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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
A  very common question this days'
 I often  ask  first back  why not.
 Here  some answers
  It  takes too long  for an assessment. ???
 Well not really a  physiological  argumentation  that's  for sure  but  for sure a  good business question  or  answer.  We  actually  not have a  5min   step length , we have a  10 min step length.
  I will show   in some  follow up why.
 Here   to start out.
a) time lag  for a  complex  system  to react  in a  1 - 3 min  step length.
  The main delivery systems  the  respiratory  as well as the cardiac system    need a  certain amount of time  to get  all the possible   actions  in place  to have an optimal most efficient  and effective  ability  to    deliver  the energy  and in our case  O2.
 Lets' look at   fast  the cardiac  option  to improve   on the one side  delivery  for the     working muscles  but as well to    create a  save    O2  supply  for the    heart it self.
  Functional  reaction in alarm phase is    HR .increase.
   . Most often  HR  first, as we  do not have  yet an optimal blood return   from the periphery  to    have a  good preload. Once we have the  blood shift  towards  work  and extremity muscles  the    preload  will improve  and HR  can   even drop  by the same load  as  now Stroke volume is increasing..
 The  activation over  a better preload    increases  SV    and with it often EF %  ( ejection fraction ).
. Depending on  Blood pressure reaction  we have  as well  a  follow  up over  vascular reactions  the SVR  ( systemic  vascular resistance )  to  maintain   and create  an optimal  BP.
  An increase in  O2  demand  over time  will as well change the  ejection time  in the heart  so that the heart itself  is getting less blood per minute  but a  healthy heart  is able to desaturate  the blood  much much better than the desaturation   of the blood in the extremity.
  What we see  in many tests is, that trained  athletes  with a relative  small SV  have a  much  longer LVET  and therefor  if we  multiply LVET  with HR  a  much longer CCT  ( cardiac  contraction time.
 This seems an additional ability of the heart muscle to try  to compensate  for a   relative  small SV.

 All this  adjustments  take some time.  Equally to the respiration  where we have RF  and TV  and   location of respiration.
 . When we look  hundreds  of test  closer  we  could see, that a critical time   is around 3 min.  so  if  we give it another  few minutes we will see  not just the trend of possible adjustment , but  whether the adjustment  actually was successful  or  had  to readjust.
 I show you randomly here some pics  form 5  and 4 min loads    in different  ideas  and  form different people  and you   can look carefully  at the time units  and decide   optically  first where yous see a  clear change  and than look  at the time.. Plus  some  real    writings  form  accepted   sources on how long a  step   should at least be.
 Last but not least in   good  vasulcar trained  people  we  need time  do not  just increase  blood flow in  the  big vessels but as well to recruit    some    not always   open blood vessels.  and this  needs as well time.
 In MOXY we see that  in the change in tHb  as a sign of  better vascularisation structur  compared  with  other  people.  Now here we have a problem  as a discussion thsi week  with a leadng NIRS  expert  and  Univeristy profeesor     showed  us, that our thinking is very very different.
  The   "educated"  person    tells us, that tHb  is  always  stable  , meaning that the blood flow  and the total hemoglobin  under the    MOXY or any NIRS will never change???
 We     see it very very different. We  see thatthis is true , if we ,have a proper   arterial occlusion. Than  we have a stable tHb.
 In any other case  we  can have a  stable  blood volume  but in a step test  we  will have depending on intensity  an  increase  of tHb  a  stable section and depending on what  influences   the blood vessels, a  drop in tHb ( Blood volume.)
 If  the educate   idea is  true, how come , that when we    make an occlusion and we  do it  too slow ,we see an increase in tHb as a sign of a  veneous occlusion  showing and proof  enough that tHb  can actually change.
  What is true is , that many NIRS  equipment  base their readings on a  stable tHb assumption   and that's  why we have  different open questions with some of the " research " graded  NIRs  equipment. See pic of a  verneous occlusion  and change of  tHb. See  a great article   from a NIRS producer    on that issue.
( we did not made  a friend  in that discussion.( Smile)  And here  some exampels  to think through on the time needed  and time lag  for step test  for  endurance information.   Can  vasular  situation change. See here short. This is one of the reasons why 6  or  8 week HIIT studies  who change  enzyme activity in the mitochondria   are  a functional reaction, but we need a structural adaptation to maintain the    reactions and   performance.

