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CraigMahony

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 #16 
In the third one minute recovery and onwards, except for the eighth and maybe the last, there is an initial drop of tHb before it recovers and rebounds. This to me indicates a minor outlow obstruction, maybe a venous occlusion. It may also indicate that Stuarts proposed delivery problem is unable to overcome the muscular compression. So either a delivery problem or a strength problem? Strangely though, the tHb as mentioned rebounds / overcompensates immediately in the eighth one minute recovery for which I have no explanation.
juergfeldmann

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 #17 
Stuart
 Agree I would also go towards a  delivery limitation. So  for the advanced   Ryan this is a great  start  to  go into the next  few month   with still using classical   wattage and  HR as a guide  but  I would start to integrate   NIRS  so  he is getting used  to understands  that  the same  wattage   is not always the  same physiological   stimulus.

 Now  looking ahead  on Ryan's  Pro   training program  we  have to look what   does  delivery limitation mean.
Here  some key words.
-The cardiac  system is  for sure a   delivery system , But in  survival mode  it may be a utilization system. 
- Is  the  respiration system a  delivery system. Most likely  yes  as it delivers  O2  but we often forget, that  pO2  is never a  real  issue in a  working  systems as it is protected   as long as possible. So  if we have a  delivery limitation   and we keep pushing  we may create a  situation, where there is less the question of  delivery  but rather  to try to  maintain a H + balance  so  respiration now has  to  "deliver " a sufficient  ability  to   get rid  of CO2.
Easy to see at the end of  races where the only task  the athletes have is  to breath and get  rid  of  H +   to get as  fast as possible   at least normocapnic  so the  can load  O2  again    form the lungs to the  blood.
- capillarisation  a  very  important delivery system  and often  overlooked  when we  talk about delivery.


Now  below  some more points   to  the great  points  Stuart  makes we  can  discuss  as  there may be some different views.

Looking at Sm02 and tHB graph towards the end as CO becomes very high, tHB levels in 1 min rest equal or go higher (last 1 min) than original rest calibration value. So I would suggest that local vascular network was not limiting here?

That is  true  for the  second assessment it  appears  we have a higher  tHB in the rest period. which than as  Stuart  points out   would give some indication of a  higher  capillary   blood flow than  at rest.
Interesting is  that that  is only  at the end load . One may think , that if we have a great  nice  capillary bed  we  may see this  possibly  earlier   at the rest  l   levels ?
 See below an example.
col thb l leg.jpg 
Now
, if  you look at Ryans   1 assessments and you make a  line   in the first assessment  for  resting tHB ;levels  so no activity  to  resting  tHB levels  with a very high CO  and most likely high  VE  than we have a minimal  to now increase in tHb in the  first assessment  and we  have a   short  spike  at the   second one.
See below

colour   zines  tHb.jpg 

But remember  the   possible   limitation I showed  in the second assessment, where we  have this  tHb  spike was where he pushed   harder. 
Now  we looked  at this section closer  and let's  go back there. You can see the tHb increase is  due to a higher increase in  HHb  as a sign of   problems getting rid  of HHb  so possible pooling.

biased 5 1 5   hard  end load  oct.jpg 
So if it is  a higher  vascular bed  which now  opens  we  would have this  after  he stopped  as  muscle pressure is gone  and  CO  and VE is  still high  enough , there is no cardiac limitation so  the cardiac system has no problem to maintain BP  and tHb  can go up . Well that's  why we  have live feedback  so lets  see  that closer.

51 5  2nd  spike  due to pooling.jpg  Now we  can see, that  the increase in tHb  is before  we  have an increase in SmO2 . So  2 options to look  closer.
 1. Respiratory limitation   O2  disscurve  shift  to the right  hypercapnia
 or 2. pooling  ?
What is it. ?  If 1  how  would  tHB  look .
 if 2     ?
In both cases  we would have a  tHb increase due  to other reason  than  actual higher  capillary bed. 





juergfeldmann

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 #18 
Craig
 In the third one minute recovery and onwards, except for the eighth and maybe the last, there is an initial drop of tHb before it recovers and rebounds. This to me indicates a minor outflow obstruction, maybe a venous occlusion.
It may also indicate that Stuarts proposed delivery problem is unable to overcome the muscular compression.

So either a delivery problem or a strength problem?

