SmO2 did not recover that much as "normal" (lot of / more CO2 means O2 diss curve to the .. and utilisation ... => something with VE? (RF?) Had imho not to do with better CO because then you would have seen a better SmO2
sandor

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Posts: 61
 #13 
interesting interesting

purely as the athlete talking:
i physically felt no different during the sessions.
the pace difference for the slower/lower HR/higher tHB was approximately 107 min vs 104 minutes. so about 10 watts or so. it felt easier to me, but i also had a live feed of HR, which could very well manipulate my brain!
resting heart rates for all days were in my normal range, 42-44.


and again, i have no answer, but i have a thought that 3 months ago, this would have been a session where i pushed to keep my HR where it "should" be, and RPE would have been modestly higher, and i would have woke up the next morning feeling negative.




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