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. This may relate to the inherent difficulty of improving arterial function which 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 least with respect to the impact of endurance training.

Arterial adaptation may, 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,

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
And here just for  fun  for the educated   person  an accepted  study   on  evidence  on change in blood flow  and volume  and  why we use tHb  in combination with SmO2  as a great way  to read  interesting trends  out  during a 5/1/5  assessment.

Evidence for restricted muscle blood flow during speed skating.

Foster C, Rundell KW, Snyder AC, Stray-Gundersen J, Kemkers G, Thometz N, Broker J, Knapp E.


University of Wisconsin-LaCrosse, 54601, USA.



We have previously hypothesized restricted muscle blood flow during speed skating, secondary to the high intramuscular forces intrinsic to the unique posture assumed by speed skaters and to the prolonged duty cycle of the skating stroke.


To test this hypothesis, we studied speed skaters (N = 10) during submaximal and maximal cycling and in-line skating, in both low (knee angle = 107 degrees) and high (knee angle = 112 degrees) skating positions (CE vs SkL vs SkH). Supportive experiments evaluated muscle desaturation and lactate accumulation during on-ice speed skating and muscle desaturation during static exercise at different joint positions.


Consistent with the hypothesis were reductions during skating in VO2peak (4.28 vs 3.83 vs 4.26 L x min(-1)), the VO2 at 4 mmol x L(-1) blood lactate (3.38 vs 1.93 vs 3.31 L x min(-1)), and cardiac output during maximal exercise (33.2 vs 25.3 vs 25.6 L x min(-1)). The reduction in maximal cardiac output was not attributable to differences in HRmax (197 vs 192 vs 193 b x min(-1)) but to a reduction in SVmax (172 vs 135 vs 134 mL x beat(-1)). The reduction in SV appeared to be related to an increased calculated systemic vascular resistance (354 vs 483 vs 453 dynes x s(-1) x cm(-1)). During maximal skating there was also a greater % O2 desaturation of the vastus lateralis based on near infrared spectrophotometry (50.3 vs 74.9 vs 60.4% of maximal desaturation during cuff ischemia). The results were supported by greater desaturation with smaller knee angles during static exercise and by greater desaturation and accelerated blood lactate accumulation during on-ice speed skating in the low vs high position. The results of this study support the hypothesis that physiological responses during speed skating are dominated by restriction of blood flow, attributable either to high intramuscular forces, the long duty cycle of the skating stroke, or both.



[PubMed - indexed for MEDLINE]



Development Team Member
Posts: 49
Hi Juerg,

I understand the setup of the 5/1/5 test quite well, thanks in large part to your posts, but with regards to the other assessment you've developed, the IPHAR, I just wanted to clarify a few things. In looking at the example you posted that you did with Xeno Mueller, I see that you place the athlete under a load and their SmO2 level drops significantly. Subsequently you remove the load and allow the SmO2 level to recover and stabilize and the place the athlete under the load again.

Has the athlete done a warmup before this? Or like the 5/1/5 assessment is it started from a state of rest? I understand in the 5/1/5 assessment we're trying to see all the reactions happening in the body, but doing hard intervals without warmup is pretty uncomfortable. In addition, I know that without a warmup the numbers that would be produced in an interval type workout would differ significantly. This leads to my second set of questions which is how is the initial load chosen? Can it be picked as an educated guess? Does it just have to be hard? Or would I use the information from a previous 5/1/5 assessment to set the load to the High Intensity zone i'd identified there? 