Craig   for me  the same thoughts.
 and  to add on, this two support  each other. If  you have a  delivery limitation due  to a  not optimal capillarisation density  and you push harder  you may  push above and beyond  the ability  for the blood vessels  to  maintain  optimal flow. So  if we see this  you have two options depending on the sport .
 a)  improve strength
  or  improve  capillary  density.
Below a  many times  used  picture  here, sorry a very old  one  from my  University years but still true.

blut geafeass und muskel contraction.jpg 


 tHb as mentioned rebounds / overcompensates immediately in the eighth one minute recovery for which I have no explanation.

Look  my  explanation suggestion in the above  reply

ryinc

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 #19 

Craig, Stuart, Bobby and Juerg thanks for your willingness to share thoughts. Everybody has added a great degree of insight.

 

My thoughts so far:

 

  • The general consensus of a delivery side limitation is aligned to my thoughts
  • In the last load, I think there is definite evidence of respiratory system in trouble (right shift of dissociation curve), but is the respiratory system the limiter or is it a compensator that reaches its own limitation?
  • The THb rebound pattern for the 3rd last and last rebounds seems to be causing some debate. Please see my notes on the protocol here in the first post.  On the last recovery (i.e. what is being described as 8th and 10th loads by some, but I would describe as 5B and 5B to be more clear) I unclipped and rested my foot on a chair next to the bike. Note this was not done at all on the 17 September assessment – right leg was always at 6 o clock approximately. I think this is quite crucial in making interpretations.

 Having said that I am battling to wrap my head around this issue. Just to summarise what we see when the leg is in the 6 o clock position.

  • Recovery after 1A and 1B THb increases immediately after the load.
  • For other recoveries. There is an immediate drop in THb as the load finishes, and it drops for about 20 seconds and then THb increases for the remainder of the break, normally to a level that was higher (or at least similar) to what it was during the load. Even though it was a similar protocol on the 17 September – this pattern of an initial drop and then recovery does not show up for the majority of the rest periods for the 17 September.
  • The size of the drop generally tends to get bigger with harder loads.

 Now for the 7 October assessment, for loads 4B and 5B (8th and 10th if you count 1,2,3…) where i put foot on the chair the THb increases immediately at the end of the load.

The graph below shows the markup:
THb drops.png 

 

Personally I think the drops in THb trend (in general) is less likely to be a venous occlusion for the following reasons:

  • The drop in THb on recovery starts very early in assessment, where muscle strength is not likely to be a limitation
  • The drop of THb after the end of the load, occurs even in some instances where during the load the THb was flat or even slightly decreasing (if it was an occlusion we would expect THb to be increasing during the load). See the brown arrow in the graph above.
  • When the leg was rested on the chair, we don’t see the THb drop. Are we saying that putting the leg on the chair increases a venous occlusion at rest? Sm02 trend on recovery would not support that would it?
  • It occurs on 7 October assessment but not on 17 September assessment. I don’t think muscles were more fatigued on 7 Oct (it was done with at least a days’ rest before and a normal training load in the week leading up to it), and if anything I actually expect that pure muscle strength might be slightly higher for the 7 Oct assessment, given the training that took place between 17 September and 7 Oct (some high force, slow cadence drills). To me it is more likely that one of the other systems with a greater level of day to day variability caused the differences in pattern.

 

  • Related to various point above, Juerg has shown a number of graphs for the last load on 7 Oct. What I think is helpful here is to show where the load actually ended.
  • Last Load.png 
  • You can see that the load ends before THb rises sharply. Now to me this could be:
  1. Right shift of dissociation curve. I.e. the load is removed and because of the C02 buildup THb rises sharply and Sm02 is sluggish to recover. There are opposite forces possibly acting on THb here, if there is a bloodflow related limitation i.e. C02 acts as vasodilator but if there is a BP limiter it might act in the opposite direction, so C02 "wins" initially but then BP reaction takes over which is why we see a drop again?
  2. A minor occlusion caused by the act of unclipping pedals.
Finally, to me it looks as the on load 3A, HR goes out of balance (probably as the compensator) and THb reacts to the increased CO (this is the bottom of the U-shape of the THb curve). It looks to me more likely that THb is increasing here as a function of increasing HR than out of occlusion trends or out of respiratory at this point.

THb vs HR.png 


juergfeldmann

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 #20 
  • In the last load, I think there is definite evidence of respiratory system in trouble (right shift of dissociation curve), but is the respiratory system the limiter or is it a compensator that reaches its own limitation?
If  it is a  compensator , than it had  to kick in  when ever   it  try to compensate  for  a limiter 
 So  somewhat before  it breaks down    on its compensatory  work.

he THb rebound pattern for the 3rd last and last rebounds seems to be causing some debate. Please see my notes on the protocol 

 Yes  that's  why you have to  forget  too much interpretation on this   section as you  changed  the  tHb reaction by  a lot  by changing this  position. Now     even if  you stay  the same position but you pushed  very hard  you often will have some problems  to relax.
 That's where I love the additional  MOXY on a less priority  muscle.  which   is  more lily  not that  much influenced. by  leg position.

