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DanieleM

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 #1 
When looking at the graph of short and high intensity intervals I noticed that the graph of SmO2 is delayed few seconds compared to the actual intensity.
Here for example the first 30 seconds all-out interval discussed in a different post.
SmO2 start to drops approximately 6 seconds after the load is started.
load1zoom.png

Perhaps even more evident in some very short sprints I performed before that.
shortsprint.pngThis was approx a 5 seconds sprint, and SmO2 will basically start to drop after that.

Physiological or just a delay due to the algorithm?
I would really appreciate a feedback on that since it will help with the analysis.

Thanks
Daniele




Juerg Feldmann

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 #2 
Thanks  for the  interesting graphs. I   would like to  talk this  out of this tread  as we discuss  some specific  cases  here  for some specific groups, about interpretation  of tHb  and SmO2 ,  as there are  some very different ideas out there on what we  may be able to read out of tHb   and what we   for the moment know   we  can. So kind of  Dream versus reality.

 So here therefor a  very short answer  as the  question and the topic  was discuss   in the forum  somewhere a  few  times  already  so here just a summary  for  readers, who  may have missed it in my mess.
 1. There is  for sure a  small  delay in   live feed backs  like in any equipment. For practical use it has most likely  no relevance  at all.
 It is one of this interesting questions  we seem to ask  when something new  shows  up, but we seem to accept the delay in data  in existing , so called established  and heavily used ideas.
 Here  an example  for  all LT  believers and defenders  and  Lactate users   in interval or any training ideas. 
As well   I showed this  many times  before. Look below   the lactate delay  in the blood after  all out  300 and 600 m runs. Look at the incredible  delay variation and time. Now  ask the question on  the  for the moment discussed 1 - 6  seconds  perhaps delay but look later  what  MOXY/NIRS really may show.

This is  what surprises  me   since many years  and in  hundreds of discussions, where  coaches  and exercise physiologists  desperately hang on the  idea, that lactate can be used in  interval and strength workouts. It is  up  to the reader  to  ask the critical question , whether you may like a  small ( if  it exists  ) delay  of  1 - 2  seconds in a  NIRS equipment or the   many minutes  delay  of  lactate with a never  true  real lactate  value   which happened in the  muscle.

  lactate post.jpg
Now  here  an additional answer  from  the physiological point we discussed  as well  somewhere.
 There is a  slightly time  discrepancy    between some research groups on how  fast the O2  will be used  in a sudden high intensity  load.
 As  some may remember   the group  around Shulman thinks it is in the seconds  and faster, where O2  is used  to  help to  maintain ATP   levels.
 The group around Richardson  has a some what  longer delay in O2 use  as they  think from their studies  that   ATP kicks  in, than has to be protected  and   the  firing  of CrP  will help  ,  but than O2 immediately will follow.
 The time lag  between the  O2  supply  for ATP  maintenance is seen by this group in the 5 +- 2  seconds  range.
 

Med Sci Sports Exerc. 2015 Mar 31. [Epub ahead of print]

MRS Evidence of Adequate O2 Supply in Human Skeletal Muscle at the Onset of Exercise.

Richardson RS1, Wary C, Walter Wray D, Hoff J, Rossiter H, Layec G, Carlier PG.

Author information

  • 11Department of Medicine,      Division of Geriatrics, University of Utah, Salt Lake City, UT, USA      2Department of Exercise and Sport Science, University of Utah, Salt Lake      City, UT, USA 3Geriatric Research, Education and Clinical Center, Salt      Lake City VAMC, UT, USA 4Norwegian University of Science and Technology,      Faculty of Medicine NO-7489 Trondheim, Norway 5Department of Medicine,      Division of Respiratory and Critical Care Physiology and Medicine, Los      Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, CA, USA      6Institut of Myology, Paris, France 7CEA, I2BM, MIRcen, IdM NMR      Laboratory, Paris, France.

Abstract

PURPOSE:

At exercise onset, intramuscular oxidative energy production responds relatively slowly in comparison to the change in ATP demand. To determine if the slow kinetics of oxidative ATP production is due to inadequate O2 supply or metabolic inertia we studied the kinetics of intramyocellular deoxygenation (deoxy-myoglobin, Mb) and metabolism (phosphocreatine, PCr), using proton (H) and phosphorus (P) magnetic resonance spectroscopy (MRS) in 6 healthy subjects (33 ± 5 yrs).