Once the SmO2 level ceases to drop how long do I have to keep the athlete working to ensure that the load doesn't continue to drop later on? The information you've posted here for the 5/1/5 assessment talks about how we need time to see whats going on in the body. My understanding of the IPAHR is that we're looking at the time it takes the body to recover from the decrease in SmO2, but in doing 5/1/5 assessments I've seen tremendous variation in the lowest SmO2 level that athletes can achieve. You've talked in other posts about how SmO2 is not an absolute value, which makes sense, but I'm struggling a bit with how to properly perform an IPAHR then. In the 5/1/5 assessment we simply slowly increase the load and watch the reactions, but the IPAHR doesn't have those steps. My assumption is that we set the load off the High Intensity zone we identify in the 5/1/5 assessment, as I can't see using a fixed SmO2 number due to the day to day variation one sees with it.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Wowww  great great  question. No fast answer, because  I have no fast good  direct answer.  Need  help  in that one.
 I will  come back hopefully today and like to explain , what is the ideas  and thought s behind  the  difference between  IPAHD  and the IPAHR as we named  it  and how IPAHR  has to be adjusted   even more to the sport specific   demands  than  IPAHD.
 The  questions  NKrause  raised   are exactly questions we  turn  through our heads  since   10 years and NIRS. Every time we  do a different sport    in a slightly different way  we  get more questions  so we  have now  some  relative simple ideas  and need  help  form the specialists  in the different sports.
 In the past  all was easy. You had  an ice hockey player, a tennis player, a  soccer player  a  cyclists a  swimmer  and what ever.
 You made  either  a  VO2  max test  and trough all the results into the same idea  VO2  max/kg   body weight  for endurance , took you calculator   and gave  zones  for any thing , from   endurance to      high intensity  all based on  max  VO2   or max HR  or  220 - age  or FTP wattage.
  simple no question straight forward  and even any research  is or was based on this.
  Than you had a Wingate  and the same  idea  simple straight forward.
 Now we  have MOXY  and  many  questions show  up  when looking to the "classical'  versions.
  Now we can go sport specific   but we  can  get better  even in that.
 The  key  words  in the explanations I will try to give is :
  O2  deficit . delivery situation ,  what is the   stimulation goal.  So please give me some time  to get a decent smart  answer  to a  super great   c critical question.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Okay  here some  closer thoughts  on the above    feedback.
 We  have  2 main  protocols.
  a)    to find intensities  , where we  can control physiological reactions  to improve  structure.
( Blood vessels  density, mitochondria  volumina  and  "numbers"  and    possibly myoglobine,  Bone density , tendon density,  muscular hypertrophy,  Costo vertebral  function, )
b)  to find  intensities where we  can improve  function  of the existing structure.
  Most discussed  one is the  enzyme reaction  in mitochondrial  function. . Discussion between HIT  and  LSD.
  , where all the  studies on HIT  have a length of  1  week  to  6   weeks.
  How fast do we  create a  solid  structure in    many of the physiological systems  and tissue ???

 The 5/1/5  is  a assessment to see  reactions  and  changes over time ( but as usual  as well some will change in a short term as a functional reaction.)
  Than we look at a n assessment, where we look on functional reactions  first but as well   we will see structural changes  over time.

