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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
An ongoing discussion now again is, whether  we replace VO2  with MOXY.
We add a value added  product  top your existing experience and hep that it will exactly do that: Add value to an already great coach or test center.
The key is to  open up to the new opportunities, rather than trying to force  NIRS information into our "classical" school and education models.
 Try to avoid the task to see, whether you can "proof" that your  classical ideas of LT and ANT and AT and VT  and slow VO2 component and all the ideas we created over time to try   to cosmetically create answers to questions, which we can't or could explain, when we based it on the  old classical ideas of VO2 max and so on.
 Try simply to use all your experiences and see, whether  areas and situations, where we tweaked the answer  so nobody could understand the answer but it sounded at least very intelligent  no can give a better and more logical and easier to understand  the answer.
 Here   a very interesting and nicely written article, which exactly  targets our problem with the classical model.
 One of the reason is  the  lag time  of the reactions  and one of the lag time reasons is the way we  where able to test in the past.
 Again the idea of being  on an ice hockey game versus reading the game report the next day at home.
 Lactate testing on your finger is a very indirect information  with a lot's of questions, what may have happened in between the lactate production the the working muscle  and the  finger tip test area.  The same is true with VO2  testing  at the mouth  and what may have happened  in between the   active muscle  area and the  and of the vascular and air piping system before we test it  at the mouth.
 MOXY  now  will give a   live info and one of the fascinating  next steps you will experience is that interesting lag time between what you will see  live   from the working area and what you may test at the same time in blood values and VO2  reactions and than the shift in MOXY data's   into the opposite direction as  you may see in lactate and  VO2  due to the lag time.
 I hope you understand what I mean, and why , if we are ready to open up and combine  this new ideas, we may have in some situations review our old idea.
 The whole question of using a performance intensity as the tool to  define workout intensities  has lot's of flaws and risks. Using a fixed wattage  an delivering , that it is physiologically always the same load because it is an objective absolute value  is a great  simple tool   to make computer programs and sell them but  if we look more critically we all have to agree, that we have to combine   this performance with bio markers , if we like to understand  and  if we like to know , why certain workouts  show progress  and some times do not show progress.
 With MOXY you have a d daily live info  and recalibration of your  energy supply ability.
 This means for all new users, there is NOT and absolute % of SmO2  you  work over weeks but a daily re adjustment and you can do that now  with using the different combinations.
 Now here a link to a great article and when you combine T.D. Noakes critical view , the above  open discussion  and this article you are a huge step forward  to be a MOXY expert soon.
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Got a great response I lie to share.
 Think again what MOXY NIRS is doing and how it may just be a nice addition to the discussion of the slow VO2  component.
Med Sci Sports Exerc. 2011 Nov;43(11):2046-62. doi: 10.1249/MSS.0b013e31821fcfc1.

Slow component of VO2 kinetics: mechanistic bases and practical applications.


Sport and Health Sciences, College of Life and Environmental Sciences, St. Luke's Campus, University of Exeter, Exeter, United Kingdom.


The V·O₂ slow component, a slowly developing increase in V·O₂ during constant-work-rate exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V·O₂ slow component and describes practical interventions that can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate exercise, the development of the V·O₂ slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a "mirror-image" V·O₂ slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V·O₂ slow component, although the greater fatigue sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several interventions can reduce the magnitude of the V·O₂ slow component, and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability or by enhancing bulk muscle O2 delivery or local Q·O₂-to-V·O₂ matching. Future honing of these interventions to maximize their impact on the V·O₂ slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.

 "These include endurance training, inspiratory muscle training"

VO2 = CO X (a-v) O2 diff

Remember the many discussions  we had over the years.
 First the problem with CO  = HR x SV. Now with  the physioflow as a standard  integrated part of our  assessments this questions for the coaches are answered.
  So than we got stuck on (a-v) O2 difference.
 Well where doe this takes place. YES  exactly under the MOXY and under your eyes as you workout. NO delay.  with MOXY
 What can change the ability to load and or release O2.
 YESSSS think about the O2 Diss curve  see repetition in the pic below.
. Now what can we " manipulate"  or enhance  from the factores, we see in the pic.
  What system is the one, who decides, where we can help  to maintain pH  and H +  and CO2 levels  in our body on a relative  homeostatic level.
 Well   for all new MOXY users   and old Spiro Tiger users. here a simple idea.
 Use a SpO2 sensor a Spiro Tiger and a MOXY and load   with a simple movement like squatting and see, what is going on  as you start to run your system  out of homeostasis.
 Have fun  and try to understand, why we think somewhat different when looking at  classcial ideas and wattage or performance alone.

Now  when we start looking at more and more MOXY workouts  try to follow this idea of the direct information and the delayed and therefor sometimes not optimal information of lactate  and VO2   information.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
They are so right :
Eur J Appl Physiol Occup Physiol. 1998 Apr;77(5):445-51.

Oxygen uptake does not increase linearly at high power outputs during incremental exercise test in humans.


Department of Physiology and Biochemistry, AWF-Krakow, Cracow, Poland.


