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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
I like to separate this topics for critical readers.
 Here again the pdf  by T.D. Noakes.
 If  and just IF his ideas are even close to  a possible better   idea than the current classical thinking , than we  may have to look back and re- think what all the thousand's of master work and PH. D   papers have to be looked at. Alone this idea  makes it understandable that we not just  simply can accept this possible  scenario.
 Nevertheless future and current MOXY users  may have an advantage if keeping an open mind, when suing MOXY an not just try to force the result in the existing " logic" of our past education.
 Here a very interesting  argument done  by using  NIRS.
 

Effects of incremental exercise on cerebral oxygenation measured by near-infrared spectroscopy: a systematic review.

Source

Department of Kinesiology, University of Georgia, 330 River Road, Athens, GA 30602-6554, United States.

Abstract

We conducted a systematic review and meta-regression analysis to quantify effects of exercise on brain hemodynamics measured by near-infrared spectroscopy (NIRS). The results indicate that acute incremental exercise (categorized relative to aerobic capacity (VO(2)peak) as low - <30% VO(2)peak; moderate - ≥30% VO(2)peak to <60% VO(2)peak; hard - ≥60% VO(2)peak to <VO(2)peak; and very hard - ≥VO(2)peak intensities) performed by 291 healthy people in 21 studies is accompanied by moderate-to-large increases (mean effect, dz±95% CI) in the prefrontal cortex of oxygenated hemoglobin (O(2)Hb) or other measures of oxygen level (O(2)Hbdiff) or saturation (SCO(2)) (0.92±0.67, 1.17), deoxygenated hemoglobin (dHb) (0.87±0.56, 1.19), and blood volume estimated by total hemoglobin (tHb) (1.21±0.84, 1.59). After peaking at hard intensities, cerebral oxygen levels dropped during very hard intensities. People who were aerobically trained attained higher levels of cortical oxygen, dHb, and tHb than untrained people during very hard intensities. Among untrained people, a marked drop in oxygen levels and a small increase in dHb at very hard intensities accompanied declines in tHb, implying reduced blood flow. In 6 studies of 222 patients with heart or lung conditions, oxygenation and dHb were lowered or unchanged during exercise compared to baseline. In conclusion, prefrontal oxygenation measured with NIRS in healthy people showed a quadratic response to incremental exercise, rising between moderate and hard intensities, then falling at very hard intensities. Training status influenced the responses. While methodological improvements in measures of brain oxygen are forthcoming, these results extend the evidence relevant to existing models of central limitations to maximal exercise


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
In the Noakes paper is a very interesting section and it may need a few times reading to follow it up critically and with an open mind .
 Here a very short part of it :
 "

Richardson et al have concluded that: ‘‘…intracellular pO2 remains constant during graded incremental exercise in

humans (50–100% of muscle VO2max)’’ so that: ‘‘With respect to the concept of the ‘‘anaerobic’’ threshold, these data

demonstrate that, during incremental exercise, skeletal muscle cells do not become anaerobic as lactate levels

suddenly rise, as intracellular pO2 is well preserved at a constant level, even at maximal exercise’’ (p. 63168). They also

conclude that: ‘‘Net blood lactate efflux was unrelated to intracellular pO2 across the range of incremental exercise to

exhaustion’’ but was ‘‘linearly related to O2 consumption’’ (p. 62768). Another study confirmed these conclusions: ‘‘…consequently these data again demonstrate that, as assessed by cytosolic oxygenation state (deoxy-Mb) during incremental

exercise, skeletal muscle cells do not become ‘‘anaerobic’’ as lactate levels rise, because intracellular PO2 is well preserved

at a low but constant level even at maximal exercise’’

 This would create an interesting discussion between what we thought is teh gospel to what we may have to learn to discuss as a possible alternative.
 Here what I mean where we  all struggle as we have to try to justify why we do what we do .

  " Moxy Monitor@MoxyMonitor

#HIIT - Integrating Anaerobic and Aerobic Systems for Peak #Performance -

3 Ways to Increase Your Lactate Threshold - http://hub.am/16eMDQM


A New #Metric to Determine Lactate Threshold: The Muscle #Oxygen Monitor -

Certainly teh last Metric to find  lactate threshold is something I have some usereses with.
Why do we force a great new opportunity in a theory or system, which we started about 10 - 15 years ago to look upon more critically. So for all   new and daily growing numbers of MOXY theres. Try to maintain an pen mind when collecting the informations  and try not to force belietheas into our existing differentf lactate threshold and VO2 max but simply start  by observing teh differetn  conclusionns and trends before jumping to a ableely theclsuion manipulated by what we had to be examto repeat to pass teh  exame.
  ( Smile ) Have fun to give this some critical thoughts

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Some ask us how complicated MOXY is to use.
 Here an alternative  for you  in case you really like to get  confused.
 :
 

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance.

Source

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

Abstract

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (VO2) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1 (SD 1.4) years, body mass 73.6 (SD 7.4) kg, height 179.4 (SD 7.5) cm, maximal oxygen uptake (VO2max) 3.726 (SD 0.363) l x min(-1)], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70 rev x min(-1). The test started at a power output of 30 W, followed by increases amounting to 30 W every 3 min. At 5 min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1 ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]pl, partial pressure of O2 and CO2 and hydrogen ion concentration [H+]b. The lactate threshold (LT) in this study was defined as the highest power output above which [La-]pl showed a sustained increase of more than 0.5 mmol x l(-1) x step(-1). The VO2 was measured breath-by-breath. In the analysis of the change point (CP) of VO2 during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: Xi = at(i) + b + epsilon(i) for i = 1,2, ..., T, and E(Xi) > at(i) + b for i = T + 1, ..., n, where X1, ..., Xn are independent and epsilon(i) approximately N(0, sigma2). In the first phase, a linear relationship between VO2 and power output was assumed, whereas in the second phase an additional increase in VO2 above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-VO2). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP-VO2 as described in our model. The power output at CP-VO2 amounted to 136.8 (SD 31.3) W. It was only 11 W -- non significantly -- higher than the power output corresponding to LT. The VO2 at CP-VO2 amounted to 1.828 (SD 0.356) l x min(-1) was [48.9 (SD 7.9)% VO2max]. The [La-]pl at CP-VO2, amounting to 2.57 (SD 0.69) mmol x l(-1) was significantly elevated (P < 0.01) above the resting level [1.85 (SD 0.46) mmol x l(-1)], however the [H+]b at CP-VO2 amounting to 45.1 (SD 3.0) nmol x l(-1), was not significantly different from the values at rest which amounted to 44.14 (SD 2.79) nmol x l(-1). An increase of power output of 30 W above CP-VO2 was accompanied by a significant increase in [H+]b above the resting level (P = 0.03).

Now the interesting part here really is the result of lactate  and H+

It would be really interesting to have an answer here from the "Lacatic acid" believer.
. Than another direction we may look is  who actually may regulate the H +
 Could it  just be, that if we can  keep the H + in  balance, we can increase lactate easier, as lactate may be a part of the  buffer system of H +.
 Than where is the H + moving , once it is released in the ciruclatroy system.
 Kidney , respiration  , do they support each other and  who is  during activity most likely the faster and better help in H +  control.
  Why is RQ not RER   in an incremental exercise test and why is RER   often far above the  1.0  level of  complete glucose  use ?
 And last but not least, why do we see athletes  on sea level  having a great deoxygenation ability and  at altitued there oxygenation level barely drops in the working muscels.
 ?
 Many questions  and  possibly some potential interesting answers for all new MOXY users. Stay tuned as the fun just starts   here now.

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