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DanieleM

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 #1 
After few attempts, I managed to (hopefully) perform a good TIP.
Steps: 140/180/220/260/300 Watt
First on the Left Leg VL (stop after first 300 load due to lack of time)
tip_left_vl.png 
Then Right Leg VL (two days later) where I've added a couple of 30sec All Out at the end:
tip_R_20140117.png 
At a first sight the trends look similar:
Alarm phase on SmO2 during the first 2 or 3 loads, then on all harder loads fast drop and then SmO2 recovers a bit and remains almost stable during the load. Recovery SmO2 reach the same level during all the loads.
tHB had a downward trend on the first loads then stabilize.
On the last load there is a clear increase of tHB during the load and overshoot when the load is over, perhaps with some delay due to short occlusion/restriction?

Thanks in advance for any feedback about possible limiter/compensator.

One more question: if I compare the first TIP attempt and the last one I can notice SmO2 overall level much higher in this last one.
Could be this a sign of better recovery condition?


 
Attached Files
xlsx tip_r_vl_20140117.xlsx (149.79 KB, 78 views)

Ruud_G

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 #2 
Hi Daniele. I have a question as well. In your lasts steps you SmO2 goes down to about 30. It seems to me that level is still quite high for a last step. Were you at your limit?
DanieleM

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 #3 
Hi Ruud, I could have done another step like that or slightly higher.
If you see the 2 hard loads after, SmO2 did not drop that much either.

Juerg Feldmann

Fortiori Design LLC
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 #4 
Will be back later, but    try  NOT to look at   numbers  and compare. You can compare intraindividual  but not inter individual just like that.
 I can show you  5/1/5  assessments  from absolute world class  cyclists   and they can't  go lower than 40 SmO2 in any of many assessments in a 5/1/5
 Remember it is a %  of  O2Hb  in comparison to tHb   but it is  NOT  and absolute information on the  amount  of  O2.
 Here a stupid example    first by using SpO2  on your finger.
  You can have a 95 %  SpO2  meaning that 95 % of the  Hb is loaded  with O2.
.  Now you may have an other person  with 90 %  of SpO2  .   so 90 % of the Hb is loaded. 
But , which one  has more O2   as an absolute number ?
 So  lets  make it even more simple. We  have in the first case 100 Hb  and  98 %  are loaded so  98   O2 pieces.
 The other   person may have 200 Hb  b and 90 %  are loaded  so he has how many pieces  of O2 ?

 So next up  we look for an answer.  You have  a  increase in tHb on the graph  so more  total Hb. . If you assume  you use the same amount  before it  climbed  and  now  you increase tHb    what will SmO2  most likely do  ( some exceptions  apply ).
 Or  tHb is dropping indication a  reduction in total Hb   and you use the same  amount of  O2  what will SmO2  do.. Now  tHb  drops     and you as well will use more O2   as you go harder  and  higher muscle compression. What will SmO2  do ?
  Try to think this way  and you see why we do certain zoning's.
  No cook book as you can see, as you have to take  all the   possible   bio markers into account.
DanieleM

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 #5 
Juerg, for the absolutes values, I was mainly referring to the differences between my first TIP and the last one. On the first I had general lower levels of SmO2, as a possible sign of weak delivery?

Regarding the trends, I would say that if tHB (delivery factor)  is increasing during a constant load, so same amount of oxygen needed, SmO2 (delivery-consumption) should increase as well.
If tHB is decreasing, SmO2 should decrease as well.

I am instead seeing something quite different:
First steps: tHB drops but SmO2 increases, in particular on the second step @140W and first step@180W.
Middle steps: more or less a balance
Last step: tHB increases but SmO2 stay stable.