A group of 12 healthy non-smoking men [mean age 22.3 (SD 1.1) years], performed an incremental exercise test. The test started at 30 W, followed by increases in power output (P) of 30 W every 3 min, until exhaustion. Blood samples were taken from an antecubital vein for determination of plasma concentration lactate [La-]pl and acid-base balance variables. Below the lactate threshold (LT) defined in this study as the highest P above which a sustained increase in [La-]pl was observed (at least 0.5 mmol x l[-1] within 3 min), the pulmonary oxygen uptake (VO2) measured breath-by-breath, showed a linear relationship with P. However, at P above LT [in this study 135 (SD 30) W] there was an additional accumulating increase in VO2 above that expected from the increase in P alone. The magnitude of this effect was illustrated by the difference in the final P observed at maximal oxygen uptake (VO2max) during the incremental exercise test (Pmax,obs at VO2max) and the expected power output at VO2max(Pmax,exp at VO2max) predicted from the linear VO2-P relationship derived from the data collected below LT. The Pmax,obs at VO2max amounting to 270 (SD 19) W was 65.1 (SD 35) W (19%) lower (P < 0.01) than the Pmax,exp at VO2max. The mean value of VO2max reached at Pmax,obs amounted to 3555 (SD 226) ml x min(-1) which was 572 (SD 269) ml x min(-1) higher (P < 0.01) than the VO2 expected at this P, calculated from the linear relationship between VO2 and P derived from the data collected below LT. This fall in locomotory efficiency expressed by the additional increase in VO2, amounting to 572 (SD 269) ml O2 x min(-1), was accompanied by a significant increase in [La-]pl amounting to 7.04 (SD 2.2) mmol x l(-1), a significant increase in blood hydrogen ion concentration ([H+]b) to 7.4 (SD 3) nmol x l(-1) and a significant fall in blood bicarbonate concentration to 5.78 (SD 1.7) mmol x l(-1), in relation to the values measured at the P of the LT. We also correlated the individual values of the additional VO2 with the increases (delta) in variables [La-]pl and delta[H+]b. The delta values for [La-]pl and delta[H+]b were expressed as the differences between values reached at the Pmax,obs at VO2max and the values at LT. No significant correlations between the additional VO2 and delta[La-]pl on [H+]b were found. In conclusion, when performing an incremental exercise test, exceeding P corresponding to LT was accompanied by a significant additional increase in VO2 above that expected from the linear relationship between VO2 and P occurring at lower P. However, the magnitude of the additional increase in VO2 did not correlate with the magnitude of the increases in [La-]pl and [H+]b reached in the final stages of the incremental test.

Oxygen uptake does not increase linearly at high power outputs during incremental exercise test in humans.

Well they are so right,  but  do we need that  complex assessment to find that out. How about we look at  where O2 is used and what can happen  at the end of an incremental test with the  O2 use. Is SmO2 dropping so VO2  will go faster up or is SmO2 leveling out so VO2  increases less intense.
  Here some pictures instead of words. You  look and you give it some thoughts.  Look how the SmO2 trend is  in this 2 exampels at the end of the step test.. What do you expect  may show up in the VO2 trend ?

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Some may remember my  short intro in the option to be able to see VO2  use from the different system, when you combine  our "IPAHD" with  VO2.
 Here a pic  of an IPAHD. Your   task.
 How  would the VO2  trend  curve look like.
 Than the question:
 Does   SmO2  recovery will look the same as VO2  recovery.
 Here a study  who   looks at this.
 Now you combine the fact , that as we  show SmO2  recovers   the same  and VO2   not    so you have a difference between a resting muscle  but a still active  cardiac and respiratory system   and than you load  and have a lag of respiration and cardiac  respond  but you see the SmO2  drop due to delivery problems.
 The  advanced MOXY users  can now see, whey we have  developed a 5/1/5   idea  and what  we can see   besides the trend in SmO2    during load  but as well the trend in Smo2  in  the deloading  situation as well as the VO2  if taken at the same time.

Reproducibility and sensitivity of muscle reoxygenation and oxygen uptake recovery kinetics following running exercise in the field.


Laboratory of Exercise Physiology and Rehabilitation, EA 3300, Faculty of Sport Sciences, University of Picardie, Amiens, France.


The purpose of this study was to assess the reliability of postexercise near-infrared spectroscopy (NIRS)-derived measurements and their sensitivity to different exercise intensities in the field. Seventeen athletes (24·1 ± 5·6 year) repeated, on three occasions, two 2-min submaximal shuttle-runs at 40% and 60% of V(IFT) (final speed of the 30-15 intermittent fitness test) and a 50-m shuttle-run sprint (Sprint), with (OCC) or without (CON) repeated transient arterial occlusions of the medial gastrocnemius during the postexercise period. NIRS variables (i.e. oxyhaemoglobin [HbO(2)], deoxyhaemoglobin [HHb] and their difference [Hb(diff)]) were measured continuously for 3 min after each exercise. Half-recovery (½Rec) and mean response (MRT; monoexponential curve fitting) times of muscle reoxygenation and muscle oxygen uptake (mVO(2)) recovery were calculated. Reliability was assessed using the typical error of measurement, expressed as a coefficient of variation (CV). Postexercise recovery of muscle reoxygenation revealed CVs ranging from 16·8% to 37·3%; CV for mVO(2) recovery ranged from 6·2% to 20·9%, with no substantial differences shown between NIRS variables and exercise intensities. While running, intensity did not affect MRT or ½Rec for muscle reoxygenation, and differences were found for mVO(2) recovery (e.g. [Hb(diff)]-mVO(2) MRT = 28·7 ± 5·2, 34·2 ± 5·1 and 37·3 ± 6·2 s for 40%, 60% and Sprint, respectively, P<0·01). To conclude, the kinetics of postexercise NIRS measurements showed CV values ranging from 6% to 37%, with no substantial differences between exercise intensities or NIRS-derived variables. However, exercise intensity did influence mVO(2) recovery kinetics, but not that of muscle reoxygenation in an occlusion-free condition.

© 2011 The Authors. Clinical Physiology and Functional Imaging © 2011 Scandinavian Society of Clinical Physiology and Nuclear Medicine.

[PubMed - indexed for MEDLINE]

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