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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
We hope to  have n short a E book ready  for   MOXY users  with teh goal  to use  same wording and same  explanations  as we   fast increase  MOXY users  all over teh world  and we have to talk a common language.
 One of our goals is to avoid     from the beginning the idea, that we  try  to   push moxy trends  and information into a : classical: system  with   compassion  of  ANT, AT. LT, VT  and  all the threshold concepts  out there.
 We like to have a new  start here  for us   and  simply use  MOXY  information to explain what we  see  and how we use this information.
  Here an interesting paper:
Can J Appl Physiol. 2004 Aug;29(4):504-23.

Muscle oxygenation trends during dynamic exercise measured by near infrared spectroscopy.


Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Canada.


During the last decade, NIRS has been used extensively to evaluate the changes in muscle oxygenation and blood volume during a variety of exercise modes. The important findings from this research are as follows: (a) There is a strong correlation between the lactate (ventilatory) threshold during incremental cycle exercise and the exaggerated reduction in muscle oxygenation measured by NIRS. (b) The delay in steady-state oxygen uptake during constant work rate exercise at intensities above the lactate/ventilatory threshold is closely related to changes in muscle oxygenation measured by NIRS. (c) The degree of muscle deoxygenation at the same absolute oxygen uptake is significantly lower in older persons compared younger persons; however, these changes are negated when muscle oxygenation is expressed relative to maximal oxygen uptake values. (d) There is no significant difference between the rate of biceps brachii and vastus lateralis deoxygenation during arm cranking and leg cycling exercise, respectively, in males and females. (e) Muscle deoxygenation trends recorded during short duration, high-intensity exercise such as the Wingate test indicate that there is a substantial degree of aerobic metabolism during such exercise. Recent studies that have used NIRS at multiple sites, such as brain and muscle tissue, provide useful information pertaining to the regional changes in oxygen availability in these tissues during dynamic exercise.  

between the lactate (ventilatory) threshold   We   all know the ongoing discussion  due to lack of  real  values. We know  that in some cases  studies  show that the lactate is increasing  at the same time , where we  see a  clear shift in  respiratory response  like  in VE.
 Therefor   this groups  state  that VT = AT  or LT. On the other side  there  are great  studies  showing that this is not really  the case.
 We argue, that  it is not the case , but if  respiration is a LIMITER  than we see the need of the body  to find  energy  ( ATP ) production  with less  help of O2   so   we  will see  an increase in lactate as a metabolic marker  that  glucose is used  with  some less help of  O2 .
  In this cases  the  lactate increases   at a similar place  as VE may increase.
 If  the respiratory system is the Limiter, than we will see  at that  stage  a  drop in SmO2    as a  sign of   delivery problem  due to  respiratory limitation  and now  we  have  at the same place   a change in lactate ( metabolic  sign [wink] , a change in VE ( respiratory  change)  and a  change in SmO2 (  oxygenation information.)
 In this  case  we have   logically  at the same time  all the reaction we  would expect , if respiration is the limiter   as the body tries  to  change the  behaviour of  respiration  with VE  up  ,  but we have to look  why  RF  or TV  or both  or  one down the other more  up . Than  we  can see, if the respiration is the limiter as a metaboreflex  reaction, so we not only have  SmO 2 drop  but as well tHb  drop  due to vasoconstriction.  This leads  to less O2   delivery  for the same   load  and  lactate will go up as a sign of a metabolic shift. CO2  will go up  stressing  repiration even more    and  this is the reason why  in that client VT   and SmO2  drop may be  close  to or at the same  place in the same step.

  Now  for  "players"  if  at this  stage  you force  yourself or the client  to breath  either very fast  or  very deep and slow ,you will have a change in lactate  as well as a change in VT  VE.    but  as well a change in SmO2  trend  depending  what you do.
 Try ity out  and come back.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here is an example   we like to  show  to avoid confusion.
  The  regular reader  is  well aware  by now, that we   use  the idea of LIMITER  and compenator.
 So  as  an example.
 If I have in  my clinic  a  client  with  a  cardiac problem  I know that the cardiac   problem my be the Limiter.  This is not always true    as the respiration  could have been the limiter and over years  the cardiac system  had  to compensate  so that it finally fails. That's when we have to go back and work on respiration and on  cardiac    training.
 Now back to our point.
 If the cardiac  system is a limiter, the ECGM    system  will  create  under load a  reduction in motorunit recruitment  and as  such  by a simular load   compared to a  non cardiac limiter client  the  SmO2  will   drop earlier and tHb  will    drop earlier. ( Portection of the vital systems   on cost of the  extremity  muscle systems .
 The    drop in  motor units  will create a   higher  contraction  for the  left over,  still working  units  , to achive the same   performance, there will be a  compression on capillarise  and as such tHb  will drop, which makes  it even  harder  to maintain performance  as less O2  is delivered  so SmO2  drops   further ( delivery problem ) .
 The  task  to try to maintain performance is now  moved  to  more involvment of the O2  independent    energy deliver  which creates a higher CO2   output  as well as a higher H +  production. so lactate   will  besides    be used  as energy , help as a buffer  system  moving H +  out of the overloaded area  .   therefor we  add to the already higher CO2  level additional CO2  over the  H +  situation, which increases  the respiratory load  which may now  hit a limitation and  vasoconstriction  will increase ( metaboreflex).  and so on.
  This has  very little, in fact  for us ,nothing to do  with  the lactate threshold, but  it  is still used    from many places  as they belive  l lactate is the reaosn of fatigue . Here to enjoy 

Monitoring skeletal muscle oxygenation during exercise by near infrared spectroscopy in chronic heart failure.