METHODS:

Specifically, utilizing dynamic plantar flexion exercise, rest to exercise and recovery was assessed at both 60% of maximum work rate (WRmax) (moderate intensity) and 80% of WRmax (heavy intensity).

RESULTS:

At exercise onset [PCr] fell without delay and with a similar time constant (τ) at both exercise intensities (∼33 s). In contrast, the increase in deoxy-Mb was delayed at exercise onset by 5-7 s, after which it increased with kinetics (moderate τ= 37 ± 9 s, and heavy τ= 29 ± 6 s) that were not different from τPCr (p > 0.05). At cessation, deoxy-Mb recovered without a time delay and more rapidly (τ ∼20 s) than PCr (τ ∼33 s) (p < 0.05).

CONCLUSION:

Using a unique combination of in vivo MRS techniques with high time-resolution, this study revealed a delay in intramuscular de-oxygenation at the onset of exercise, and rapid re-oxygenation kinetics upon cessation. Together these data imply that intramuscular substrate-enzyme interactions, and not O2 availability, determine the exercise onset kinetics of oxidative metabolism in healthy human skeletal muscle.

 

Now  as you can see the initial  O2  may even  come from what we  once postulated long before  it may come  initially  from Mb    before it comes  from Hb. Most likely it will depend  on what happpend  directly before the incredible hard  load. ( Remember  the study we showed  about    sprint  and O2  use ) The reasoning  for Mb  before  Hb is  rooted in the  property  of the O2  disscurve.
 see below

oxy and myo o2 curve.jpg 



Now  this is a great  question as well as  a nice  criticlal discussion.
 Again, nice  would be, when  we critically look at accepted   indoctrinated ideas in this situation.
 The  question, why we  still have lactate tolerance  trainings, why we still have  ideas like  we  see   on tHb  that we  go " anaerobic  " and so on.
 The question :
 Where are the  papers  and studies  who proof that  LT is existing  and not just  fabricated  with   many different interesting concepts  and formulas.
 What we  try here with NIRS is to show  that we have a unique  chance to  actually see live  what  is going on  with possibly a  very small delay  and  what we desperately  try to find,  the  metabolic reactions  where we  start to  shift  delivery  and utilization   to try to sustain performance.
We looked  for  " anaerobic  " and aerobic  and used indirect  feedbacks  to hope  we  are close. We  where searching  where we  may  run out of Oxygen  or  more carefully  started  to  have not  enough O2. We created ideas like  aerobic  threshold  or LT 1 and  anaerobic threshold, LT2, delayed  VO2  and different mathematically calculation in case we  where not ready to  look for a FTP  60. All great  ideas  as we had no other  choices.
 Now we  can see live , where this  O2   "fight"  for balance or  out of balance happens  and we  simply  do not  at least try to  integrate it in our  existing ideas ????
 That's where I have  so much fun to  listen  and hear  argumentations  and defences from what we all did.
 Do you get this ??? 
Daniele  hopefully  some  ideas , which may help to give  you some answers  to your  question ?


Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #3 
After  short  but not unusual  sidestep let's go back to our  case discussion  form a workout.
 We  are still stuck in the first section so  let's   put it together    for a  recap.
Case we discuss.

full discussion idea  with three sections.jpg


And on this  pic  we discuss the first  part ( the green  slightly overlapping into the yellow.
The discussion is  on what do we  see and  in case this  was a planned  warm up , what  did  we physiologically created  or achieved  with this planned  warm up.
 It is  NOT  about , w2as  it a good or bad  warm up , as we do not know the goal  of this warm up done  by this  person.
 It is all about  what NIRS feedback's    can tell us  , what this  warm up created   when looking at O2  reaction and at  blood flow reactions.

So below    where  I try  to give  some  feedback on what we  see , may see and what more we need on information's to make a  better  conclusion.

thb smo2  first part.jpg


First  thoughts where  discussed already.
1. Do we increase  oxygenation. Answer  was  NO  . How  do we see that in the  graph ?
I showed the biased graph  as  an easier optical   feedback.

bias first part.jpg 

Now here as  an optical comparison of  a  workout  from  one of our athletes with the goal  to try to increase  O2  as well as tHb  for a very specific  targeted  workout goal.