Juerg Feldmann

Fortiori Design LLC
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 #6 
Dan yes  all is true.
 So the question is :
 What does  that mean, when I  see a situation, where we have an  increase in tHb  for example but a stable  SmO2   in connection with O2  use ?
  or any other combination, . Think  about the influence of  blood increase  or decrease  .
Than there is  one  small part we have to consider.
 .
 Is the in-flowing blood always   loaded  with the same  amount of O2.  Or what situation could  deliver  lover saturated blood  from the  heart to the muscle  or better from the  lungs to the muscles.
 If that would be the case  what   could have caused this  situation  and how  would that influence tHb  and SmO2 trends. ( than there  are  some medical problems  who could be  the reason as well but keep them out of the discussion.

 Last  add on:
 The change in absolute   SmO2 trends  like Daniele  has  seen  can have different reasons.
 Here the 2  most common.
 a)  very different placement of the  MOXY on the muscle.
 BUT.
 If you are relative  accurate  than there are  2 points  or thoughts to consider.

 1. SmO2 trend is an information or indication of  O2  delivery  and or  utilization.
 So depending what you did the Day before  and you  for example target  in the day before  to workout  your respiratory  system  and you did a good   workout, meaning you are  actually  worse  ( loosing for a while performance till the body adapted  and reacted  on your target stimulation )  you will have the next day a   not so optimal delivery.
 Now  if you   did  NOT overload the utilization  as well ,you will   try  the next  day  to push the same wattage. ( as  many at least cyclists  still believe  the same wattage is the same physiological load.) The result on the MOXY  will show you that this can be  but often is not the case.
 If you push the same wattage  so some  wattage  zone  than you may see a very different physiological reaction. The overload of the respiratory system  reduced  the delivery  and if you have the structure   in mitochondria    you may be able to compensate  a little bit with a better utilization. So you will see  today  by the same wattage a  much lower  absolute SmO2  reading.
 
 Now the opposite  could  be  created. You do a specific   overload of mitochondria density  and or vascularisation overload.  So you have a problem  with utilization  but not  with delivery. So you may try to compensate if possible with delivery   but you can't utilize  it ,so absolute SmO2  will be higher  than usual by the same  wattage .

 We use this information in   strength workouts  and or in team sport  workouts  by  using the " warm Up " the next day to see changes in SmO2 trend  by the same  load.
 So you do for example intense  squatting or plyometric  exercises  you will see  situation, where athlete  will in the " warm up " reach  much higher than usual SmO2  absolute values but than despite  an " all out "  workout " the  SmO2  will not drop at all. Very  poor  or  disrupted   utilization. Here an old picture  on why this may happened   under forced  workouts.
eccentric muscle dammage.jpg

DanieleM

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 #7 
Hi Juerg,
I thought about that and below some loud thinking:
First step 140#1 seems "normal" alarm-phase, slight increase in tHB and SmO2.
Second and third step 140#2 and 180#1 tHB has a decreasing trend while SmO2 is increasing.
Possible explanation:vasocostriction due to hypocapnia (tHB does not bounces back to baseline in the rest period) and O2 diss curve shift to left.

Last 2 hard loads @300W.
tip300w.png 
Here the upward trend of tHB and stable SmO2.
Let's see the possibility:
Vasodiladation due to increase CO and/or CO2 OR venous occlusion.
HR is increasing during the load (on the first load, it goes from 151 to 158, second load 152-161 during minute 1-5) so I can guess that CO is increasing (assuming SV stable but I don't have this value).
The stable SmO2 despite increase delivery makes me think that there is also a CO2 component and now a Diss Curve to the Right.
CO2 accumulation could be due to venous occlusion trend but also due to respiration limitation (bad loading of O2?) or O2 independent source.
At rest after first 300 load:
tHB overshoot, SmO2 just get back to previous resting value.
Could be CO2 due to respiration or use of O2 independent. How could I distinguish between them?
After second load, it looks like there is short outflow then tHB start to rise but slower than before.
SmO2 as well takes the entire minute to get back at "baseline" and this would confirm the high component of CO2 especially in the second load.
Here in combination to the above it could be a small component of venous occlusion.

Lots of speculations...feedback much appreciated.

