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Development Team Member
Posts: 94
OBLA (4 La) correlate EMG correlate HRV (SD1) correlate VT2 correlate EMG/NIRS correlate Thb/SmO2 plato.

Are the variability not only OBLA? HRV trends correlated with some NIRS patterns? Someone in the tried to watch?

In terms of the fact that some have growth, others have a decrease in Thb.
Is there a relationship between these parameters and the parameters of variability at rest and during exercise, after they are performed.

As an example, overtraining can worsen the variability, will this be accompanied by a change in Thb's dynamics? Fall of absolute figures, change of pattern in response to intervals (rise / fall / unchanged level of Thb).

This thought came to me when I noticed that the Thb indicator as a whole falls from excessive overeating, and does not grow in response to intervals, the return to normal takes 24-35 hours.

I have Polar H7, I usually use the android program cardiomood - it's free on the website (not android) allows you to look at the dynamics for 10 or more minutes of all the variability indices, so you can search for the SD1 plateau threshold, download data.



Development Team Member
Posts: 1,501
This is a  fascinating  topic. We did  far before  MOXY a lot of  workouts  with Portamon  and HRV using Bioharness  and Physio flow  looking at cardiac hemodynamic.
The fascinating part is  the  connection between  HRV  and cardiac hemodynamic   but as well between HRV  and  respiratory overload.
So we  separated  cardiac  overload   workouts  and looked  at  thB  and SmO2 trends  and what  cardiac parameters   besides HRV  would change, as well as  we did  severe  respiratory overloads  without  cardiac    or minimal cardiac  loads  and than assessed  the HRV reaction and tHb  SmO2  ( TSI %    and  Hb difference  reactions ). The  first fascinating  information  was, that when we  looked  as well VO2    levels so FeO2 %  and  Et  CO2 levels we  could see, that any calculation of  O2  use or needs in combination  with  VE was not  predictable as we often believe.
 So we can have  50 l VE  and a very different   use of  O2  by the same  person  all depending on  his respiratory pattern and chnage in TV  and therefore  change in %  dead space  moved. You add to this the change in O2  dissociation curve  due to the change in  pCO2  and we  are even more off any calculated  classical  information.
 The chnage in   the respiratory behaviour  than  chnage the    trend in HRV  nearly more  than the cardiac  hemodynamic changes. What  you  can look is  at  the LVET  and you calculate  this  x  HR  so you get what we  discussed ion the forum  the CCT  cardiac contraction time, which is very different in trained  and untrained  athletes, but  which changes as well with cardiac overload. 
There are    possibly  very few  if  any (  can not  find  yet )  studies  done , where they combine all of  this  ( Live cardiac feedback live   VO2  feedback , live  respiratory  dynamic  and breathing pattern , live  NIRS feedback , live  SEMG feedback  and  delayed  blood   ( lactate  and otehr  feedbacks ) see Red bull  feedback on   blood values changes  during squatting on this forum )
The only  big  study I am aware of  is the one   done by Per  and his  Red bull team  in or on sea level death valley and  compared to  high altitude, when they as well had  internal core temperature feedback  and brain NIRS  and different additional feedbacks.
We did   a  few years back this   above combination daily over  many month ( see  forum pics  with   Frank Bour  and others) The simple  reason of all this combination was to understand  how  the correlate  with each other as all is  the same idea  at the end   energy supply and demand and utilisation.
We  than had  the discussion on here on  FTP  / Max Lass  and NIRS  and  had  teh tend  feedback  that   when we have a  relative  stable SmO2  and a  relative stable  tHb  we often see a  relative close  connection with   MAX lass ( Not  4 mmol  [wink]  but stable  lactate  dynamicon any different values) but as well a  relative stable  performance over a longer  time.

Now  why  was this fascinating.
 It  started  to get fascinating, when we added  live   cardiac hemodynamic  and live  VO2  and respiratory  feedback to it.

In  short. Once we   where in a    metabolic  homeostasis  (  name it as  you like  steady  state   for example )  we had in  many  of the  tested  physiological systems a  balanced  situation. 
 Cardiac  parametres  for example.
 Relative  stable HR, SV, LVET, SVR
 Stable  TV,  RF  and  stable FeO2  %  and EtCO2 but as well a very stable  respiratory wave  from  bio harness.( we used  sometimes  2  belts  so we had  abdominal and  apical pattern feedback  to  be more  secure on location of  respiration.
Stable  SEMG in   involved muscles   ( we  sometimes  used  SEMG on auxiliary  respiratory muscles  [wink]

And than we  looked at  Portamon NIRS in three different  depth  so T1  T2 T3  and we had TSI %  and we looked at  tHb difference  as well as  tHb. The tHb diff correlates  very nicely in many cases  with SmO2   we get  from MOXY.
  Now to make a short  story out  of  many month  and   many tests.
 We  started in this   steady states to  manipulate different parameters we had.
 Example  TV  naturally  with respiratory  manipulation  or  artificially  with increase  dead space ( hypercapnia  situation )  or  change in   inspiratory air    with added or  O2  content.
We  did  local  heat or  ice  application where we had  the portamon ( see examples on this forum )   but we as well did systemic    changes in temperature  with  warm  rooms or  outside cold    situation.

