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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
I got  a  few mails  asking  me, why I believe  that  we  can make it that simple :
 Delivery problem  and utilization problem.
 A;  Most likley  you are  right it is not that  simple  and as in many cases there  will be a lot  of  exceptions  and interesting cases.
 The reason  why we make it    easier is  to  be able to use MOXY.
  So may  question  back would be:
 Is it that  simple, that we can take a VO2  "max" value  and  simply use a  calculator  and every body  with  60 %  of  a  ' VO2  max"   will train  physiological the same  systems ?

 If  your  answer is  yes  it is  that simple  great. If you hesitate  than the question would follow:
 How  can we  have " accepted  " research  and intensity ideas  , which are based on this  assumption.
  The latest  review on VO2  max test shows a summary of  over  33   accepted  publication on VO2  max  tests, where  49 % of the  tested people showed  a tendency to a  "plateau"  and 521 %  not at all.  Form the 49 %  tendency    most of them had  to  be in a  kind  of an agreement on  what  we may consider  an all out test.
.  The  other part is , that  when taking  %  of VO2  max  and or  ant  test res7ult   we    may forget the  real physiological    reason, why we  are not able to function every day  exactly the  same  like a  motor. We   depend on physiological reactions.
 So  the MOXY  concept  we use  is based on the simplification of delivery  and  utilization trends  and  there  are some  overlapping situation , where we  can't  deliver  and are not allowed  either to utilize    O2  further down. ( Limit  of  ATP depletion).
 Here a nice   summary  and read carefully to see the idea  of    delivery limitation.

O2 Arterial Desaturation in Endurance

Athletes Increases Muscle Deoxygenation

RENAUD LEGRAND1,2, SAI¨D AHMAIDI2, WASSIM MOALLA2, DOMINIQUE CHOCQUET2,

ALEXANDRE MARLES1, FABRICE PRIEUR1, and PATRICK MUCCI1

1Laboratory of Multidisciplinary Analysis of Physical Activity, Faculty of Sport Sciences, University of Artois, Lie´vin,

FRANCE; and 2Laboratory EA 3300–Physical Activity and Motor Behaviour: Adaptation, Readaptation, Faculty of Sport

Sciences, University of Picardie Jules Vernes, Amiens, FRANCE

ABSTRACT

LEGRAND, R., S. AHMAIDI, W. MOALLA, D. CHOCQUET, A. MARLES, F. PRIEUR, and P. MUCCI. O2 Arterial Desaturation

in Endurance Athletes Increases Muscle Deoxygenation. Med. Sci. Sports Exerc., Vol. 37, No. 5, pp. 782–788, 2005. Purpose: The

aim of this study was to compare the muscle deoxygenation measured by near infrared spectroscopy in endurance athletes who

presented or not with exercise-induced hypoxemia (EIH) during a maximal incremental test in normoxic conditions. Methods: Nineteen

male endurance sportsmen performed an incremental test on a cycle ergometer to determine maximal oxygen consumption (V˙ O2max)

and the corresponding power output (Pmax). Arterial O2 saturation (SaO2) was measured noninvasively with a pulse oxymeter at the

earlobe to detect EIH, which was defined as a drop in SaO2 _ 4% between rest and the end of the exercise. Muscle deoxygenation of the

right vastus lateralis was monitored by near infrared spectroscopy and was expressed in percentage according to the ischemia–hyperemia

scale. Results: Ten athletes exhibited arterial hypoxemia (EIH group) and the nine others were nonhypoxemic (NEIH group). Training

volume, competition level,V˙ O2max, Pmax, and lactate concentration were similar in the two groups. Nevertheless, muscle deoxygenation at

the end of the exercise was significantly greater in the EIH group (P_0.05). Conclusion: Greater muscle deoxygenation at maximal exercise

in hypoxemic athletes seems to be due, at least in part, to reduced oxygen delivery—that is, exercise-induced hypoxemia—to working muscle

added to the metabolic demand. In addition, our finding is also consistent with the hypothesis of greater muscle oxygen extraction in order

to counteract reduced O2 availability. Key Words: EXERCICE-INDUCED HYPOXEMIA, HEMOGLOBIN SATURATION, AEROBIC

PERFORMANCE, ENDURANCE TRAINING, MUSCLE OXYGENATION  

Why  where  O2max, Pmax, and lactate concentration were similar ???
  We  still use  O2 , we  just use  it  from strorage,   if possibel  and not take  it from delivery.  If  we have it in storage  we as well  do not  (NOT )  run into a  O2  deficit.  Give this some thought  looking   form teh classcila  VO2  max idea  and  from  our MOXYGENATION idea




 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Roger

Moderator
Registered:
Posts: 266
 #2 
In the paper, they concluded that the additional deoxygenation in the EIH group was not due to shifting the hemoglobin dissociation curve because they didn't see a difference in lactate readings between the EIH and NEIH groups.

