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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Many  test  and mail's I am getting  are incredible great feed backs  on how to use  SmO2  trends  and information  for  training intensity control.
 I like  to start slowly here to add  the second  metric  we have with MOXY  the tHb into the discussion.
 I believe  that both SmO2    as well as tHb  can increase  immensely the feedback we get  from the working area , but as well from the total systemic  respond.
 tHb is a great  indicator  of blood flow (  volume  )    respectively Delivery.
 tHb  can change fast   and with fast I mean  fast  or immediately. This most often indicates  a immediate  direct  mechanical change in blood flow  ( volume ) on the tested  area.
  Possible mechanism  are  ( Gravity / direct compression  from outside.  Direct compression  due to  muscle contraction )  so mechanical reasons.
  Than we  can have  slower reactions in  connections  with feedback information  from the systemic    blood flow  or  circulation.
 This reactions are  clearly slower (lag)    and a reason of longer steps  needed to see this reactions ) but as well the systemic  reaction  are slower in the recovery  like a  vasodilatation due to  CO2  or a vasoconstriction due to CO2  or  a vasodilatation  due to  blood pressure corrections  or more often a vasoconstriction due to blood pressure correction.
 Last but not least   tHb changes  due to  shift of  blood volume  as well as  O2  to  more  important working  body areas ( muscles.)
  Here  to  just warm you up with some of the interesting  reactions we  can actually see, when integrating tHb into the full assessment picture.  
One pic is a local mechanical reason of tHb changes.  another  pic is a systemic blood pressure   reaction  and one is a systemic blood volume  shift. ???
mark workout thb smo2.jpg

field 1 nice occl.jpg

involved  and not nvolved.jpg

And here some  add on  to show  how  systemic reactions will be visualized if looking properly on tHb reactions.
Here a nice  example  and  sooner or later NIRS / MOXY will be used  to  look at this interesting trends  , as soon we start to look more  on tHb  and not just on oxygenation trends.
  At the end  delivery  ( tHb) is a big part of  oxygenation. No delivery no oxygenation.

J Physiol. 2012 Dec 15;590(Pt 24):6285-96. doi: 10.1113/jphysiol.2012.241190. Epub 2012 Oct 1.

Skeletal muscle vasodilatation during maximal exercise in health and disease.

Calbet JA1, Lundby C.

Author information

  • 1Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira, Las Palmas de Gran Canaria, 35017, Spain.


Maximal exercise vasodilatation results from the balance between vasoconstricting and vasodilating signals combined with the vascular reactivity to these signals. During maximal exercise with a small muscle mass the skeletal muscle vascular bed is fully vasodilated. During maximal whole body exercise, however, vasodilatation is restrained by the sympathetic system. This is necessary to avoid hypotension since the maximal vascular conductance of the musculature exceeds the maximal pumping capacity of the heart. Endurance training and high-intensity intermittent knee extension training increase the capacity for maximal exercise vasodilatation by 20-30%, mainly due to an enhanced vasodilatory capacity, as maximal exercise perfusion pressure changes little with training. The increase in maximal exercise vascular conductance is to a large extent explained by skeletal muscle hypertrophy and vascular remodelling. The vasodilatory capacity during maximal exercise is reduced or blunted with ageing, as well as in chronic heart failure patients and chronically hypoxic humans; reduced vasodilatory responsiveness and increased sympathetic activity (and probably, altered sympatholysis) are potential mechanisms accounting for this effect. Pharmacological counteraction of the sympathetic restraint may result in lower perfusion pressure and reduced oxygen extraction by the exercising muscles. However, at the same time fast inhibition of the chemoreflex in maximally exercising humans may result in increased vasodilatation, further confirming a restraining role of the sympathetic nervous system on exercise-induced vasodilatation. This is likely to be critical for the maintenance of blood pressure in exercising patients with a limited heart pump capacity.

and here  another  nice  information.

Acta Physiol (Oxf). 2010 Aug;199(4):393-406. doi: 10.1111/j.1748-1716.2010.02125.x. Epub 2010 Mar 25.


Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?


Calbet JA1, Joyner MJ.


Author information


  • 1Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira s/n, Las Palmas de Gran Canaria, Spain.




In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [approximately 300 mL (100 g)(-1) min(-1)], but the pumping capacity of the human heart is limited to 20-25 L min(-1) in untrained subjects and approximately 35 L min(-1) in elite endurance athletes. This means that when more than 7-10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when approximately 80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Great   question:
I got a great question  from Slovenia.
  Can we use this  idea of tHb  practically  and  do you have  an example   for  swimming.
  I like to show you a  swim workout  done  by Dominique a  top  coach in Montreal  with  some world class swimmer.
  I  do not like to discuss the result on here , as  this is  a  part   we do  with the coaches.
 I like to show  you here simply the  workout and the very different  reaction  and as you will see SmO2  gives only  a feedback on the utilization reaction of O2  but tHb  actually will tell you why we see this specific  utilization trend  and what was  limiting  further  changes or    the actual workout. Here the SmO2  workout  picture    followed by  the tHb workout picture  and than the PP  with an example on how we look at the information closer  with coaches  and test centers  to  make  individual adjustment  and understanding the effect the training  may have had  on the athlete, or whether the feedback was expected  from the training  I set  up .

Smo2  3  sets all.jpg 
thb all 3 bl.jpg

Attached Files
pptx Dom_A_3_sets.pptx (1.12 MB, 104 views)

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

Time will tell.
 The question I discuss  in an email exchange is the ability to use THb  as a trend information of changes in vascularisation.
 My answer.

 I  do not know.
  Time will tell. I have a group of clients, where  I try to see, whether this is possible.
 The idea is to see,whether the THb is increasing  
a) more  after 3  and 6 month of specific  " vascular "  intensity workouts. ( if it  is really a vascular stimulation) compared  form the start by the same load.
 Problem is, that many other factors will change the behavior of THb. 
 Here  for example some of them :
  Respiration  , muscular strength and therefor % of contraction force by the same load, even flexibility  on a bike  and so on.
 The reason of this idea  is based on a very nice  article  I showed long time ago once here already.
 Here again the interesting  read.

Vascular adaptation in athletes: is there an ‘athlete’s




Daniel J. Green1,2, Angela Spence2, Nicola Rowley1, Dick H. J. Thijssen2,3 and Louise H. Naylor2


1Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK


2School of Sport Science, Exercise and Health, The University of Western Australia, Australia


3Department of Physiology, Radboud University Nijmegen Medical Centre, The Netherlands




Whilst the existence of a specific phenotype characterized as ‘athlete’s heart’ is generally acknowledged, the question of whether athletes exhibit characteristic vascular adaptations has not been specifically addressed. To do so in this symposium, studies which have assessed the size, wall thickness and function of elastic, large muscular and smaller resistance arteries in athletes


have been reviewed. Notwithstanding the caveats pertaining to cross-sectional comparisons between athletes and ‘matched’ control subjects, these studies reveal increased conduit artery size, including enlargement of epicardial arteries and those supplying skeletal muscle. Evidence that peak limb blood flow responses are enhanced in athletes further suggests that resistance


arteries undergo increases in total cross-sectional area. Such increases can be localized to those arteries supplying active muscle leading to speculation, supported by exercise training studies in humans and animal and cellular data, that arterial enlargement is associated with repetitive episodic increases in arterial shear stress which elicit endothelium-mediated remodelling. Such


structural remodelling at conduit and resistance artery level may play a role in accommodating the substantial increase in cardiac output apparent in endurance athletes; arterial pressure is not increased at rest or during exercise in athletes (versus control subjects). Arterial wall remodelling also occurs in athletes but, in contrast to the impact of shear stress on remodelling


of arterial lumenal dimensions, the impact of endurance athletic status on wall thickness may be a systemic, rather than localized, phenomenon. Finally, the question of whether the arteries of athletes exhibit enhanced function is moot. Somewhat paradoxically, measures of conduit and resistance artery endothelial function may not be enhanced, compared with healthy control


subjects. Thismay relate to the inherent difficulty of improving arterial functionwhich is already normal, or the time course and transient nature of functional change. It may also relate to the


impact of compensatory structural remodelling, as arterial lumen size and wall thickness both affect functional responsiveness. In summary, there is clear evidence for an impact of athletic status on arterial structure and function, at leastwith respect to the impact of endurance training.