The  whole  idea was to simply  forget  theories  and calculation and look  what happens  really.
In  a  short  summary>
 There seems  ( needs  much more independent studies )  a  trend  where we have a feedback  form tHb  and SmO2 trends  whether we have a  cardiac  overload  or a  respiratory overload.  despite the same HRV  reaction.
 So a  change in HRV  we see for  example  after a  heart attack  and  after a  respiratory distress in COPD  has a different NIRS reaction. 
 So  when we in the future  combien HRV  and  NIRS we  may be able to  have  information on  the problem area ( cardiac versus respiration ) In both cases  we see a  problem in the delivery  situation and therefore a  drop in SmO2 but we have  an opposite  tHb reaction . ( Why )

Below  some  key feedbacks in what we  talk above  from this  fun  times. Below a  example  of a  T1 T2  T3  feedback  from Portamon  courtesy  Andrea  from Switzerland  and his  team

yama 3 levels.JPG 
Below   one of  our first combination of MOXY  and Portamon  to see how SmO2  and  tHb difference correlate.

5 m r Port Mox.jpg  green SmO2  purple  tHB  difference

Below  same athlete   manipulate   situation skinny  traces  are T3   , thick are T 1

1 break relatibve nyumbers baised from start.JPG

biased zero first stop  to see 2nd 200 watt.JPG 

est to look is    Yellow trace. Now below   where we  tried , whether we  can manipulate  this trace  as we  go    when ever we like  with different physiological  ideas.

vascularisation and time lag.JPG 

Summary : .
 The  fact that we  can manipulate  the reactions in certain intensities ( Mainly in the OXY  intensity  [wink]  shows, that  in reality this  happens all the time, we simply   do not know  it  and or  do not accept  it as it difference  to many ideas and theories.
This  reactions  are natural   "survival "reaction and kick in to   just do this  , try to maintain as long as possible metabolic  balance.

As  higher the  intensity as more  the  intensity  dictates  this reactions and we loose  control. As lower   the intensity as   more option we  have  to decide what reactions we like to  create.

  This is the fundamental difference  between physiological  guided training stimulation  and performance   dependent, forced uncontrolled but needed reactions.
 This is where I started to forget  ZONING  based on intensities,  but rather in  the     goal or stimulation I like to achieve. 

Thanks for this great feedback  and it shows how interesting in the future  it will be once we have many more  groups looking at  this connection from all different   viewpoints


Development Team Member
Posts: 227
I was experimenting with HRV as well.
Some time ago I did very intensive and long hypoventilation session, goal was to see if I can overload right ventricle without heavy cardio workout, as Juerg suggested we should be able to do it, but it sounds kinda "impossible" He was 100% right, it is more than possible and it is visible when looking at Moxy calibration.
On Jan 15th I had easy session, this shows on Jan 16th in my 10min calibration period:
tHb (brown 3rd from the top) nice amplitude and good recovery during 1 min stop at the end.
Jan 16th

On Jan 17th, 5 hours before my cycling session I did intensive and long hypo-ventilation session, this affected my tHb quite a lot, no initial tHb dip and no increase after 1 min stop at the end, tHb went actually down...(legs were fresh so it was not related to muscle compression etc.)
Jan 17th

I took fairly easy on Jan 17th, and we could see slight improvement(not big but better than day before) Jan 18th I also took easy on that day.
Jan 18th

My RHV showed it as well, I have ithlete app and their ECG sensor as well HRV4training, will try CardioMood as well since it shows data real time.
I'm one of the people who extra stress increases HR variability, I'm always taking reading standing up right after I wake up. 
What I really didn't realized until today, how my HRV increased since I bought Moxy, I use Moxy 10 min calibration routine to guide my day to day load since end of October:

Blue line represents HRV (higher more recovered I am) You can clearly see how my recover increased since I started using Moxy, I'm at the same 60min power and increased by sprint power by quite a lot.



Development Team Member
Posts: 66
How does your 10 minute calibration look like? What conclusions do you see from it?

Development Team Member
Posts: 227
Hi Gunnar,

We had good discussion about it here:

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