Is it possible that the dissociation curve shifted due to CO2 concentration differences instead?  If one makes a guess that those athletes with low SaO2 (the EIH group) might also have high PCO2 in the blood, then this could be a cause of dissociation curve shifting.  Is this effect large enough for the magnitude of deoxygenation difference that is observed?


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Thanks  Roger  great   question  and a great chance  not  to critics  but to show  the disconnect   in many  exercise  physiological studies  to the real world  of  physiology.
  1. Lactate has  only a limited   feedback ability  to the trend in SmO2.
  a)  we  can have   4  different situation  and it is up to the regular reader  to  explain  what  happens in the body  when I  explain the 4 different  options.
 a1. We  can see  an increase in SmO2    and  an increase in lactate  at the same time  Why   and   when ?
a2. We  can see  an increase n SmO2   and a  decline in lactate
a3  We  can see a  drop in SmO2  and a drop in lactate
a4  we  can see a drop in SmO2   and  an increase in lactate.
  Reason:
 Lactate   has no  direct impact on  the O2  diss. curve  at all.
 It is  the H +  (  lactate is a buffer  of H + )  as well   CO2  besides  other reason , who shift   the O2  diss curve.
.
 In this case above,  the  fact , that VO2  and lactate where not different  in the two groups  simply indicates, that they did a  step test  ( classical VO2) test  with  too short steps in the first place  to actually create a  clear information on  what and  why  some where   low in SpO2    ( nearly 50 % ).
  A  drop in SmO2   means , that they where looking  at the end of the test  for O2     and the  O2  was  found  in the storage  and the  regular  training  stimulated  in this  people the ability  to   deoxygenate  better. ( Different reason  for this ability  like CO2  levels H + levels   change in  hormones as  explained in the  articles  before.)
 The fact remains, that they  still had O2  they where able to use  due to the better deoxygenation ability  and there was   a similar amount  of VO2  used over all.
  In the group  with a  " normal'  SpO2   there the  O2  needed    or used  at the end  was  delivered over  blood  flow ,   so they  where not digging into the storage,  as it was  not needed as the delivery  system to the blood was  still  working well. So  same O2  use  just delivered  instead of used   from storage.
. This  examples show exactly the big  reserve  we have to improve  performance.
 Athletes with  an EIH  have a  different limitation  and a different compensation. Limitation may be  respiratory system or  vascularisation  or  muscular  . Compensation is a better utilization of  O2    ( bio availability ). The other group  has  a utilization limitation   and  has a compensation over ,   for example , muscular ability.

So the  key is  to find the Limiter  and   than work on the Limiter  to improve  performance.
 So the EIH  group  would have to work on the ability  to  load  O2   and   maintain the ability  to utilize  and they have immediately more O2   available for a better performance. The  other group would have to work to improve  utilization   and maintain delivery  and again a  performance gain.
  That's  and exactly that is , why we  do  our  2 different assessments. Finding  delivery limitation  and utilization limitation  with MOXY  and  combine it in  actual test centers  with Physio flow  and VO2  equipment.
  The main   reason  why this is not  common used  as of  yet is the  inability we all have to accept, that we  can make progress and  do not have to hang on a  now  nearly 100 year old  concept  of VO2  max  or  2  and 4 mmol lactate, when we  actually  agree, that there is no such thing  like a VO2  max  but a VO2  tested peak.   and that lactate is most likely   an energy source    and a great  shuttle tool  for  many  important   ideas in the body.So the  "effort'  from many groups  to  force  NIRS result into a mythical idea  of LT  ANT  and  so on   slows  done the progress of looking  at new  options.
  So the fact  than in this study  VO2  and lactate is used  but did not correspond  with  NIRS trend shows  nicely  why we desperately try to avoid , that NIRS  MOXY is getting used  to be a  part of an artificial  kept  alive   theory    to all costs. For us  MOXY is a new start into a new area  of  life  in the field information , which can be  combined  with " classical " ideas but is  so much more direct than  lactate and VO2  , that   it is  not   a great idea  to try to force  MOXY trends in non existing  lactate thresholds  or    % of  VO2  max  and so on.
  VO2  and lactate  have a direct   result  based on  test protocols and  we  can't use them as  actual physiological information in most of the  short term  test ideas.
 See here a  small statement  form the University of Maastrich   research  ideas  in Cycling  Pro  and amateur  comparison.