Daniele



Andrew

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 #8 
Just thinking aloud also, based on the just the quick look at the picture in the previous post from Daniele...
I appreciate all the possible scenarios you give to explain the rising THb and stable SmO2, and have this question. Is it not possible that the slowly rising THb is a reflection of the slowly increasing cardiac output, which in turn is a result of the slowly rising HR? If this were the case, the stable SmO2 would be a reflection of the stable wattage, and the athlete reaching the point at which no further drop in SmO2 is possible, which is what triggers the rising cardiac output to compensate for the peripheral system reaching its limit. This explanation wouls also yield "overshoot" during the recovery phase, as the cardiac output would continue to be high for the duration of the one minute recovery period.

I look forward to further discussion to help me understand how we can determine which of the possibilities listed are actually occurring in this picture.
juergfeldmann

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 #9 
Teat thoughts.
Here where  we  can discuss some  options:

 Is it not possible that the slowly rising THb is a reflection of the slowly increasing cardiac output, which in turn is a result of the slowly rising HR? If this were the case, the stable SmO2 would be a reflection of the stable wattage, and the athlete reaching the point at which no further drop in SmO2 is possible, which is what triggers the rising cardiac output to compensate for the peripheral system reaching its limit.

1.The increase in tHb is as Andrew  points out  a  potential indication of  an increase in Cardiac out put ( CO = HR x SV) so here  , if we have HR we can look , whether this is more  due to SV  or due to  HR . If we see a  flat HR  during the load but an increase in tHb  than it could be  an increase in SV.
BUT as usual  it could be as well a  CO2  increase  duet to  hypercapnia  and  the  CO2  could trigger an increase in vasodilatation  and  an increase in tHB during the load.
 But if that would be the case  we would see SmO2  lower  due to the soccer case studies  explanation of  O2  diss shift. So SmO2 lower n the recovery but tHb  higher  in the recovery.

So the point of  increase in tHb  during load  could be a  sign of an increase in CO  to try to compensate  for the higher  O2  demand..
 2. Stable SmO2  and stable wattage. ? Could be,  but I would  more   go towards what we see which is   NOT a  stable  SmO2  as it is only the same %  of Hb loaded.
 SmO2  would be stable  , when tHb  is stable. a  stable SmO2  means that the % of loaded  Hb  is still the  same.
 So  IF: tHb  ( blood flow  or Volume  is stable  than the  flat SmO2  means  a  balanced delivery  and a balanced  utilization  of O2   or  as Andrew  points out a limitation for no further  utilization at that time. in this activity. Remember  you always can drop SmO2  down to very low  levels or 0. But in an activity  it just may be that the " discomfort for that muscle is so high  that you may  start to compensate  with another muscle. so you simply maintain this level.

Now let's go back.
 We  do NOT have a stable tHb in our  case. We have an increase in tHb  out of the  different reasons we discuss.
 So if we go with Andrews  suggestion ,  the tHb  is increasing due to an increase in CO  either over HR  and stable SV  or over  SV  and a stable HR  or  an increase in both, than we have  an increased  volume of blood  getting pushed out of the  heart into the lungs. Depending on the O2  Diss curve  we may load  perfect or less optimal ( CO2  high ).
 Never the  less the  higher  tHb indicates  more Hb . So if we load perfect   than a higher HB  would as well mean  more O2 . Example. 100 Hb  pieces  80 %  loaded  = a SmO2  of 80 %. Now to make it simple. We  use  for the  current activity 20  O2 pieces  so we unload  20  from the  80 once it is in the muscle  so SmO2  really  is now  60 %. That is  what we read.
 If  we have now a stable tHb  and we have a  flat  60 %  SmO2  than we  use all the load time the same amount of O2  and this could be  as well by the same performance.
But in our case we have an increase of tHb during the load. so we do not have 100 Hb like at the start  we may have 150 Hb  at the end  so  from start to end we increased  the Hb  from 100   to 150.
 By 100  we had   80 loaded  and used 20  for this load  so we  where left  with a  value  of  60.
Now  if we load in the lungs  the same  at the  beginning and  at the end  we  have  now 80 % loaded  of  150  which  would give us  120  loaded Hb  so much more O2  really , but it is the same %.
 So when we see  a " stable SmO2  of 60 %  now here at the end  as well we really  would have  90 Hb loaded as this would be 60 %  of the tHb. Hope it makes sense till here ?