As we suggest  we do  a  5 min   start calibration and have 21/2  min  6  o'clock  and 2/12  min 12  o clock  to see   the individual reaction of our client  so   when we see  similar trend  we keep this weakness in mind.

 The next step  before   we  get to exited  about interpretation is  that we  normally  will do 5 - 10  physiological assessments  and they are all involved in the  training  itself  as a part of  calibration for the upcoming training  session or goal.
 Lie  in any workout  every body  will  do  what some call " warm up "  and  instead of simply moving   without plan  we do a  relative strict   " warm up "  we name it calibration for each  workout  and therefore  have  very early on  after  10 - 15 min  a certain trend , whether we can actually follow our  plan or whether we    do a different workout.

Are we saying that putting the leg on the chair increases a venous occlusion at rest? Sm02 trend on recovery would not support that would it?

Or  is  this a  " normal " relaxed position  where the chair  may be higher than  the 6  o clock  position so perhaps  closer to   having the legs  on 12  o clock.  Now  I have to go back and look at SmO2  level  when  Leg  was on the chair  closer  and compare  to the  leg 6  o  clock    by  similar loads.. Foot  on  6  o clock  has a very different relaxation  SEMG  than  foot  at  12  when you look the  reaction  as the MOXY  is on RF. So   hip flexion  versus  hip extension including  leg  down  would be a  fun  way to look  at SEMG  reaction. May play  w  around  next week.   What i would  do is a  workout  and prior  to the workout  I  would  "   warm  up  like  you did  like  the fist 2  double step  or  the   first 4  steps  but single but with a 1 min rest  to see  the  common reaction  form your  body .   6  o clock  the next workout in the  warm up the same but  leg  at 12  o  clock   than see , whether there is a pattern   here.

Than  when  ever you  do a  hard workout  anyway. You not even need a MOXY  and  you  do  for  example  some   interval with the  highest  loads you had.  try  once  you    just do it  , than the  second interval you  concentrate  of  breathing much  more  deeper  and faster  than   do it  than repeat  again and see  how  you react. You can do this with  or without  MOXY on the leg.
 Look as well HR as  you  do   this.  If  the limitation was a occlusion trend  due to a  delivery limitation than  what would  a   increased  VE  do ?
 If  it is a  repository limitation    than  what  will you see ?
ryinc

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 #21 
If  the limitation was a occlusion trend  due to a  delivery limitation than  what would  a   increased  VE  do ?

I have to think some more about the answer to this question. However, i first want to ask a question on the part in bold "limitation was an occlusion trend due to a delivery limitation".

I had previously thought the occlusion trends were normally a sign of muscle strength limitation not a delivery limitation. Normally when CO is not overcoming muscle compression we see a drop in THb, e.g often in the start of a load? Can you expand on what you mean by this.
bobbyjobling

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 #22 
I think if it was muscular occlusion during the rest period THB will go up and depending on CO or BP THB will overshoot the calibration THB level until it reaches a max level. If it was CO or BP problem then this overshoot will be suppressed due to BP/CO limitations .
High capillary might cause this THb suppression, but THB shape throughout the assessment would be different too, maybe flat or inverted U with "little" THB response during rest period but all depends on BP regulations.
But I could wrong


juergfeldmann

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 #23 
Question:
Personally I think the drops in THb trend (in general) is less likely to be a venous occlusion for the following reasons:

Not  sure whether I understand this properly.
 If  we have an  outflank restriction from an area due to  muscle compression which reaches  a pressure  more than  venous  pressure, (see a mechanical occlusion I showed  from the Artinis  website )  than we  may see a  slowly   or faster pooling of  blood  before the restriction. This  than  can be a venous occlusion.
 The  outflow restriction  my more likley show an increase in tHb. 

juergfeldmann

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 #24 
Ryan  great pont 
 I had previously thought the occlusion trends were normally a sign of muscle strength limitation not a delivery limitation. Normally when CO is not overcoming muscle compression we see a drop in THb, e.g often in the start of a load? Can you expand on what you mean by this.