bias leg hypoxic hyper cpan.jpg

 You can easy see in the first section the attempt to  try to increase  oxygenation  from  above the resting baseline.
 This was successful.
 The tHb  as an  indication of  local increase in blood  flow  was not yet successful after the  initial  preparation.
 So  we than in the second sections  where looking for the current  " balance " in O2 intake  and utilization as well a balanced   blood flow. ( some may have named it  FTP performance  or some may have named it MAX LASS. We simply  name it  O2 balance as that is what we see  a balance in O2 intake  and  utilization. So no need  to   test for  an indirect  feedback over lactate or  over performance. The physiological  reaction  which creates to day this balance  will  give us a feedback on what  wattage we  can push today as  FTP?
 It is not the other way around,. The  tested  and possibly current FTP wattage may not  created  today a balance O2  intake  and use ? . In our case we may have  exactly that feedback  but  wait  to see this later.
 You can easy see, that we  achieved  this  and therefor started  a specific workout to stimulate  blood flow  so we could move into the  actual workout  see  last section where we   had the target to get optimal blood flow  and optimal oxygenation.

Now   direct discussion on the SmO2  trend in SmO2  and tHb in our first discussed section. I use the time  axis  to tell you where I look at the data.

thb smo2  first part.jpg


- 0 - 60 Often seen  initial drop in tHb and SmO2  from a baseline calibration value. Reason.
 Immediate  need of  energy  including  O2 , but delayed  increase in blood flow, in fact initial compression of blood vessels  due to muscle contraction  so  contraction force  overrules the still low  CO pressure.

- 60 - 240  On going drop in SmO2 as an indication, that O2  is  faster utilized  than it can be delivered.
                 Ongoing  drop  with some  up and downs  of tHb  as  an indication, that the muscular contraction force  seems to  still overrules the CO pressure ( other possibilities  to discussed. )

Speculations: To get rid of the speculations we  need additional feedback's like HR   or  direct performance.
 Now here  what  SmO2  and tHb  may reveal  when we  would look at HR  and   wattage.

SmO2  when looking at absolute  direct basic  reasons  : SmO2  drops  after  the expected initial drop because we  have not  sufficient enough delivery of O2  for what is  needed  to either keep a balance  and or  even an increase in SDmO2.
 This can mean, that after  an initial  start  wattage   this  person may actually not have waited long enough to see, whether the cardiac output (  small feedback over HR0 had  enough time to try to get an optimal delivery  value  going. Instead  the performance may have been steady increase asking      steady for a  somewhat higher O2  delivery but the delivery system  was lagging behind hing in   volume  due to lag time of  HR  and or  lag time of increase in blood  volume available  for   the circulation..
 So  when we  speculate  how the  wattage  may  look in this case  based on SmO2  than  we have 2  options.
a) A stable wattage but too higher  to sustain a chance  to get O2  in balance.
.b)  A steady increase in wattage  too fast to give the CO a chance to try to deliver  and as such balance  O2  intake  and utilization.

Now lets' look the tHb trend. A steady decline  but short before  240 we have a trend of a potential  flat tHb indicating  at least a balance between   compression and CO pressure..
 The steady  drop in tHb   with the speculation for  s a steady  increase in wattage  but a   too short time   for  CO  to react  would fit  the idea of a steady increase in wattage.
 The increase in wattage  will over time  try to stimulate  a higher CO  and if   the cardiac system is a  compensator    rather than a limiter  we would over time see a possible increase in tHb to try to deliver.
 We  may not see an increase in SmO2 if the utilization is still higher than  the  delivery ability despite  a higher delivery  volume. We  could now  go much further but just leave it here.
 So the next sections  shows  4  loads.
 What we  for sure  can see, that the second load  most likely  was  wattage  wise the   lowest load.
 What we  can not tell is the actual performance in wattage  as  MOXY is a metabolic feedback and  NOT a performance feedback. . But there is some  more w e  can see.  There are  most likely short bursts and wee see a fast  drop in tHb  and a fast recovery  so relative explosive loads  . The same wee see in SmO2.
 What is interesting is , that in the off load  we  do not have an overshoot in SmO2  nor in tHb  above  baseline  . This indicates, that in contrast to a 5/1/5  where we  stop load  completely so we  get rid of one  guy who uses O2  , we have In this case  most likely  still a load in between the bursts. When you look at the tHb  recovery values in between the bursts   than you see, that they reach  a level  like we see in 0 - 60  area . Indicating in this initial  stage that  the wattage   in  between the burst is  possibly similar like the wattage  at the 60  time marker..
 Due to the fact , that the initial 0 - 240  did  not  improved   tHb values nor SmO2 values we  can  assume , that even during the bursts the  CO  was not yet  working well over SV. Most likely  just over  some HR  reaction. The drop in tHb   during the burst  anyway  was not beneficial  for preload   of SV in the first place.  Now  after the 4  burst.
480 - 780 we have a similar trend in tHb  and SmO2  ( level  with a   flat SmO2 level indicating now a balance between  input  an utilization.
 The short burst  for sure  stimulated the  HR , the  lower  wattage now   will allow  a better   preload  so   most likley the HR  was now  stable or  not increasing  so  speculating of  similar wattage load now   like at the start.
 Similar  HR but most likley not increasing  so  close to a balanced SmO2.
 Where we  have some open questions is the  tHb  trend  towards a  drop in this section..
 Here we would need to  get a feedback what is going on in the respiratory section as well a feedback  from a MOXY in an non involved  boy part.