 Now  at the start we used 20 pieces of O2    at the end we used 30 pieces  of O2  but the %  and SmO2 is a % of tHb is the same.
 So despite[.  a  flat  SmO2  but an increase in tHb  this athlete used  more O2  over the load  time  and really SmO2  would  drop but as it is a %  of tHb it does not drop . If you tilt the graph  and make tHb  flat  than  SmO2  would drop.
 So despite a flat SmO2   this athlete  still uses more than at the end   but he can compensate   with more delivery. Or in other words  he  maintains a flat  SmO2  despite that fact he uses  more . A  good example of a compensation  due to a higher deliver  which maintains the  SmO2 % level. but really  he uses  more  O2  as the time goes on  and it is a  question of how long the compensator  can deliver the O2  ( tHb )  up
Summary:
 I believe that we have to look in situations , where  we discuss O2 use  tHb  and SmO2  in combination. This is what makes me wonder in many research articles, where they use just O2Hb or HHb  and without  combination of tHb trends , whether the conclusions  they come up with  may have to look upon more critically.

 One of the discussion s well is , that in some NIRS equipment. the calculations  for SmO2  or other wording  we may use  is  based on the assumption, that  tHb is  always stable.
 This may  be true in specific situations but in field testing or sport  this  is not  always the case  due to factors  like CO  change  and body position change  and   respiration  and so on.



DanieleM

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 #10 
Juerg, the explanation about tHB rise and stable SmO2 makes absolutely sense.
The part I am struggling to understand is this:
Depending on the O2  Diss curve  we may load  perfect or less optimal ( CO2  high ).
My interpretation is that if we have high CO2 (respiratory limitation), would cause a dissociation curve to right and not optimal load of O2 from lungs to the blood.
 
So if I can summarize so far, my options are:
1. tHB increase due CO increase as compensator and trend towards more O2 consumption during the same load (same as slow component of VO2?). If this is the case who is the limiter?
2. tHB increase due to both CO and CO2 increase (could be more evident in the second load due to longer time for SmO2 to recover). If this is the case we will have more tHB but less O2 loaded and therefore O2 consumption probably flat during the load.
Respiratory as limiter?
3. How about the other option to have an increase in tHB due to high O2 independent?
The picture of last two same load overlapped:
load300overlap.png 
 
Finally any suggestions about the first part of the test?
My initial thoughts were:
First step 140#1 seems "normal" alarm-phase, slight increase in tHB and SmO2.
Second and third step 140#2 and 180#1 tHB has a decreasing trend while SmO2 is increasing.
Possible explanation:vasocostriction due to hypocapnia (tHB does not bounces back to baseline in the rest period) and O2 diss curve shift to left.





juergfeldmann

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 #11 
Daniele, Thnaks for great feedback as usual.
Lot's of great a  questions  and I  try to work my answers  step by step through  and  please comer back whne I am getting stuck. Start  first section

1. tHB increase due CO increase as compensator and trend towards more O2 consumption during the same load (same as slow component of VO2?). If this is the case who is the limiter?

tHb increases  as a possible compensator, so the question is as  formulated , what  creates the stimulation to increase  tHb  and as  such delivery of more blood  and  hopefully as well of more O2.

So if  I have to deliver more O2  as it  is a demand  for te load I perform  and I have the chance to deliver  like in our case  ( increase in CO ), than  the limitation  could be in the problem of  actually utilization  ( deoxygenation further down.)
let's see whether I can formulate this  in simple term but other readers  can jump in.

 Hb   can load in simple terms  4  O2  molecules. In a  "normal "situation we can release  easy one . T release more, there  needs to be some training done  but 2  seems to be  relative easy.  So there are 2 more left  on Hb. What we  do NOT know with NIRS really is  how mu8hc has to be  released  that we actually have a  clear feedback  due to the change  of  colour of a less loaded b piece.