 The " warm up " is included in the 5/1/5  so we   have always   a  feedback how the body reacts  all the time.
 We basically use the  warm up as a  calibration  for the physiological systems.
  Now  shall I warm up in the   high intensity assessment.
  It all depends  on what we like to assess.
  If  I  do NOT warm up  I am  sure I  start  more  or less   at the same baseline  and  have a very low CO  and a very low VE . That means  in an all out start  I  have to  get the energy  form the storage  area  rather than  fro the delivery   system.
 This will allow  me  to assess over time, whether  I.
  increase  storage area
 b)  improve  the ability to dig deeper into may  existing  storage.
c)  how deep    does  my body allow  to get into the safety storage  before It will push me into a hypoxic    situation.
  Here 3 pics  who  will demonstrate you the  situation.
 To   get your head into that  idea  you may have  to  accept the fact , that there is no O2  deficit  at  all at a start of a load.
  Deficit  means  you have  less than  what  is  zero.
  You have nothing on the bank but you go  ans pent  100 $   now you are in a deficit.
  You have 200 $  on the bank and you spend  100 $  you are NOT in a deficit  you just have less in storage.
 The physi9ological bank  does NOT allow you to go into a deficit  otherwise  you get a rigor  mortise  and it is over.  You are never  during a  physiological assessment  anaerobe.
 You just will spent as much as your body allows  you  to dig into your storage.
  Some  train and can  go deeper  but even top athletes  will be stopped  to avoid  an O2 deficit.
 I will show later    pictures  and test  where we  can show this.
  So  if I am interested in my " account"  and how far I  can go down  you do not like to warm up.
  If you just like to see  how  the Business  works  under stress  and when you may go  back into the storage  you  have to warm up.
 Warming up means  you add to the existing storage  some additional   O2  (  dollars )  and or  you   now  spent  first  100 $   than you business starts  to work  and you   bring more in than you use  so  your account  storage increases  or you are just stable  or  you may still   need  some help from the storage.. In the 5/1/5  that is what we look for.
 In the short   high intensity  we  have  just one  load  ( all out)  and look  whether we     and how we dig into the storage  or if we warm up  how far  do we dig into the storage  with the  problem, that I am not sure  how much  is  delivered   and how much is  from the storage.
. We will go much deeper into this options as we progress over the next  few  month. This just a guide  for  people trying stuff out.
  Short  steps in any assessment  you do  have the risk of using storage  but never   give enough time  to see, whether the delivery  will not just deliver  on what you need  but " over deliver" on what you not need  yet  so you  can increase  storage.
.  .
 Now in a short HIT assessment you  have  some additional challenges.
   The challenge is the  different safety  pins  your  body  has to  safe  your   systems.
  We know already that in the 5/1/5  we look for limiter  and compensator.
 In the short  assessments  we  have mainly the risk  for  "killing" peripheral  structures.  ( Pushing the ATP level into a  dangerous  low  level.
 We know   from Connett et all, that the body rather tries  to  avoid using  further ATP  , than trying to create limitless ATP  when in danger.
  So  there has to be a safety    system   doing exactly that. Avoiding  further splitting of ATP into ADP  and P.
 Different ideas floating around  since  many years.
One  very popular is the  reduction  of  recruitment of motor units   so less motor units  less ability  to drop  ATP further.  Protection of the  cardiac  systems.
 The question is, whether  when I do a biceps  curl   that this drop in local ATP  is enough trigger   to  get the brain worried  about the  one single muscle.
 That's where  the   proponents  of  Peripheral  governor  and the Central governor  clash.
 Perhaps both  have great points  and we  can combine them.
  So  peripherally there  are ideas, that  Ca++ may be one of the limiter  so  more or less Ca++ release   and more  or less ATP splitting.
 Mg  may be another   factor  same    reaction.
 P +  may be another one   but where now  more in problems  to  rebuild  ADP  to ATP  than avoiding  splitting ATP.
  H + is one  who shows  up again.
  Not as a  sever  change in pH  but as a   disruptor  of Ca++  and Mg --  coupling  so  it takes  the spot  from Ca++  and avoids  a further ;splitting.
  If we  can get rid  of the H +  we   can  split longer  . How do we get rid  of it.  Key words.  lactate.  MCT 4  CO2 )
  For any acyclic  sport we therefor  can use the same  idea  but adjust the duration of the assessment accordingly to the real sport situation.
So what we do is : we asses the athlete in his real sport  and than  look at his   trends  and  design the  assessment accordingly  to the reality of the load in his specific  sport.
 Here   2 example  from an on ice  game  ( first period ) assessment.      2 very different   players, one  super fit  the other one a great player.
 You can see the first period  and the  rest  between first and second period.
  You can see how often they  had a  shift  and you can see over time, what  caused  the limitation  and how their  body was digging in  during the shift  to  maintain performance.
  So here  what we  add  just  for fun and you can see    how very different the reaction during load    and recovery.
  The assessment show  exactly this  physiological behavior  so we  can use  the assessment and  are able  to  tell the coaches  what  and where they have to focus   either during  the summer to improve  or  during the  season    not  to loose.