Yes  if  we have a  straighten limitation  and we reach  35 % +-  of    maximal strength we start as Rhomert presented  in the early  1960 , to reduce blood low   till up  to  no flow.
. Now  there  are different options . I  can improve strength so that by he same load  I only  use  15 % of maximal strengths.
 or  I can improve  delivery  systems  like more  capillarisation  so  I have a higher chance  to actually keep some blood flow going.
Cardiac  and respiratory  are looked  upon as  clear delivery systems. But as mentioned  above  you  can have a local  limitation of delivery  which is in man  beginner the case.
 Beginners have   very likely not  cardiac  and respiratory limitation but local  mitochondria  and  capillarisation limitation.
 That's  the reason, why you can do nearly any  thing with them  if  you not overload  daily but get a 3 x  / week  activity going  for a  while.  They will improve no matter what testing system  and  ideas  you  use.
 The problem  comes, when hey are reaching an  adaptation, so we have to  change stimuli The famous   dialectic contradiction.
 Adaptation means  you  have  the  ability  to make  progress , but   because you make  progress and adapt  you stop making progress

Now in the case of  strength  in improvement  versus  higher  capillary  entity   the question is  what is better for the particular sport you may  do.
 In cycling   sprint  or   mountain   time trials.
 The famous  body weight comes into  play  and the duration  you   have to  load.  But as well   time of the years. what is easier  time  wise  for the moment improving strength or  building more  blood vessels. The   fight  shall I go  functional or shall I go structural.

 The fascinating part is , that  when we  get into an external stimuli like  in altitude  we have this incredible adaptation from nature.

 Some  early researcher suggested, that in altitude  we increase  capillary  density.
 In fact  depending on the duration we  actually loose  muscle mass  and maintain density    for a  while  which than looks lie  a Gehrig density per   square mm  but in fact same  density  in less muscle mass . Makes sense  to reduce    weight  as muscles  so easier  to  feed  less muscles  with reduced  O2 pressure   over the same delivery   system.
If  we say longer  we  surprisingly loose  mitochondria density as well  so long  time   people  living  at altitude  or  Sherpas  have  actually a lower  mitochondria  density   and we would expect  the opposite.

So in your case. Strength  versus  capillary density.
Hope it makes some sense.
ryinc

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 #25 
Question:
Personally I think the drops in THb trend (in general) is less likely to be a venous occlusion for the following reasons:

Not  sure whether I understand this properly.

 If  we have an  outflank restriction from an area due to  muscle compression which reaches  a pressure  more than  venous  pressure, (see a mechanical occlusion I showed  from the Artinis  website )  than we  may see a  slowly   or faster pooling of  blood  before the restriction. This  than  can be a venous occlusion.
 The  outflow restriction  my more likley show an increase in tHb.

Juerg, i think we are missing each other on the above? Let me summarise the points I made to make sure we are on the same page.
  1. If you look at the 7 Oct assessment, at the end of the loads (from 2A) there is a immediate drop in THb (see the picture where i marked this up - i added it again to the bottom of this post).
  2. Some contributors to this thread are saying this could be indicative of a venous occlusion.
  3. I am not yet 100% convinced it is an occlusion for the following main reeasons (1. It happens at early loads, where unlikely to be high mechanical pressure; 2 in some of the early loads there is no evidence of pooling of Thb during the load itself - we actually see Thb dropping during the load; 3 we don't see it on the 17 September assessment, a muscular limitation does not seem likely to be there one day and gone the next, unless there was particularly different workouts in the days leading up to the assessment - which i can confirm was not the situation).

If you understood that these were the points i was making in your response above, then i think i have totally missed the message in response post. There is nothing i disagree with in your post, i am just not sure how it disagrees with what i put in my argument?

THb drops.png 

juergfeldmann

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 #26 
will look this evening much closer 
BUT  in the  circles  you see a  drop in tHb
 (from 2A) there is a immediate drop in THb (see the picture where

Some contributors to this thread are saying this could be indicative of a venous occlusion.

If  we have  an occlusion  or  outflow restriction ( venous  occlusion)  and  in  case it is just at the start of a  1 min rest, no matter what intensity, than we  would have still a   relative high CO ,  So lots  of blood coming  from the  heart  arterial  but   less or no  outflow   due to a venous  occlusion. Would we   expect  than  that the tHb  would  drop ???? That is  the question  of the  venous occlusion suggestion.

I am not yet 100% convinced it is an occlusion for the following main reasons (1. It happens at early loads, where unlikely to be high mechanical pressure; 2 in some of the early loads there is no evidence of pooling of Thb during the load itself - we actually see Thb dropping during the load; 3 we don't see it on the 17 September assessment, a muscular limitation does not seem likely to be there one day and gone the next, unless there was particularly different workouts in the days leading up to the assessment - which i can confirm was not the situation). 