Arterial adaptationmay, to some extent, emulate that evident in the hearts of endurance athletes, and it is tempting to speculate that similar mechanisms may be at play.


(Received 18 October 2011; accepted after revision 13 December 2011; first published online 16 December 2011)


Corresponding author D. J. Green: School of Sports Science, Exercise and Health, The University ofWestern Australia,


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now going back to the great data collection  from Dominique.
 Here  some  directions  for regular  user of MOXY  and some thoughts.
  Each of this  different blocks  had a very  specific  stimulation on the system.
 True , there  are all swim related workouts but each had a very different physiological outcome.
 You can see this much better, when looking at THb than when looking at SmO2.
 The loads   are all in the range , that SmO2   most likley never reached a critical low level  to create  a hypoxia stimulation.
  There where just different reason why we had this  3 different reactions in SmO2. More  interesting is the very different reaction   when looking at the delivery system  and as  such  at the THb  trend.
 #  completely different out comes  with   the first  set a very different reaction in the recovery phase  compared to the other  2 sets  and the last 2 sets  a direct opposite  reaction with one decreasing the  delivery ability  in the rest phase  and the other  reducing  delivery during the load phase.
  if we look at this three options we  can make some very interesting planning.
  Here a suggestion how we do this.
  1. Assess the athlete  in a race situation.
 2. Look  how  the body reacts  in SmO2  and THB.
 This gives you a direct information, whether we  have a delivery problem  and whether the delivery problem is  based on  respiratory  limitation or on muscular limitation or in very  rare  cases   based on the cardiac system.
 In any case the race information will show the limitation as it is  an all out  case.
 Than we know  form this three  sets, what we can stimulate  and now you can go back  and instead of doing all three sets you may focus on the set, which most likley  will reduce the limitation we found during the race.
 Here  an overview  with some  additional  directions on where you can go

3 blocks thb smo2.jpg  .

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here  from the same  great  source  ( Dominique )  and another great example how MOXY  can give us feedback .
 This is a  swim set  with 12  reps in the same set.
 First the overall information.
D K dfirst set all.jpg 
Even if you are a new starter  you can easy see, where the delivery  of  O2  tHb  ( brown ) is going  in a very different way  than at the start.
  See the last 3   loads. Now  if you look at this situation closer it looks like this :

D K  frist set close.jpg 
Now you can see, that  thnaks to teh " intervall" interruption of teh kload  we  get a lot  of  feedbacks.
  So in a test, where we  simply  add step by step load  we never ever get the feedback whether   we  create a delivery problem  and  or an  outflow problem.
 This here is a great example of an  ???????
If you look closer  in the overall  info  of the 12  reps  you can see the change coming in the way tHb  reacts  what can you see   ?

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now here just  for fun a comparsion  of the 2  swim athelets  in tHb  and SmO2  behaviour over the full workout inclsuing warm up.

a and K  smo2 poly.jpg

a and K thb poly.jpg 


Development Team Member
Posts: 264
Hi Juerg,

I am loooking at one of the last pictures ( the set of 12 swim repetitions) and very interested since as I recreational cyclist I often perform this kind of workout.
That is quite tricky.
If I look at only tHB I would say that this guy is recovering (tHB increases) but from SmO2 there is still a load applied.
My only explanation is that he is not able to strongly contract the muscles so the load is low but the dissociation curve is shifting to right causing the SmO2 to still drop.
...but I am not fully convinced..