Summary > the  short assessment to design   interval workout  for   high intnsity  ideas     can be done   depending on your   goal  and what you like to assess.

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Development Team Member
Posts: 49
Thanks for the response Juerg, that clarifies a bunch of things! So if I understand correctly the 5/1/5 assessment is to track and identify the structural changes necessary in an athlete to help them improve. So this could be things like a weak heart, poor diaphragm strength, capillary density etc. Either way the changes I'm tracking in the athlete with this assessment should be longer term, I won't see improvement over a day or two, big changes will likely take months or years.

The IPAHR helps identify a functional constraint that we might need to improve to help an athlete get ready for race season or a specific competition, and its structure is determined by what function we're trying to improve in the athlete. I suppose this would tie in quite strongly with a lot of the questions you've received about sport specific protocols.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
N. Krause,
Well I have to admit , that when I read  your  great and clear  formulation in English  it make s  even more sense  for me.  Great  simple   and short  summary.
 As usual there  are overlapping situations  but  to make it simple  and clear  , that is a  big part of it.
  I like to show you a very  practical example here.
 Problem   in an athlete  is  deoxygenation.  The picture in the  5/1/  is a great  watt performance   a  great  cardiac hemodynamic ,  a great respiratory improvement    but still problem  with deoxygenation.
  So we ruled  out  the  hyper    hypocapnic  situation . He  could try  somewhat  more hypercpanic   breathing but too difficult under  all out  stress.
 So we are   left  with 2 common  additional helpers  moving the O2  Diss curve to the   right. Temperature   and  2.3 BPG hormone.
  Att 1   a little bit  better  explanation on   the 2.3 BPG hormone. As you can see   : Hypoxia   would improve  the  level   of 2.3 BPG.
  Now  we have  to find out, whether a  certain interval  really creates  a  hypoxia  and if or whether it is   just a hard  interval with optimal deoxygenation  or whether it is a   slightly local  hypoxia  or whether I  can create  the needed general body hypoxia  to    stimulate the  hormone. As this is a functional reaction  it is a preparation for a  race  or an important  event.
  So what we did  we    where  using MOXY  to create a general  hypoxia . To do this  we used  2 MOxy's  to  test locally  and than  general  to see, whether  we  could  produce  a  deoxygenation effect  in the working muscles  and finally in a  not  at the activity involved  muscle as a sign of a  desperate   search  for O2.
  See the three levels  of   workout   to  create deoxygenation   than   local hypoxia  and than  general hypoxia.
  After 4  workouts  spread apart  accordingly  to some hormonal research groups we improved the  deoxygenation  from a  low 55  SmO2  level to a possible  30 SmO2 level  an increasing the ability  to short term  hang on in a  specific  race   to  perfect.  see att.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
And here a replay to the 2  hockey player  live feedback info  from a real game.
  Why do we  see, what limits  each of this players  ability on the ice.
 Well 2  things.
