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Exercise induced arterial Hypoxemia EIAH and Cardiac Contraction Time CCT (FaCT term). I think both of these terms refer to the same thing. Where CCT = LVET x CO and EIAH is when blood moves too quickly through the pulmonary capillaries due to too high a CO, that full oxygen diffusion cant occur.

Have you through your own testing seen if CCT is acute enough that we can see this with Moxy? What would the trend in SmO2 and tHB look like? Do you have any graphic examples?
Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Marcel , thanks for this great  input.
 As usual  you are far ahead of the game  with your thoughts.
Now  2  3  add ons.
 1. CCT  as you point out is the term we use  when we calculate  LVET ( left ventricular ejection time in ms)  x  HR.   Example  300 ms  LVET  and 150 HR  you get a CCT  of 45 Sec.
 meaning that during a  1 min workout  your  heart muscle itself  is not getting a lot of  O2  as the heart itself  get's oxygenated  during  the  relaxation phase  and not during the contraction phase. Below a  Physio flow   graph  so HR left to  x LVET  dark blue  lower row  middle  = CCT

pf overall picture - Copy.jpg    

2. Exercise induced arterial Hypoxemia EIAH .

 It took,or it still takes a lot of  convincing to the exercise physiological groups and coaches ,  who still argue  that  this does not exist, that respiration is never a limitation  of anything. ( look at the strange  justification  , as they use  MMV  as the reasoning of never being on a limit with respiration.

 I am not  completely sure, whether  just the high CO  and the  actual transition time is the main reason of EIAH.
 As the wording explains it is  an exercise  induced arterial  hypoxemia.  Meaning  they believe  it is exercise  so activity induced    and    pushes   for the believe, that CO  has to be high.
    Yes if CO  is high and with it the  speed of the  blood flow paired  with a very high respiratory frequency  and possibly a  small TV  we    can create this arterial hypoxia.
But we  can  as well crate it without    high CO . We simply shift the  O2  disscurve to the right so we have a great  de oxygenation but a  poor  oxygenation  and SpO2  is low   and SmO2  is dropping  fast    and we have  an arterial hypoxemia as well.
 Do we see it with  nears  .

Yes  we  can see it  with MOXY  or NIRS  but only  when we  actually  allow the time as well  when we  create a situation, where we stop using O2  in the working muscles  but keep  CO up  so we still deliver  blood  but not fully oxygenated.
  Here  are some case study, where  we produced  this .  Red is O2 Hb  Blue is HHb  Below  a  " normal "  reaction in a TIP. At the  1 min rest your tHb  increases  and  due to lag time of CO  and VE  we have a  very high  CO  and VE  despite   no muscle activity. So  over delivery  from the heart and the respiratory system but over delivery  because a   few seconds  before it was needed  as the  muscle has  full activity.
 So we create a delivery  without the  proper  utilization and we see an increase in tHb  and  SmO2    due to  an inflow of  saturated blood ( O2Hb ) See below  and a  drop in HHb  as  not a lot of O2  is used anymore

healthy example.JPG

Now  below a situation, where we created  a hypoxia in the arterial blood  so we  where hoping , that when stopping the  action we still again deliver a lot of blood  but this blood is not fully oxygenated. So as well tHb increases  but  we  not only increase the  amount of O2 Hb  loaded coming in  and  is not used  but as well we get  more HHb in .  see below 
 This is the first  an only picture  of a EIAH .
 Problem . Just nobody really  accepts this and we need  some   studies  who  will   for sure be done  earlier than later  to have an accepted publication.

starngae data.  2jpg.jpg

I hope this answers  your question in words  and pictures.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Thanks  for some nice  emails on this topic.  Yes  here a short  feedback showing you  that this is an ongoing discussion.
 Here  for your information a nice article  from the  last century .
  May be  respiration  can be a limitation in some cases???

 Now look at the date  and you can see, that w with the availability of MOXY we  in fact  can as   baseline coaches  actually assess what was  of a big  discussion point  now.


Send to:

J Appl Physiol (1985). 1999 Dec;87(6):1997-2006.

Exercise-induced arterial hypoxemia.

Author information

  • 1John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA.