Servizio di Cardiologia Riabilitativa, Istituto Lancisi, Ancona, Italy.


Patients with chronic heart failure (HF) have a reduced skeletal muscle blood flow which can in part explain reduced exercise tolerance and increased ventilation. All the techniques commonly employed to measure skeletal muscle blood flow have limitations that reduce their accuracy and clinical application. Near infrared spectroscopy (NIRS) is a noninvasive, inexpensive, and reproducible technique able to monitor muscle oxygenation both at rest and during exercise, providing information about tissue perfusion. The principle of NIRS is based on the observation that the light absorption characteristics of hemoglobin (Hb) and myoglobin (Mb) in the near infrared region (700-1000 nm) change depending on their relative saturations. In humans, NIRS has been employed to monitor skeletal muscle oxygenation during exercise and/or after cuff-induced limb ischemia in normal subjects as well as patients with chronic HF. Patients with chronic HF have a reduced Hb/Mb oxygenation at any matched work rate and a more rapid deoxygenation above the anaerobic threshold than normal subjects. More recently, NIRS has been used to determine the kinetics of muscle oxygenation in recovery after constant work rate exercise, providing evidence of an inverse relation with cardiac function as assessed by peak oxygen uptake. In conclusion, NIRS appears to be a new promising noninvasive technique for studying muscle oxygenation in a variety of experimental models. (c)1999 by CHF, Inc.

 For us  it is NOT  the anaerobic threshold  as the  system is  not anaerobic in the first place . it is the limitation of delivery  and  in some cases  utilization of O2  due to protection of vital systems  as well   to avoid  a critical  drop in ATP.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
As  mentioned , the  key is  to try  to  have an open mind   towards  a new  idea   and try  to blend out   common  confusing  "classical"  concepts.
 The main   info on mails  I am getting  from people is that they try to find a common   value in classical ideas we have in our  brains  and  MOXY  an than they often  do not fit together.
  Interval  MOXY and lactate.
  If you do a  200 or  300 m  interval on your track   and you take a lactate sample  at the end of the run  immediately,  you may have a  very low lactate value, which never ever  fits the  " feeling "  you have. A  few  minutes  later you may have a very  high lactate value but. With the low value  at the end of the  run  you felt "terrible"  and with the high value  5 min later  you are ready to go again ?????

 The SmO2  value is very low  as well immediately after the run.Therefore  fits  your " feeling" after  you just  made a very strong  energy demanding effort  and as a part of the ATP  demand  you needed  to take O2   as long and as much as possible. If  it  was not anymore  delivered  or  the utilization was higher than the delivery  SmO2  will show  that immediately as you  go.  At the moment  when you stop  lactate will be low  and SmO2  will immediately shoot  up as a sign of  refueling the O2 storage ( Mb )   and reloading Hb.
  So now you have  actually a very high SmO2   and a very low   lactate. During the run  you  have a  steady dropping  SmO 2  till to a  certain level and you may  have a  plateau.
  A few minutes   after the load  SmO 2  may actually  come down again  but lactate may still go up.
 This is the difference between a  real live on  sport  assessment with MOXY  and an indirect  information over  a blood  sampling on a finger  . The lactate is a trend information of  some metabolic  changes  but has very little info on where this  problem may have occurred  and where  we may take lactate as energy source  before it even shows  up on the finger.  When you start using  MOXY  try to add the info  tHb  can give you and  start to think   that your body works as a  team  ( rowing team)  so  what can influence  what reactions  instead of looking , where you may find a  specific  mathematical  angel,  a threshold  or what  ever.
  Here a  direction    more an more   groups take now  when using  NIRS  ( MOXY ) and it is great for us to see, that our  many years  of   insisting  in the idea  of using more than just  TSI %  or SmO2  we  can look at additional trend s  from NIRS/ MOXY.

Haemoglobin oxygen saturation as a biomarker: the problem and a solution.


Optics Division of the Martinos Center for Biomedical Imaging, Harvard Medical School, Massachusetts General Hospital, 149 13th St rm 2301, Charlestown, MA 02129, USA.


Near-infrared spectroscopy measures of haemoglobin oxygen saturation are often used as an indicator of sufficient oxygen delivery to assess injury susceptibility and tissue damage. They have also often been used as a surrogate measure of oxygen metabolism. Unfortunately, these measures have generally failed to provide robust indicators of injury and metabolism. In this paper, we first review when haemoglobin oxygen saturation does work as a robust indicator, and then detail when and why it fails for assessing brain injury and breast cancer. Finally, we discuss the solution to obtain more robust measures of tissue injury and cancer by combining oxygen saturation measurements with measures of blood flow and volume to more accurately estimate oxygen metabolism.

[PubMed - indexed for MEDLINE]
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