 

"A study protocol with 3-minute stages was used in this study, starting with 2 W/kg and

increasing every workload step with 0.5 W/kg. Other research investigating differences

between professionals and amateurs, mainly Lucia and Chicharro, used different study

protocols with stages of 25 W/min (17, 18, 37, 39-44). Sallet et al. used a ramp protocol of 30

Watts every 1 minute and 30 seconds (55). These differences in ramp protocols may hamper

comparisons between the several studies. For example, the ramp protocol of 25 W/min

generally requires less total time than the protocol used in this study"

 If  we have real physiological parameters, than protocols  should not influence   physiological reactions if the body  had a chance to try to react. If the protocols  are based on physical ideas  too much  and the lag time  of some of the physiological systems,  including the lag time  for the equipment.  ( VO2   testing at the mouth  to  concluded, what happens in the muscle,  lactate testing at the finger  to conclude what happens in the muscle ) , than we   simply  create  nice looking ideas    with very little ability  to find limiter and compensator.
 Summary.
  The drop in the study  of  SmO2  is  due to the shift in  O2  diss curve  due  to respiratory limitation. There is a fundamental difference in metabolic acidosis, where lactate can be one of many bio markers  to show, that we  start mixing  o2  dependent ATP production with O2  independent ATP  production,    which can create a shift in O2  curve due to change in H + level  and pH.
  and the respiratory acidosis  which creates  H +  and CO2   an therefor a shift in  O2  diss curve  as well. We  can create a  respiratory acidosis  with low SpO2  and   high CO2  and a shift in  SmO2   and a better deoxygenation with out even  moving a leg  or an arm  and  with put increasing HR  really. See  pic  from a case study  done by Brian Kozak. look the deoxygenation    and he  did this  by simply sitting at home. What was he doing.
  Many questions  you have to answer in this respond. I am looking forward  to a critical response  and   ideas.  Here a  short  info on  acidosis  and  alkalosis

Acidosis/alkalosis

 

Some  basic information

 

 

 

Normal pH value for the body fluids is between pH 7.35 and 7.45. If the pH of body fluids is below 7.35, the condition is called acidosis, and if the pH is above 7.45, it is called alkalosis.

 

Metabolism produces acidic products that lower the pH of the body fluids. For example, carbon dioxide is a by-product of metabolism, and carbon dioxide combines with water to form carbonic acid. Also, lactic acid ( lactate +  H ) is a product of oxygen independent metabolism, protein metabolism produces phosphoric and sulfuric acids, and lipid metabolism produces fatty acids. These acidic substances must continuously be eliminated from the body to maintain pH homeostasis. Rapid elimination of acidic products of metabolism results in alkalosis, and the failure to eliminate acidic products of metabolism results in acidosis.

 

The major effect of acidosis is depression of the central nervous system. ( Feedback loop  over the Central governor  and for us  over the ECGM  extended central governor) When the pH of the blood falls below 7.35, the central nervous system malfunctions, and the individual becomes disoriented and possibly comatose as the condition worsens.

 

A major effect of alkalosis is hyperexcitability of the nervous system. Peripheral nerves are affected first, resulting in spontaneous nervous stimulation of muscles. Spasms and tetanic contractions and possibly extreme nervousness or convulsions result. Severe alkalosis can cause death as a result of tetany of the respiratory muscles.

 

Although buffers in the body fluids help resist changes in the pH of body fluids, the respiratory system and the kidneys regulate the pH of the body fluids. Malfunctions of either the respiratory system or the kidneys can result in acidosis or alkalosis. (Mal function can be create  due to limitation of the task   the respiratory system suppose  to do. )

 

Acidosis and alkalosis are categorized by the cause of the condition. Respiratory acidosis or respiratory alkalosis results from abnormalities (or weakness /limitation) of the respiratory system.

 

 Metabolic acidosis or metabolic alkalosis results from all causes other than abnormal respiratory functions.