 I believe  before we  make a  lab test  it would  make more sense  to actually see, how an athletes  body reacts  during a race.
 This than will help us to see, what limits  his    ability or hwy is he  better than the other.
 In the past we  had no tools  to do this as  the equipment  where not  feasible.   There would be a major  problem to talk an athlete in an ice hockey game  to wear a portable VO2  max  equipment  (??  , Taking lactate is  worthless to find out   the limitation. Using a HR  either.
 BUT  we  have now  MOXY , cheap  and  perfect  and   the athletes  not  even are aware of it.
  So we  have this 2 athletes  see  where they  limit the performance an than  go back  and use this information to set up the    short intensity testing accordingly to the sport   in reality and the 5/1/5  to  add  the  endurance intensity info to the needed interval  training  with individual    load  and recovery  intervals  instead of 5   fingers    5  set   1 min rest  and so on.
  Now we see  changes improvement  and  retest  during the game.
  So here an inside  look on what we do.
 Like  any great  researcher  we share the information on here  as we need feedback  and critics  to try to improve.   Here  the 2 players  you    think  which one belongs  to what overall game picture. So based on this pictures  we know  whether we  can improve   the athlete in a short term  or whether we  have to maintain his  performance  for the season  ( retest  and see ,when  we  fry the athlete  and when he  needs a rest  and than work on the structure  the  off season or whether it is a functional  limitation and we  can improve this  to a certain extend  for this  current season.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
More to step length.
 We  argued, that we see,that the design of your VO2  max test or LT  test  or  Max Lass test or  maximal Hr test of  FTP test directly influence  you  " tested " maximal result.
That would mean,depending on our believes , in any  test  idea , the  training intensities  and zones depend  much more on the type of protocol you choose , instead on the actual physiological response  your body may give you or you plan to achieve.
 So the question is :
 What is the goal of an assessment ?
 Is it to find a tested maximal  and than base the  zones  on a mathematical  formula, or  do we like to  actually learn , where  and  how  physiological systems may  be limited or  may  start to compensate.?
So when we  discuss step length, we always  try to keep in mind, what we  look for. We never look for a maximal watt level or  any maximal  physical information. We always look for physiological reactions.
Now over the next few month we will discuss this further, as  many  new  MOXY users  will learn very fast, that the drop in SmO2 ( Level) depends  a lot on the design of the test you choose.  The same happens  when you look at  lactate  values or VO2  max results.
 For us, it is important to understand,  why SmO2  drops   or not drops, as we look on the  question:
 Do we have a delivery problem of energy ( specific of O2 ) or  do we  have a utilization problem of  O2.
 Depending on the answer, the training intensities and zones will be different as  we may  plan a structural improvement  or a functional  adjustment. Than we like to see, how we  can  specifically target  one  physiological system  and  give another physiological system a break.