 Last speculation we  can make is, that the reactions we see,which  does not show a great SmO2 or tHb  increase  can be an indication, that the  load was relative  high  to start the  optimal stimulation for  tHb  and SmO2.
 When I  say high , than that is in comparison to the  possible   optimal  balanced load.
 We know  from VO2  that  when pushing 50 %  of  VO2  peak  we  already have a FFA  stimulation. So I would guess that the  start load din this case  from this  person  was at least 50 %  of his FTP  or  slightly  even higher . So too   hard  to start out  an initial  stimulation of blood flow  and  respiratory reactions  and too fast increase in loads.
 So next up will be section 2 in our discussion.

Juerg Feldmann

Fortiori Design LLC
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 #4 
Hmmm  my  big mistake  , Daniele  was  perfect I messed up my part here as the  first section closer discussion should be under recap  and not  as an add on to Danielle's  discussion.
 That's  when I am not   focused  and rush on the forum in between  treatments. So need your imagination  to see that  first part discussion moved  to recap as we will follow  through there with the second section in our discussion on possibilities  to  make  NIRS interpretations.
 Sorry  for the mess up.
Roger

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 #5 
In the default update rate mode on Moxy, there is about a 5 second delay due to the smoothing algorithm.

The Moxy calculates a new SmO2 and THb reading every 2 seconds, but the number it displays is the rolling average of the previous 5 readings (10 seconds).  This has the effect of smoothing out quick changes in SmO2 or THb.  The data looks like it is shifted about 5 seconds later.

Some researchers are interested in what is going on during that 5 second period so there are 2 options on the Moxy to update faster.  There is a "No Smoothing" option that eliminates the rolling average so each new reading is only based on the previous 2 seconds.  There's also a fast update rate option which updates every 0.5 seconds.

I've attached a document that goes into a lot of detail on this if anyone is interested.

pdf Moxy Update Rate.pdf     

Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #6 
Roger  thanks  for the  great add on.
 I had an email on how to change  that  and I try to explain it but Roger  may have to jump in.
 You change the   rate in the MOXY  app and you have there the different versions  Roger  explains.
 For  coaches  and  live feedback the default  is a great way  as otherwise  the data's  get very restless.  For us  as we all   depend on the top  researcher it will be fun to see how that plays  out. Is it an O2  integration based on Shulmans  ideas in the range  of  very short  times  like second  and faster or the   study I showed you , where they think it  may be more in the 4 - 6  second range.
  Lot's of interesting times ahead. 
DanieleM

Development Team Member
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Posts: 264
 #7 
Great thanks!
It was really good to have this clarified since there are workouts/test based on very short sprints.
It now makes a lot of sense and shifting back the SmO2 and tHB by 5 seconds to be in sync with the power reading, it means that SmO2 starts to drop almost immediately.

This will also match with the graph from Bucheit et al. using a different NIRS instrument (Niromonitor NIRO-200)
Performance and physiological responses during a sprint interval training session: relationships with muscle oxygenation and pulmonary oxygen uptake kinetics.
bucheit30s_sprint.png 
TOI is the tissue oxygenation index and should be the same as SmO2.
And, on here as well, TOI/SmO2 seems to start dropping almost immediately.