ATTENTION
 pure speculation due  observation
 If  I manipulated  O2  disscurves  and see a change in SmkO2  than this could be a part of the trends we see.
 So  if  I have a situation, wheretehO2 disscurve is    normocapnic  I may release 1  or2  easy. If  I shift  more to the right I can release O2  easier  and   ( speculation)    more  than 1  easy.
 If I shift to the left  it is the opposite.
 So in our cse If  I  am normo capnic  and  I still  could  use O2  for utilization and I still have the capacity but I am stuck  with just releasing 1  or 2  per Hb than I  can  use more , when I  actually  deliver  more  so higher CO.
 To " proof " this theory  I  try in this cases  to simply  go hypercapnic  so  we see tHb not increasing  as  CO is not stimulated    so tHb flat but SmO2  dropping  as change in %. Hope it makes sense.

DanieleM

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 #12 
Juerg, I fear I am getting lost here...

You mentioned about the possibility that utilization could be the limiter (not able to further desaturates).

Does it mean that despites a very likely H+/CO2 increase (O2 independent making part of the job?) there is not much Diss Curve to right to allow a further desaturation?

Thanks

DanieleM

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 #13 
I would like to add another piece of the puzzle.
I performed a short 5/1 step (same wattage used in the double steps) but this time moxy was placed on the biceps so not involved muscle with very interesting results.
Below the graph:
tip_biceps.png 
What is evident is an almost full desaturation of the biceps in the last step.
The tHB trend at the last step: it drops in the first minutes and then sharp increase for the full rest of the load then drops again to base level at rest. 
My interpretation is that there is a strong vasocostriction on the arms and this coupled with some isometric tension has created an almost full venous occlusion and, as a consequence, a full desaturation.

Looking at the overall picture, this may possibly explain the sharp increase in tHB as a sign of systemic vasodilation. CG shuts down blood flow to the arms to direct it to the legs. 

As usual all the feedbacks are highly appreciated.




Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #14 
Hallo Daniele.
 First to the  question of `confusion `you had a above I missed. The answer is in r the discussion with Fred.
 You can have a utilization limitation    but you actually do not see a very far drop in SmO2. Summary again here.
 If you have  a limitation in capillarisation and mitochondria density than you can see a  very low SmO2  if the delivery is not keeping up with the O2  demand  and you simply utilize  very low  down. An extreme  example is  in your biceps   data. A    compression  out flow of the biceps  followed  by a   occlusion trend  and by an outflow. So your delivery  far missed the O2  need  so you started  to utilize  on what you had. On the other  side  if your  delivery is huge  but the utilization is limited  than you  will have a  `pooling `of  O2  there  but you can utilize it as there is only so much you  can turn over. Seen in beginner s  and in overloaded    top athletes.
  If this was a   bike test I  do not think biceps is an  non involved muscle   in high intensity . We prefer  the  delta pars  acromialis but even there in a very hard load  every thing  is  in activity. ( one of the reason of a  limited information when we  have systemic  feed backs  of performance like lactate   or VO2.. What we see in your biceps is most likely a combination of a  isometric muscle contraction   combined   with a perhaps systemic  vasoconstriction.
 This would be the case, if we really have a systemic limitation,.  In your next    workout  you do  fix a MOXY on the delta  pars  acromialis    no matter whether it is a  endurance  and or  interval workout  just in any workout  you do. Now  what you can see is , that when you push into a STEI    intensity  you  can  fix  the mOXY nearly anywhere or   if you like to  move in the STEI  as well.  . As  soon you see a drop in a  less  involved  system you know you either use this  body part as a compensator  for  maintaining performance  and or  your body tries s to avoid sending  O2 in the less important  sections. Remember the  energy or supply O2  pyramid  we showed  so often and it may make  more and more sense as we go along.
DanieleM

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Posts: 264
 #15 
Below a short workout with Moxy on the Delta.
Short warmup then fixed wattage (220W) except at approx time 600 to get off the bike and back again. Workout finished at time 2500.
deltapars.png 


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