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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
We mentioned this often  and  we have a blog on this  website on cardiac  output.
 Here     to start out  some    discussion:
 " For the average adult, stroke volume at rest in a standing position will be between 60 and 80 milliliters, resulting in a resting heart rate of between 60 and 80 beats per minute, although resting heart rate can be as high as 100 beats per minute. Therefore, resting cardiac output is typically between 4.8 and 6.4 liters per minute. These numbers, however, are for an average person and not an athlete. Elite athletes have been found to have resting heart rates as low as 28 to 40 beats per minute, resulting in a much lower corresponding cardiac output."

 We  would argue  her e that we see it different.  and test different  see pics  on how we test live  cardiac out put  as a result of  HR  x SV.
 The    cardiac output in a top  athlete  at rest is  equal or higher than in average people . So a  resting HR  of  40   will  give you a very  big resting  Stroke volume  as it  is still HR  x  SV.
 So we  see  resting SV  in   rowers  and cross country skiers  of 120 ml  and more. Pic  is a  untrained    client   
.
 We  can show  if the discussion  goes this  way, how we  can use   MOXY  and  HR  to actually get some inside  view in  hemodynamic  interactions, as  we   use  MOXY  for  information on cardiac hemodynamic   when nw we combine it in our  assessments  with Physio flow.
  This as well will show  one big  difference  between the " classcial" idea  on Stroke volume reaction  and what we  really see live in reality testing.

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Here  some additional info on the   blog   on Cardiac output.
 We  are  interested in this  with MOXY use, as we compare    cardiac hemodynamic  and its connections to   MOXY  trends.
  We   had the info, that CO = HR x  SV.
  What is  for us  as well important  is the fact, that   CO  resp  SV  and HR  depend  on many different  situations. One of them is  Preload.  In simple  terms. The amount of  blood moving back to the heart   can have a direct influence  on SV  due to the  elastic elements    in the heart .  A  bigger   volume return  creates a bigger pre load  and as such  we may see  an increase in SV.
  We often look in this situation as well on EF  %  Ejection fraction  volume or how much  form the total blood in the heart is  pushed out.
 Preload  can have a direct influence on EF.
 So where is MOXY coming in.
 When we  do a 5/1/5    we see the changes   between load  and  rest  in an  interruption of homeostasis.
  If we now  not only look at SmO2   but as well  on how tHb  reacts  we  can see  a  connection with  SV  and HR.
  If we have a vasodilatation   tHb  up  as a   reaction of hypercapnia  ( CO2  ) up we have a  better  blood return  and therefor a higher SV  and as  we   maintain or keep the same CO it  will show up with a  drop or at least  no increase in HR.
 If  we have a  tHb  drop  meaning   a vasoconstriction  due to different reasons  we have  a lower  return  on blood  and a lower  SV  so  we see a  jump in HR.
 If  we  have  an increase in tHb  due to a  venous occlusion  we  have a lower  return  of blood  to the heart, a  drop in SV  and as well an increase in HR.
 We tested hundreds  of   cases  with  the combination of   Physio flow    NIRS  and VO2  and blood  sampling  to see, whether this ideas  really  have some merits.  Now we    can use MOXY  and look at HR  and RF  and often have a very nice   information what we would see with the more   sophisticated  equipment. In the field   or as a coach  you can't   use this equipments  easy   and or  costs  are too high.
 So  with MOXY  HR  and RF  we  have a pretty  cheap  version  easy to use in the field  to   actually get   many of the above in formations in.
  I show you 2  pics   from  many of  our  case studies , where we  tried  and successfully  could manipulate  SV  and   than  where comparing how tHb  and  Hb Diff  would react in NIRS.
 Here 2  examples  just for  fun.
  Than  some  ideas   with LVET  and  filling time   as well as a simple example, how the body will keep a  stable CO  but if you change position you will change HR  or SV.
  Last but not least  a not accepted statement  we did many years back, that there is no(NO) prediction  in what SV will do in a  step test as there are all   different options  depending on limiter  and compensator
  This  are examples  we took  from other sources, as  when we  show our  results  it is not  accepted  at all.    Have fun to  give this some thoughts.

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Some  emails on this topics  and here some answers  .
 1. Yes  SV  will change  due to training ( if  we train and stimulate the cardiac muscle properly ) Great  studies on  cardiac  remodel ling ) The result is   lower  resting  HR  and  higher resting SV.
   see pic  1

2.   A    drop in  resting  HR in a  short  period  ( over night  or the  situation , that you  can't get  HR  up  the day  after an interval workout  or a  long  training  where you most likely dehydrated)     can be a sign of a   higher plasma  volume  as a  reaction on the day before.
  This leads  to a  better  preload  and a higher EF %   and therefor by the same load  and same CO needed  to a  lower  HR  due  to the higher SV.
 ( Influence  of  temperature  on  SV  and Cardiac  output) This is  one other reason, why  using wattage alone is  not an optimal guide  for  physiological training intensities. If you pair  wattage  with some bio marker  you are  far   better off  with information's on what you  stimulate  and what the workout   ends  up with as a  result.  


 3.SV  will  reach a plateau  very early on  and will stay  stable.
  True  that can happen  but you can as well  ( and  most likely in  a healthy  heart ) see an ongoing increase in SV  till to the end of a  test.
 As well   if the cardiac system is a limiter  you may see a drop in SV  at the end of a test. Meaning  HR goes up  SV   goes down  so you may in fact see a   stable CO.
  This  than can lead  to the about  48 %  of  VO2  max tests  who may show  close to a plateau  at the end of a test.
 The other 50 +  %  never   give you a VO2  max   but only a VO2  peak  result.  Here an example of a CO HR and SV info   from a test done   in Quebec  ( University of Trois riviere   by Claude  Lavoie, Andri Feldmann and  the team)
 The  second pic  shows you a great example in the lag time of lactate info  in this test. This test  was   load  and deload  but deload  was not  0 watt  but as you can see  70  watts  and  the load was only done  once,  so no homeostasis disruption info on here as well.

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