Agree  absolutely.

There   is some other option  possible but I like to try it out  today  with some  client  I have on the bike and than like to    zoom in  and  look at  HHb  and  O2Hb trend in this section..
 The  dip in tHb  means a  reduction in  Hb in that  area  due  to  reasons we  still  discuss here but unlikely   an occlusion  see above  ideas   from myself  and Ryan. .   Great  discussion  thanks
Stuart percival

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 #27 
I am struggling here a bit.
I tested an athlete yesterday and actually had a similar tHB results. Levels never exceeded or returned to calibration resting levels- From memory the final rest equalled rest level.They did however rebound in every rest interval but never equal to or greater than rest
So what scenario allows higher tHB at rest but never returning to that level even in easier loads when CO is increasing and vasodilation to deliver more blood to locomotor muscles. I think Ryan mentioned that muscle weakness would be unlucky as loads are relatively easy. The girl I tested races and her RPE at that level was 3/10
i can post graphs later but they are similar 
ryinc

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 #28 
Stuart - just to be clear my comments around muscle strength were in relation to the slight drops in THb on rest.  They were not related to the U-shape of THb that we see as an overall pattern from start to finish.

I have a new theory that has to do with placement/attachment and not physiology on these slight drops but i need to test it first.

My thoughts to your questions are that possibly a well-developed vascular system that dilates well but where CO delivery is perhaps not that strong might lead to the type of situation you describe (i.e. ThB struggles to get back to baseline but there is evidence of increases during rest). After some vasodilation, all the "channels" are open but the pressure of the blood pumping through is simply pretty low so there is a weak rebound because majority of CO capacity simply goes to keeping up the pressure in all the vessels. So imagine an extensive network of pipes with liquid going through them. You might increase the pressure of the liquid but if you increase the diameter of the pipes at the same time, the pressure in each might actually reduce - but i have no background in physiology so take whatever comments i make with a pinch of salt. Sure Juerg will give some good insight.

There is a thread dedicated to the U-shape observed in many assessments seen here and by the sounds of things in your assessment too. (http://forum.moxymonitor.com/post/thb-ushape-7769666?highlight=u+shape&pid=1289846806) - it got quite technical (too technical for me) but there was an excellent, almost philosophical, post from Andri near the end of the thread which i found really insightful and alone was worth reading the whole thread for.
juergfeldmann

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 #29 
Ryan   will be  back but  your piping  comparison is  what  I  have  every spring  when I  add more   hoses  for  watering the  garden but  have the same  pump  ( O )..  So I love the comaprson and will  dig  back again in the  2 very different ideas din the scitifiqe  world  on   blood vessel  recruitment, where the sport science is  perhaps stuck on  an old idea  of  Krogh  and misses  the newer  ideas   form vascular  research with  great equipment not  available to Krogh  at  his time  when he  produced that theory . 

If  we look at  top  coordinated  athletes versus beginners  we  see a very different rend  as the U  shape  tHB reaction in a  complete 5/1/5  shows.
 In beginners  with a limited  intermuscular coordination so just pushing  down and this as well  just in a anticancer range  compared  to a  top athlete  with   as well pulling up. you have a very different muscular  pattern  with many more muscles   asking or   O2  but  very low   strength  demand for the same wattage  than  one muscle pushes the same wattage.  So  as you can imagine the the trend will be different. Over time  you sill be able  to use this feedback to see improvement for  intermuscular coordination versus intra muscular coordination.

If  we  chnage for example the   chain ring  and us e a  rotor crank original version or a  Q  ring  newer version we   can see this even nicer.  To set  up a  Q  ring  properly  you can combine SEMG  /MOXY  and  VO2  and you see the most efficient  way  how to mount it  for  a   TT  or a a mountain stage.
 Not sure whether   Fromme and  Sky  is doing this. I know many use lactate as  marker, ( Yo  could use intramuscular  glycogen  situation  with US but difficult  to  do and not yet great application during a race . but  the optimal set up is  that you can change  seat position very slightly and achieve very  different inter muscular coordination  depending on  the   road  situation.  A great  way  to than use  this  in  workouts as in fact you know how to shift blood  due to different   muscular involvement. You may not be  faster , but you may be able  to maintain a certain performance  longer  as you can recover  one section by using another section.
 Cross country is  easy to  be used  for this   from more leg  work  to more upper body  work depending what is the most efficient way to move the fastest  with the smallest  VO2  possible. 

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