 Example  : Working on the respiratory system as well as on the  adjustment  to  control  acidosis  ( H + )  without stressing for example the muscular system. So metabolic acidosis versus  respiratory acidosis.  For me, this is an important part,  as I have clients, they can't afford  to get the cardiac system stressed  after certain operations,  or they can't  get the  muscular system stress  and so on. So the goal is to maintain all other systems  , without stressing the injured  one.
 In sport the same  , but here you may give  an overloaded system  a  day or  2 of a break ( recovery )  to improve  , but you may not like to  rest  the other systems.
 The pic shows  you a  case study, where we  where looking , whether we  can create a  muscular  interval workout  , without  any cardiac  nor respiratory reactions  without  actually running or biking. So we  designed a specific  equipment  used  Portamon  and where looking , whether we  can  create a physiological stimulation of oxygenation and deoxygenation  similar or equal to an actual active workout. See  pic

Now  back top the start.  Many new  MOXY user  using  the ideas of 5/1/5  will have very unhappy  clients:
 Why.? because their  wattage level may be  far off  from what they where able to push  in a 3 min step test.
 Or : Their VO2  max  will be very different  in a 5/1/5  than in a 3 min step test  or even a  classical VO2 max test protocol.
  Meaning : Step length and design  will create a  result,  but is it a result, which  can be used  for   training intensity zones , or is it just a result , which looks  good  on a zoning sheet.
 If  there is something like a VO2  max  than  why  do we have this  discrepancy when we  have different  step length protocols.
 And   why is 3 min  better than 1  min or 5 min ???
 Perhaps there is only a peak VO2 value  at a common day  for a specific activity  in a very specific  test  design.
  Now to use this values  as a general  help for training intensities  ????
 Perhaps  for training , we  rather need a feedback ,as we work out, who tells  us NOW , whether we  train  in an intensity , where we may have a delivery problem  and I like to address this,  or we have a utilization problem  and I work on this  weakness. Or  whether I like  to  work   mainly "aerob"  or like to add a  certain " hypoxic "  stimulation  to it.

Can you imagine  doing this with intensity zones  based on a  %  of  a  maximal tested  end result  ???
  Or using a  wattage meter ???  or a  HR monitor  ?
 But YES , you can get this  live  feedback  by using a MOXY  and, if  combined  with wattage  and Hr you can even  see  the changes  which may have already occurred  or occur  as you work out.

 I know , whether I  use the respiration  now  as a compensator  or  I  do not stress it , or  I may have reached  its  limitation , but no  help yet  from another compensator.  Lot's  to think  about.
 Last  questions  to yesterdays  challenge.
   If you have a MOXY  and a lactate Pro.  Make a  10 - 15  second all out  load  test  with MOXY  and  lactate.
  Than  repeat  30  seconds  and so on.
 Look when you may see  lactate  increasing  and where you may see  lower SmO2  values  and  whether you reach a  flat SmO2  curve.
  Now  think:
 As long SmO2  drops , what  do you  use    to create ATP  besides   the " anaerobic"  energy  supplier ?
  If  you  not see lactate increasing , does that means  you do   NOT create lactate ?

 If you can get rid of H+  ( How  and with what  help? )    why can you go longer , high intensity.?
If  we block the removal of H +   why do we have to stop earlier?
 Why  is lactate increasing , when I get rid  of H + ?
 Here a pic  where we  artificially  blocked the ability  to easy remove H +.See  result in simple squatting numbers.
 Red is a one leg  deep  squatting  10 repetitions  to  subjective  failure.
  Followed  by a rest  and than same leg , same idea , 35  deep leg squatting  till subjective  failure.
  Red   was  with  manipulation  for    H +    so that  he could not  get rid  of  H +.  Interesting is:
 If  we  allow the release  H + , than we  see a much higher  lactate value ,  compared  with  red. where we see  nearly  no lactate in the system.

Summary :
Longer step length allow  us  to see easier  physiological limitation of different systems  and  Limiter and  compensator  are  easier to  identified.
 Short  step length allow  easier a  functional  information on how the body  can  in a  fast way react  functionally  to " survive"
So  when we  look the old  "fight :" between  HIIT  and LSD  workouts , we  have  the answer.
   HIIT  will show a  functional   reaction  on how  to fast  and  in a short term allow  more O2  extraction  so SmO2  can drop , to survive.
  LSD  will allow a structural change, so better vasuclarisation, bigger SV  ,  bigger TV  and so on due to structural changes. 
Here a  simple PP  to show you , what  or how we look at  functional and structural    reactions.  It is a summary  form a set of different ideas   sparked originally  by the G.A.S   principle    by Hans Selye  and his stress research.

Attached Images
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Study Participant
Posts: 45
Juerg, in the fourth attached pictur from your first post in this section, can you explain how they achieved an increase in tHb, without affecting oxyhemoglobin or deoxyhemoglobin levels? In the case of rising total hemoglobin, I would have expected either a balanced increase in both, or a preferential increase in one or the other depending upon the intervention that led to the increase in tHb in the first place.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530

Thanks for the question,
This is one, many new users with MOXY struggle at the beginning.
I like to show the picture in question again below. And here the question and the answer to it.

can you explain how they achieved an increase in tHb, without affecting oxyhemoglobin or deoxyhemoglobin levels?"