 

Inadequate ventilation of the lungs causes respiratory acidosis. The rate at which carbon dioxide is eliminated from the body fluids through the lungs falls. This increases the concentration of carbon dioxide in the body fluids. As carbon dioxide levels increase excess carbon dioxide reacts with water to form carbonic acid. The carbonic acid dissociates to form hydrogen ions and bicarbonate ions. The increase in hydrogen ion concentration causes the pH of the body fluids to decrease. If the pH of the body fluids falls below 7.35, symptoms of respiratory acidosis become apparent.

 

Buffers help resist a decrease in pH, and the kidneys help compensate for failure of the lungs to prevent respiratory acidosis by increasing the rate at which they secrete hydrogen ions into the filtrate and reabsorb bicarbonate ions.(  As well a   limiter   Kidney  will get help   from the compensator   Respiratory system. )

 

 In  sport  however the  short term  need  of  balance of  H +  only  can take place  over  a  perfect respiratory system. However, the capacity of buffers to resist changes in pH can be exceeded, and a time period of 1 or 2 days is required for the kidney to become maximally functional. Thus the kidneys are not effective if respiratory acidosis develops quickly, but they are very effective if respiratory acidosis develops slowly or if it lasts long enough for the kidneys to respond. For example, kidney cannot compensate for respiratory acidosis occurring in response to a severe asthma attack that begins quickly and subsides within hours. However, if respiratory acidosis results from emphysema, which develops over a long period of time, the kidneys play a significant role in helping to compensate.

 

Respiratory alkalosis results from hyperventilation of the lungs. This increases the rate at which carbon dioxide is eliminated from the body fluids and results in a decrease in the concentration of carbon dioxide in the body fluids. As carbon dioxide levels decrease, hydrogen ions react with bicarbonate ions to form carbonic acid. The carbonic acid dissociates to form water and carbon dioxide. The resulting decrease in the concentration of hydrogen ions cause the pH of the body fluids to increase. If the pH of body fluids increases above 7.35, symptoms of respiratory alkalosis become apparent.

 

The kidneys help to compensate for respiratory alkalosis by decreasing the rate of hydrogen ions secretion into the urine and the rate of bicarbonate ion reabsorption. If an increase in pH occurs, a time period of 1 or 2 days is required for the kidneys to be maximally effective. Thus the kidneys are not effective if respiratory alkalosis develops quickly. However, they are very effective if respiratory alkalosis develops slowly. For example, the kidneys are not effective in compensating for respiratory alkalosis that occurs in response to hyperventilation triggered by emotions, which usually begins quickly and subsides within minutes or hours. However if alkalosis results from staying at a high altitude over a 2 or 3 day period, the kidneys play a significant role in helping to compensate.

 

Metabolic acidosis results from all conditions that decrease the pH of the body fluids below 7.35, with the exception of conditions resulting from altered function of the respiratory system. As hydrogen ions accumulate in the body fluids, buffers first resist a decline in pH. If the buffers cannot compensate for the increase in hydrogen ions, the respiratory center helps regulate the body fluid pH. The reduced pH stimulates the respiratory center, which causes hyperventilation. During hyperventilation, carbon dioxide is eliminated at a greater rate. The elimination of carbon dioxide also eliminates excess hydrogen ions and helps maintain the pH of the body fluids within a normal range.

 

If metabolic acidosis persists for many hours and if the kidneys are functional, the kidneys can also help compensate for metabolic acidosis. They begin to secrete hydrogen ions at a greater rate and increase the rate of bicarbonate ion reabsorption. Symptoms of metabolic acidosis appear if the respiratory and renal systems are not able to maintain the pH of the body fluids within its normal range.

 

Metabolic alkalosis results from all conditions that increase the pH of the body fluids above 7.45, with the exception of conditions resulting from altered function of the respiratory system. As hydrogen ions decrease in the body fluids, buffers first resist an increase in pH. If the buffers cannot compensate for the decrease in hydrogen ions, the respiratory center helps regulate the body fluid pH. The increased pH inhibits respiration. Reduced respiration allows carbon dioxide to accumulate in the body fluids. Carbon dioxide reacts with water to produce carbonic acid. If metabolic alkalosis persists for several hours, and if the kidneys are functional, the kidneys reduce the rate of hydrogen ion secretion to help reverse alkalosis

 

 

 

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