Juerg Feldmann

Fortiori Design LLC
Registered:
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 #8 
Daniele  ,
 Thanks  for this great  feedback.
 As  all can see  different words  for  often the same ideas.  TSI is used in NIRS Portamon which is sometimes  but not always  the same trend as SmO2.
 The trend  Danile   ex-lans  would thna be much closer to teh thery   we discuss  by Shulman. Here a  recap
 

Robert G. Shulman

Department of Diagnostic Radiology, Yale University School of Medicine, MR Research Center, New Haven, CT

SHULMAN, R.G. Glycogen turnover forms lactate during exercise. Exerc. Sport Sci. Rev., Vol. 33, No. 4, pp. 157–162, 2005

 

We suggest that glycogenolytic ATP production supplies the energy for millisecond bursts. This hypothesis implies that _1 _mol·g_1 tissue of

glycogen subunits is consumed during each contraction to

refill the ATP and PCr pools. Because basal glycogen concentrations

of _70 _mol·g_1 tissue are not depleted even after several dozen contractions, resynthesis of glycogen must occur between twitches.

Without the millisecond time pressure of contractions, the ATP required for this resynthesis can be achieved via somewhat slower oxidative means.

Although oxidation cannot supply ATP in milliseconds, it could resynthesize glycogen in the _1-s interval between even rapid contractions. Measured rates of oxygen consumption vary, seemingly dependent on the measurement method.

None of the reported values reaches the rate of 1 _mol·g_1 tissue per twitch, but the fastest values measured do reach several _mol·g_1 tissue per second. Hence, it is possible that the glycogen pools, which are decreased to refill PCr and ATP in milliseconds, are replenished by the energy supplied oxidatively in the longer period, no shorter than _1 s, between contractions.

 

Evidence That Glycogen Rather Than PCr Generates ATP during Contraction

 

The conventional view of short-term muscle energetics is that PCr supplies almost all of the energy needed for a sustained burst of contractions lasting less than 10 s, after which it is replaced by glycogenolysis.

This view is not supported by experiments. In a recent review, Greenhaff and

Timmons (5) report, “It is now accepted, however, that PCr hydrolysis and lactate production do not occur in isolation, and that both are initiated rather rapidly at the onset of contraction.”

Robert G. Shulman

Department of Diagnostic Radiology, Yale University School of Medicine, MR Research Center, New Haven, CT

SHULMAN, R.G. Glycogen turnover forms lactate during exercise. Exerc. Sport Sci. Rev., Vol. 33, No. 4, pp. 157–162, 2005

 

INTRODUCTION

 

The modern age of lactate studies began approximately 20 yrs ago when George Brooks questioned the accepted findings of previous generations and proposed the Lactate Shuttle (1).

Early studies demonstrated that lactate accumulated when frog muscles contracted up to the point of exhaustion but

disappeared during recovery in the presence of oxygen. In that view, the creation of lactate by exercising muscle is caused by the deficit of oxygen.

 

However, numerous experiments by Brooks (1) and others have shown that lactate is generated during the performance of work by skeletal muscle in the presence of plentiful levels of oxygen (10). In fact, it is generated even when mitochondria are fully oxidized (10).

Lactate production under hypoxia and or anoxia is rather the exception than the norm (Gladden)

 

NMR studies of the oxygenation of muscle myoglobin in exercising humans showed that oxygen levels in working muscle decrease with load, but even at maximal oxygen consumption are well above the mitochondrial needs (8).

 No such thing like anaerobic  situations

 

The shuttling of lactate to redistribute energy led to questions about its origin, which was long assumed merely to be the result of an inadequate oxygen supply.

 This review is based on the understanding that lactate can shuttle energy

from locations where it is synthesized, such as white fibers in skeletal muscle or astroglia in brain, to other locations, such as red muscle fibers or synaptic neurons, where it can be oxidized (1). The residual reductive capacity of lactate to provide energy is not wasted by the body and its formation is not caused by a limited supply of oxygen. Lactate is not simply an unwanted by-product, but rather is purposefully synthesized during work to meet normal physiological needs.

 

However, the nature of that normal physiological mechanism has not been found. Now that the hypothesis postulating a deficiency of oxygen has been discarded, the reason for lactate generation to meet the energy needs of muscle and the brain requires an explanation. In this review, results from several  avenues of research on the energetics of skeletal muscle are coordinated to propose a model for lactate build-up during muscle work under well-oxygenated conditions, a build-up that drive the lactate


This  and other interesting new  direction due to  better technology  is  why we  have to review  the classical ideas   we all learned   and got  educated  on. This is what makes so much fun.


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