The answer is in the question itself :

"I would have expected either a balanced increase in both, or a preferential increase in one or the other depending upon the intervention that led to the increase in tHb in the first place. "

tHb (is a trend information on blood volume ) but NOT an  information in actual volume in ml or L is the result of :

O2Hb ( oxygenated Hemoglobin ) plus HHb ( deoxygenated Hemoglobin)

So always O2Hb + HHB = tHb

So the increased trend you see in this pic of tHb is the result of either both O2Hb and HHb increase together, or one is increasing more than the other, but in total you still will have more tHb.
The reason you think it is not what is, is due to the scaling of the O2H and HHb in comparison with the tHb scaling.
As you can see the O2Hb  and HHb axis is on the left side in a scale of a jump of 1 unit per line.
The tHb due to the way it is calculated and adjusted is on a scale 0.1 per unit.

 So  if   we look at the change in tHb  in units of  0.1    and than compare  to the   scale  of the left side , you have 0.1 unit  = 6.5  units    or in   more   straight numbers  1 unit tHb  equals  65 units  on the  left side. So you simply  can't see the   small change in units  due to the scaling    we  choose    in this particular  case study  to look at tHb trend  information.
  This is one reason  why we  only show tHb  and SmO2  in the MOXY   information  and just some  research groups  actually look at O2Hb  and HHb  due to some ongoing  development of  ideas  and  some ongoing data collection to see, whether  we  can  read  out some information easier    when showing   O2Hb  HHb  versus  tHb only.
  As  soon you combine tHb  and SmO2    you will over time  see the picture  of O2 Hb  and HHb   evolving when you  make interpretations  of   MOXY  assessment information.
 If we would post the  actual raw  data's  you could see  this  change easy  . So  when looking at trend  always keep in mind that the numbers  have as such no  absolute values  ( exception SmO2  % )  but  as such  even SmO2  %  does not  give you   information , whether you have more or less O2 . it just tells you whether  you  increase  , decrease or  have  a stable  %  of  O2  compared to the tHb.
  It is similar like in SpO2 .  A  90%  SpO2  means that 90 % of the available Hb  is loaded  with  O2.  It does not tell you, whether this athlete  has in fact enough O2  for what he likes  to do , he could be  severely anemic  despite a  90 %  load.
  Or in simple   stupid  numbers.
  He can have 10 Hb  and 9  are loaded  so 90 %  SpO2   . So he has  9  which  will move O2.
  He  could have  100 Hb  and 90  are loaded so 90 %  are loaded but in fact he  has  81  more Hb  who deliver O2 . or   extreme, he could have  100 and 80 % loaded  so it looks " worse" than the  10   / 9  situation but in fact  for O2  delivery it is better  as he  delivers 71  loaded Hb  more  to where he may  need O2.
. When looking at trend  you  always have to keep this in mind.  A  drop  alone  by  SmO2  does not immediately mean he  runs into trouble . He may drop to a lower  %  but may have    a  higher tHb  and as such still functions  better than with a high SmO2  and a  drop in  tHb.
 This will show  ,once  people get familiar  with ,how much more  MOXY offers us  compared  to VO2  and any other existing  data collection. What makes it somewhat  more difficult, but as well interesting, is exactly the fact, that  once  you add physiological  ideas  into the equations  you can see so much more than many  people think . True,  using a calculator  and using  %  is faster, easier  , but is  it physiologically individually  usable.
 All    MOXY users  will get  from us  all the support  they need as  we  surely  believe in a  few  month or years down the road , it changes the   ideas we work with our self  and or athletes.

 It explains so much better and more , why  we have this individual reactions we see  and why " cook books'  work in beginners, as doing something , anything , will show  always results,   than doing nothing, the question  is, when we   start to stop improving , that's when the individual approach  will have to come in.



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