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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
An increasing numbers  of  emails  since  San Diego  ask the question on the use  of  feed-backs  we  may get  using tHb.
 I will try to  get some thoughts on this  .
 tHb  is a  trend information ( no absolute values ) on potential blood flow in the tested area  and  when using multiple MOXY  placing on potential some trends in blood flow due to certain regulatory  processes  like BP  protection, anti gravity positions and so on.
I  do not   think we  can  use live  tHb    with MOXY  to make a statement  on the actual amount of blood on dehydration and re-hydration  of  blood.
 Remember  that in simple terms we have blood as  plasma  and as  cells structures  where  the cell structure  is  a combination of different cells   and one of the  is Hb.

 So when we  use  the trend information of tHb we assume, that the  concentration of  Hb  is    the same   when we push some blood out  due  to contraction or  anti gravity  ideas  as well  when we increase the blood flow in an area  due to   vasodilatation.  Many more option but in all cases  we have to hope that the concentration is  about  stable.
 What we  do not  know  how the  NIRS behaves , when we have the same  numbers of tHb in the tested  area  but they are  in a diluted plasma  volume or a  lower plasma  volume. To explain this easier  we can use the Hct  (  hematocrit.)
 So I may have  1 L  of plasma  and 100 cells in there  or I have 500 ml of plasma  and 100 cells in there. The Hct  will change as we test the blood. What we  are not sure  is how that may influence the NIRS  feedback. Roger may be able to give us  more ideas based on the  technology.
 For the moment we assume  more blood  more Hb  so  if tHb goes up we  have a better  or higher  blood volume in the tested area.
 Now there is a small  problem here.
 A  high tHb  does not   always mean as well a high oxygenation of   a high O2Hb level. Or the opposite. A low  or dropping tHb  does not always mean a  dropping in O2Hb.
 Think that  idea through. Small hint.
 Look  at the rest 1 minute tin a 5/1/5 as tHb goes up  and than look at the   biceps  contraction example we showed  on the forum where tHb goes up.
 In other words. To make a statement  on tHB  and what may  happened  you  better  as well look closely  at the SmO2 trend or reaction.
 So one  value  will support or help to make a better  interpretation than when we look just  SmO2  alone or  tHb  alone..

 Now  many  emails  asked me, whether we  could back up this ideas  with  some  accepted papers  and not just making up a nice story  which may fit the   MOXY data collection.
. Now here a  newer paper  which n fact is a summary  form  different papers  from the  late 1970 - 1980  and  before that.
 Remember the idea   of   knowing the history  to avoid too many  repetitions in  mistakes but as well in great ideas.
 Now here a  paper abstract  and summary  who  support our ideas, why we can sue  tHb  for many feed backs  we  get out of the trends. This is as well a reason why we  developed  5/1/5  so  why we  like the  one min rest in between  equal loads.
 Here the abstract.




Michael J. Joyner and Darren P. Casey

Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota; and Department of Physical Therapy and

Rehabilitation Science, University of Iowa, Iowa City, Iowa

L Joyner MJ, Casey DP. Regulation of Increased Blood Flow (Hyperemia) to Muscles

During Exercise: A Hierarchy of Competing Physiological Needs. Physiol Rev 95: 549–

601, 2015; doi:10.1152/physrev.00035.2013.—This review focuses on how blood

flow to contracting skeletal muscles is regulated during exercise in humans. The idea is

that blood flow to the contracting muscles links oxygen in the atmosphere with the

contracting muscles where it is consumed. In this context, we take a top down approach and review the basics of oxygen consumption at rest and during exercise in humans, how these values change with training, and the systemic hemodynamic adaptations that support them. We highlight the very high muscle blood flow responses to exercise discovered in the 1980s. We also discuss the vasodilating factors in the contracting muscles responsible for these very high flows. Finally, the competition between demand for blood flow by contracting muscles and maximum systemic cardiac output is discussed as a potential challenge to blood pressure regulation during heavy large muscle mass or whole body exercise in humans. At this time, no one dominant dilator mechanism

accounts for exercise hyperemia. Additionally, complex interactions between the sympathetic nervous system and the microcirculation facilitate high levels of systemic oxygen extraction and permit just enough sympathetic control of blood flow to contracting muscles to regulate blood pressure during large muscle mass exercise in humans.