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
D K dfirst set all.jpg 
DanieleM, thanks for your input   in the forum. We need more of this  here , which would free many hours, where I  now use to give feedback on emails I get. So  first of all thanks , for this input

 I hope we  talk about the same Moxy traces I  show here again as this is one of the 12 sets  we  got  courtesy  of Dominique  from a  great swim club in Quebec
 If this is the set in questions  than I assume you talk about the tHb ( brown trace) at the end  so lets  say the last 7 loads ????

here the pic  to get it better ??
D K  frist set close.jpg

If I look at only tHB I would say that this guy is recovering (tHB increases) but from SmO2 there is still a load applied.

I hope this is what you mean. The  drop in tHb  and after the T 3300 the THB  is  much higher ??? First
First of all you make a super interesting point :

My only explanation is that he is not able to strongly contract the muscles so the load is low but the dissociation curve is shifting to right causing the SmO2 to still drop.

Here  some  add on to this  interesting option:
 1. A high CO2   can in fact create a  nice  drop in SmO2  due  to your suggestion of a shift of the O2 diss curve to the right. We use this fact  often in our seminars   to demonstrate  how we can  change  O2 bio availability by doing nothing , and with nothing we mean holding your breath and SmO2  will start to drop. The    reaction a high CO2 can create is as well interesting for " lactate " believers.
 If you  ride  at   what some call MAX LASS  and you  start to create some hyper capnic  reaction ( breath slower and deeper ) than you will create a  drop in SmO2  as you release more  O2  and  for a  certain amount of time your lactate which may be somewhere  perhaps around 3.6  +-  what ever will in fact start to drop   despite a drop in SmO2. On the other side  you go  and breath hypocapnic  your  MAX Lass value  will increase  despite the fact that SmO2 is increasing.

This is one very simple test to show  that lactate trend  and MOXY  real live info simply  do not mix  and any attempt  to use a lactate idea  and   force  NIRS into the old classical system is   just an attempt  to    hang on some interesting  but outdated  ideas, which now  can be replaced  with new information's we  can gather   with new  technology.

2.  Than to your   thought. Indeed  an  increase in CO2 has  a  vasodilatation effect  and the increase in tHb  could be in fact a  sign of a vasodilatation due to an increase in CO2.  

3. now you can see, when looking at SmO2  trends,( dotted line  below  in black ) that  this athlete  desaturates    every time pretty much the same  amount
This   seems to be the current ability  to use  O2  and than she is getting a utilization limitation  and can't  for the moment or  at least  with this workout  desaturate  further down in the tested  muscle group.
 There are different reasons  and there  are different training ideas, where you can change that. In this case the coach knows now , that there is  quite some improvement left  in that area  . Any other  assessment idea  ( VO2 max  LT  At  FTP ) never would show this information.
 Can it be  improved ?

 Here an example from   TOP NHL  player   courtesy  of Brian Kozak ( Next level coaching )   changes of  desaturation ability over a  certain time   and training period.
MR  smo2 compar  legs.jpg

So back to your  question
  and an even closer look at the   area  of discussion. You can see that  before T 3300 the  SmO2 Trace as well as the tHb trace  drop   simultaneous
where as  after T 3000 SmO2 trace  drops  but tHb trace is more or less immediately increasing.

 First of all . If we believe in the  idea below.

How  come, if we believe  NIRS is actually doing what  NIRS  claims to do, that we see in any activity  of short intense  duration a  drop in SmO2  as  an indication of a  intends involvement of  O2  in the  initial muscle activity.
 How  come  that  athletes  who can desaturate SmO2    much further can sustain an all out performance  much longer ? Is there any science  paper, who proof the above graph?. Any reader please show  it on here.
 BUT there  are some very great studies  done, who  would completely disagree with the above graph   like the ATP stores  dropping as it is  learned  and thought in school.
 Here a  very short  one  out of Connett et all. 

   atp crp.jpg 

In simple terms. ATP  may not be allowed  to drop below a critical level ( Rigor  would occur). PCr. is    reloaded  or  restored over  what substances ?  and last but not least  why is the full O2  Disscurve looking like  below and  what happens  with O2 stored in the muscle ( Myoglobin ? )