Exercise-induced arterial hypoxemia (EIAH) at or near sea level is now recognized to occur in a significant number of fit, healthy subjects of both genders and of varying ages. Our review aims to define EIAH and to critically analyze what we currently understand, and do not understand, about its underlying mechanisms and its consequences to exercise performance. Based on the effects on maximal O(2) uptake of preventing EIAH, we suggest that mild EIAH be defined as an arterial O(2) saturation of 93-95% (or 3-4% <rest), moderate EIAH as 88-93%, and severe EIAH as <88%. Both an excessive alveolar-to-arterial PO(2) difference (A-a DO(2)) (>25-30 Torr) and inadequate compensatory hyperventilation (arterial PCO(2) >35 Torr) commonly contribute to EIAH, as do acid- and temperature-induced shifts in O(2) dissociation at any given arterial PO(2). In turn, expiratory flow limitation presents a significant mechanical constraint to exercise hyperpnea, whereas ventilation-perfusion ratio maldistribution and diffusion limitation contribute about equally to the excessive A-a DO(2). Exactly how diffusion limitation is incurred or how ventilation-perfusion ratio becomes maldistributed with heavy exercise remains unknown and controversial. Hypotheses linked to extravascular lung water accumulation or inflammatory changes in the "silent" zone of the lung's peripheral airways are in the early stages of exploration. Indirect evidence suggests that an inadequate hyperventilatory response is attributable to feedback inhibition triggered by mechanical constraints and/or reduced sensitivity to existing stimuli; but these mechanisms cannot be verified without a sensitive measure of central neural respiratory motor output. Finally, EIAH has detrimental effects on maximal O(2) uptake, but we have not yet determined the cause or even precisely identified which organ system, involved directly or indirectly with O(2) transport to muscle, is responsible for this limitation

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here some additional thoughts.
 I  like to show  you  why we have this discussion  and I call it  selective reading.
 If  we  simply like to believe respiration never a limitation to get rid  of any possible discussion we  follow this  specific  idea  here  from 2012.

Assessing exercise limitation using cardiopulmonary exercise testing.

Stickland MK1, Butcher SJ, Marciniuk DD, Bhutani M.

Author information

  • 1Pulmonary Division, Department of Medicine, 8334B Aberhart Centre, University of Alberta, Edmonton, AB, Canada T6G 2B7 ; Centre for Lung Health, Covenant Health, Edmonton, AB, Canada.


The cardiopulmonary exercise test (CPET) is an important physiological investigation that can aid clinicians in their evaluation of exercise intolerance and dyspnea. Maximal oxygen consumption ([Formula: see text]) is the gold-standard measure of aerobic fitness and is determined by the variables that define oxygen delivery in the Fick equation ([Formula: see text] = cardiac output × arterial-venous O(2) content difference). In healthy subjects, of the variables involved in oxygen delivery, it is the limitations of the cardiovascular system that are most responsible for limiting exercise, as ventilation and gas exchange are sufficient to maintain arterial O(2) content up to peak exercise. Patients with lung disease can develop a pulmonary limitation to exercise which can contribute to exercise intolerance and dyspnea. In these patients, ventilation may be insufficient for metabolic demand, as demonstrated by an inadequate breathing reserve, expiratory flow limitation, dynamic hyperinflation, and/or retention of arterial CO(2). Lung disease patients can also develop gas exchange impairments with exercise as demonstrated by an increased alveolar-to-arterial O(2) pressure difference. CPET testing data, when combined with other clinical/investigation studies, can provide the clinician with an objective method to evaluate cardiopulmonary physiology and determination of exercise intolerance

Or  we may at least  have an open mind   to  read this  information.

Exercise induced arterial hypoxemia: the role of ventilation-perfusion inequality and pulmonary diffusion limitation.


Hopkins SR.


Author information


  • Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0623, USA.




Many apparently healthy individuals experience pulmonary gas exchange limitations during exercise, and the term "exercise induced arterial hypoxemia" (EIAH) has been used to describe the increase in alveolar-arterial difference for oxygen (AaDO2), which combined with a minimal alveolar hyperventilatory response, results in a reduction in arterial PO2. Despite more than two decades of research, the mechanisms of pulmonary gas exchange limitations during exercise are still debated. Using data in 166 healthy normal subjects collated from several previously published studies it can be shown that approximately 20% of the variation in PaO2 between individuals can be explained on the basis of variations in alveolar ventilation, whereas variations in AaDO2 explain approximately 80%. Using multiple inert gas data the relative contributions of ventilation-perfusion ("VA/Q") inequality and diffusion limitation to the AaDO2 can be assessed. During maximal exercise, both in individuals with minimal (AaDO2 < 20 Torr, x = 13 +/- 5, means +/- SD, n = 35) and moderate to severe (AaDO2= 25-40 Torr, x = 33 +/- 6, n = 20) gas exchange limitations, VA/Q inequality is an important contributor to the AaDO2. However, in subjects with minimal gas exchange impairment, VA/Q inequality accounts for virtually all of the AaDO2 (12 +/- 6 Torr), whereas in subjects with moderate to severe gas exchange impairment it accounts for less than 50% of the AaDO2 (15 +/- 6 Torr). Using this framework, the difficulties associated with unraveling the mechanisms of pulmonary gas exchange limitations during exercise are explored, and current data discussed.

 You   are the  "judge"



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