So when we look at tHb in a 5/1/5  we have some  ideas  in font of us:
 a) is the tHb  dropping  due to mechanical reason like  compression.?
b) is it dropping  due to  some physiological reflex  reactions like BP  control. or  metaboreflex  and other reason
c) is it going up  due to vasodilatation
d) is it going up due to outflow restrictions like venous occlusion trends

  To have a  better feedback we than add SmO2 trend..

 Below  three examples  to  just try to get a grip on this ideas.

3 squatting biased.jpg 
 Look at  red   and brown. Red is O2Hb   or  Hb  which is loaded  with O2 . So when   "normally" O2Hb  drops  we have less loaded, as  HHb goes up (unloaded.) So SmO2  which really is  %  of O2Hb in  the tHb  will drop as well. So in the above example we have  an increase in tHb  but a  drop in  SmO2  or  in the pic O2Hb . Why ?

easy load.jpg 

Now  above  another  idea of a  workout and you can see what we  tried to achieve is a  drop in tHb  and at the same time a drop  in O2Hb  or  ( SmO2 ). What did we  do here  and why  is  here tHb  dropping compared  with the first example where  tHb increase but in both  O2Hb  or SmO2  will drop ?

exchnage  from  back flwo to  occlsuion.jpg 

Now here  a nice  example    where we  have a  drop in tHb  and a  drop i O2Hb  ( SmO2 ) but we  have as well a  drop in tHb  but an increase in  O2Hb  ( SmO2  ). We  do NOT have in this picture  a  increase in tHb  and a  drop in  O2Hb.
  My  grade  10 students  have  next week  to create a workout, where  we have all  different i options  on hand in one workout.
 a) Increase of tHb  and  drop in O2Hb,
 b) increase in tHb  and increase in O2Hb
c)  decrease in tHB  and decrease in O2Hb
 d)  decrease in tHb  and increase in O2Hb
 Try to create this workout  for yourself.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
The  above example  shows many tHb reaction created over the muscle contraction reactions.
 Now  here a nice  paper  form France, with an example   of the  many times  discussed  respiratory metaboreflex  and why we focus  so many training hours on the respiratory system.

Related trends in locomotor and respiratory muscle oxygenation during exercise.

Legrand R1, Marles A, Prieur F, Lazzari S, Blondel N, Mucci P.

Author information

  • 1Laboratory of Human Movement Studies, Faculty of Sports Sciences and Physical Education, Lille University, Lille, France.



We investigated the potential effect of respiratory muscle work on leg muscle oxygenation without artificial intervention in non-endurance-trained young subjects and searched for the range of intensity when this effect could occur.


We simultaneously monitored accessory respiratory and leg muscle oxygenation patterns with near-infrared spectroscopy (NIRS) in 15 healthy young men performing maximal incremental exercise on a cycle ergometer. Pulmonary gas exchange was measured. The respiratory compensation point (RCP) was determined. Oxygenation (RMO2) and blood volume (RMBV) of the serratus anterior (accessory respiratory muscle) and of the vastus lateralis (LegO2 and LegBV) were monitored with NIRS. The breakdown point of accessory respiratory muscle oxygenation (BPRMO2) and the accelerated (BP1LegO2) and attenuated fall (BP2LegO2) in leg muscle oxygenation were detected.


BPRMO2 occurred at approximately 85% .VO2max and was related to RCP (r = 0.88, P < 0.001). BP2LegO2 appeared at approximately 83% .VO2max and was related to RCP (r = 0.57, P < 0.05) and with BPRMO2 (r = 0.64, P = 0.01). From BP2LegO2 to maximal exercise, LegBV was significantly reduced (P < 0.05).


In active subjects exercising at heavy exercise intensities, we observed that the appearance of the accelerated drop in accessory respiratory muscle oxygenation-associated with high ventilatory level-was related with the attenuated fall in leg muscle oxygenation detected with near-infrared spectroscopy. This suggests that the high oxygen requirement of respiratory muscle leads to limited oxygen use by locomotor muscles as demonstrated in endurance-trained subjects. The phenomenon observed was associated with reduced leg blood volume, supporting the occurrence of leg vasoconstriction. These events appeared not only at maximal exercise but onward above the respiratory compensation point.


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