 So back  to the point but all has some merits  to it.
 Before the t3300  you can see a  drop in tHb  and SmO2  as  an indication of  immediate   utilization of O2  and this with a muscle compression  or performance, which creates a  tHb  ( blood ) outflow due to compression of the blood vessels..
 Now  after T 3300  we have the same utilization of O2  indicating a similar energy demand   or  at least similar O2  utilization ability but this time the  muscle performance contraction  in this  stroke  workout  creates  a much higher muscle contraction , in fact  withe exception of the first load, where we see a very short out flow  followed by an increase in tHb we have every load a   strength involvement  above  for sure  35 %  of maximal strength and as  such we  create a  out flow problem  due to compression of the venous  blood vessels. In  other words  the load  or  compression of the muscles  is creatingvenous occlusion  and as  such we have the same amount of  blood inflow over the arterial system  but we have a reduced  outflow flow over the venous system and blood starts  to pool in the tested area.
 In some sports  like rock climbing or motocross or strength workouts  the athlete would describe it as muscle pump  feeling.
 So the  potential idea, that we have a similar  O2  utilization but a much smaller  muscle load  would argue, that with less muscle activity we would have less CO2  production  and therefor  unlikely a  vasodiltation.
 BUT  we  can artificially produce this by holding breath  and or there would be theoretically  another option, where  we use  similar amount of  O2 but  less  muscle contraction force.  ( Cardiac  limitation with a  reduction in motor unit recruitment.
 This would end  up with a much   slower performance in the  workout but as we can see  as it is in a pool same  end time as  they all swim 25 or 50    meter. .
 Summary . The  higher  tHb in this case is a  indication of a much higher   muscle contraction force creating a  venous occlusion  and as  such  an increase in tHb.
 You can see  before T33000  as the SmO2  increases  so does tHb  as a sign of reduction of muscle tension at rest  and decompression  inflow  to  base  value.
 In the section   after T 3300  you can see  as SmO2 increases    tHb  drops as a  sign of relaxation of muscle tension as before  but now a venous  occlusion outflow back down  to base line.
Hope  this makes sense.  . Juerg


Development Team Member
Posts: 264
Many thanks for this great analysis.
First of all, yes I was referring to the workout you analyzed (in particular from T3300).

If I understood correctly, the athlete put the same "power" as in previous loads, but now the contractions is creating a venous return issue causing tHB to rise instead of falling.
I can see that from that point is completely out of phase compared to SmO2.

What are the consequences of this? Will the athlete be forced to stop after few extra loads? And last,if I can ask, what kind of training would be appropriate to improve this "weakness"?

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
uuups just  see, that my respond never showed up n here so will have to re  write it  today. Sorry. Juerg
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay  let's see, whether I can give you a  decent answer here :

 If I understood correctly, the athlete put the same "power" as in previous loads, but now the contractions is creating a venous return issue causing tHB to rise instead of falling.

a) we are not sure, whether this athlete put the same "power" into this  repetitions. Remember, it is a swim workout  so we  would have  time as a comparison.
 Now  we are not that interested yet into the time but it is helpful as well. You can see a little  or no time difference but  in this length of  an interval we would have to look accurately  at the performance.
 The fundamental difference in how we use  physiological feed backs to current ideas is, that we  look   on what we see live or in swimming short after.
 so here what we  would do  in this case.
1. SmO2  drops  similar and recovers  similar.
 So what ever was done   in this   swim  workout created a similar  O2 utilization ability for this muscle.
2. The  blood flow    ( or volume ) in the tested area  clearly changes  at the T 3300 point  from  a  compression reaction tHb    drops due to muscle contraction in this working muscle compared  to the exercise    the swimmer did  after  T 3300 , where the same muscle  created a higher muscle contraction which was  so much stronger, that  we  see an outflow  problem ( venous occlusion trend) which means  same or  more blood moves into the   working area , but less  moves out  so we  have this pooling  and as  such  an outflow  ( drop  of tHb )  as soon the load is over..
 Question " is this good or bad.
 Non of them can be answered  for a workout.
 For a race.   it is not optimal , as we  get rid of a  part of the balance of the H+ buffer ability due to outflow restriction.

Here an example  of 2  athletes doing the same planned workout of a  aerobic lacticid   workout.
 Classical trained coaches like  me  would have learned , that this is  anaerobic  alacticid.
  So the workout  was a endurance workout  for a  hockey player. Duration of the workout was planned for 45 min. The  workout was the same for both 15 skate imitation jumps  uphill followed by  an individual rest period till SmO2  (  re oxygenation reached  the same level.
 This means the rest time  was  for sure different for recovery , but the load idea  was the same  with 15  explosive jumps.
 the workout results  will show  you what went wrong with the athlete  who was not able to sustain the 45 min at all versus the athlete, who had no problem  at all.. The result of this workout  than was used to  not only individualize the   recovery time but as well the load time.
    first  you see the overall view  of both athletes.

total B  thb  smo2  workout.jpg 

  The above athlete  completed  the workout  from  Davos    1600 ma.s  to 2300 m a 45 min +- without any problem .It was a great  aerobic lacticid  workout. We  do not care about the lacticid  too much with some exceptions, when we plan to   stimulate  either MCT 1  or MCT 4 proteins.

Now the pic below is the second athlete , who  did not finished the task  and we ill show you what the difference was. This will give you the answer to your question
Will the athlete be forced to stop after few extra loads

S total  thb  smo2  workout.jpg    Look at the red  circle  and it is a similar situation as  with the swimmer.
 Now here a closer  look  at both  and we  simply take one  single load  ( 15  jumps  and recovery to base line SmO2

Athlete, where the  training was  what was planned a  aerob    ice hockey workout ( endurance is the ability to recover  fast in this sport. )

single  one  load B  thb  smo2  workout.jpg  You see the full load  of  15  jumps  and  SmO2  drops due to aerobic involvement ( opens the question of the   validity of the old classical idea of   energy   use. 



So the  workout  from this athlete  shows  a steady   use of O2  even immediately at the start  of  , what some would have called  anaerobic  alacticid  load.
 We see a steady drop in tHb  due to the  steady  increase in muscle contraction as a sign of  increasing  of  motor units  ( SEMG  would go up )  but not  hard enough to create a  venous outflow problem.
 So we have a  non interrupted  inflow  a ( some what reduced  )  and a non interrupted out flow to maintain a H + balance with all buffer abilities  we have including respiration.

 Now here the other athlete one  single load   closer view.
S  1 load  explanation  thb  smo2  workout.jpg 
 You can see  that this athlete  needed  much more time for 15  jumps  and  you can see  after  an initial  nice  aerobic involvement we have a short  " hesitation " to utilize  more  O2   but than  the body improved the utilization ( bio availability )  and    more O2  could be    used  for  ongoing  exercise. Than we reach a   less   SmO2  drop which goes to together with a tHb plateau. So   red  area   muscle compression but than    start of a venous occlusion  up to a  short arterial occlusion, short  outflow  at the end of the test  with  an immediate increase in tHb but a  not  optimal   reloading of SmO2. So energy storage  was    slow  and  very long  wait  to be able to go again.
 The tHb   overshoot is a  indication of a hypercapnic  situation at the end of the load  and the  Hyper capnic situation was a reason of a  O2  diss curve  shift to the right and  a  better O2 utilization. But the H +  balance  was gone ( metabolic plus respiratory  acidosis  and the feedback  stopped  the body  from    further workouts..
 So  in this case. the same workout had  two very different stimulus.  If the plan was an endurance  workout  hockey specific  than  the  first athlete had a good workout, the second athlete had a very different  outcome.
 To offer the second  athlete the same   stimuli  he would have workout  out in the  red zone  so only 20 + seconds  an he would have done the same .
 This i what happens    in all clubs  and team workouts.  20 athletes  and possible    even they do the same optical workout  4  - 6 different outcomes,So completely    out of control and what is good for one may be not optimal  in that stage  for another one.

 There for     we have to use  an assessment ideas like this , practical workout  to adjust  the workout  or  work on the limitation  which caused  in athlete 2 a very different outcome. Summary   in a  workout  nothing is bad    we just have to know what we  did  so we understand the responses.
 In a race or game  athlete 2  can not be  as long on the ice in a shift than athlete  1. So in the swim example. Yes the   after T 3300 load  had  some time limitation or performance drop. If that was planned great , if this happens in a race  bad.
 So   work for the coach  is  to avoid this in a race but may use it in a workout.
 . The  race has to be  as much efficient as possible , the workout can be as  much inefficient  as possible  for may   times.

what kind of training would be appropriate to improve this "weakness"?
If thi happens like in this case in a workout the veneous occlusion is not a weakness but the exercise    to produce this  trend is a strength of a thinking coach  if  he   knows that he produces this.
Now it can be used  to get rid of the problem in the race.
 If  he does not recognize this    trend , than the workout is  out of control  and the problem may be aggravated in a race.
 If we  see this in a a race, than we e  can go  and work on this to   reduce the risk of a venous occlusion in the race by  different means  to improve this situation..   MOXY is  NOT a  tool to find a   magical   mysterious  point  and we name it    like  XY  Max   or  zt  threshold.
 What   MOXY is a is a reality show  live  to see, what limits    performance  and who tries  to compensate. To find this you  go  and do a sport specific assessment. A  ICE hockey player  is on the ice  and a swimmer in the water.
 Or in other words, how many cyclist would  pay  for a VO2  max test on an Skate mill???
. After the assessment as you can see  in this cases. we  can get a lot of  information  and therefor can apply the  information in an individual guided     workout  sport specific  or  in a general workout  needed  for this sport.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
I got some nice     and very great feedback on the last post.
 Here very short  what the common    discussion was:
 1. Why    or how would I use tHb  for training planning.
A : Depending on your  assessment  for your sport you may actually use  tHb  for  some very interesting options.
If  for example you find a cardiac limitation like CO  over  a low SV or you  plan  to do some vascularisation you will use tHb to control the proper intensity  during the load  but as well after the load the  reaction.
. Depending on the   ideas  you  use as a coach   you therefor  can  control the training intensity  instead of based on wattage or HR  " zoning" on actual live physiological feedback,  where on one day  you may use  much more load  to create the same   tHb reaction than you may   produce  on  another day with less load.
 This makes a  zoning really obsolete  as  MOXY is the zoning  as we   check live what we do. Why would I calculate a zoning , than base it on a HR  or wattage level  after I did a LT  an than believe  it will work every day, when I now  can have a  live feedback  and see , whether I ma in the planned zoning or not.

Development Team Member
Posts: 54
Below is some screen shots from a recent biathlon test race on roller skis, it was a undulating course. Moxy mount was on the legs. After the start there is the initial alarm response then the tHB response is upward, after each lap the tHB seems to increase even more. Each lap was around 09min. I do not always see this upward tHB response. But it is easier to see in longer interval type workouts.

So here my question, am I right when I say that the general upward trend in tHB is most likely due to an increase in SV be it through plasma volume or actual stoke volume? SmO2 does not really change lap to lap. So utilisation is simply where it is, SmO2 is able to recover during the short downhills and during the shooting bouts. 
Oct test race moxy.jpg  Here a screen shot similar time period with Heart rate and top and SmO2 blue bottom.Oct test race HR.jpg 

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Marcel great work here what I need to get somewhat closer  to  some   ideas. Can you sent me the csv file you download  from MOXY    so I can move it in our interpretation software.
  As ell if you have your HR    downloaded  and you can move it on an excel  format  that would help so I can move it in as well.
 Will be back after I  look through your   points.

Development Team Member
Posts: 54
Juerg, attached the csv files 

Attached Files
csv 31-10-2014_17-13-51.csv (69.93 KB, 52 views)
csv 31_oct_14_race.csv (44.73 KB, 50 views)

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