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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
We  had over the last  few  weeks  some test coming in with a similar question.
  Very low SmO2  values  so  what can you do. ?  There  are different options.  Here  two of the  most common once
But first remember.

 We use  what we call bio markers.   So  any additional info you have  from a  TIP  5/1/5 assessment  will be used  to see, where and how you may  have been  still in a recovery mode.
The most common info's  you  will have is HR  and  if you are a cyclist possibly wattage.  If you are a runner  you  take  breath per  strides.  So  in your STEI  intensity zone  you may breathe 4 steps in  and 4  steps out  by a HR  145  +-  and a  stable SmO2
As a cyclist you may have HR  135 +-  by a wattage  of  190  at the STEI zone  and a stable SmO2 plus if you are advanced  you may know your respiratory frequency there  per  RPM  so 4  RPM  left count in  and 4  rpm out.

1.  If  you do an  endurance  based  workout  with your  specific zoning idea  you do not worry  about the numbers  but as  mentioned so often you look  at the trend. You can start with a  5 min  " warm  up `by using  wattage  of  HR  and look at SmO2 trend.
  So if your workout HR   is  135 as mentioned by about  190 watt  you may start  with  100 watt for  5 min followed by 150 watt 5 min  an than you go into the  190 +- watt intensity  and you watch  HR  and SmO2 trend.  You stay there for at least  5 - 10 min to stabilize  all and than you make a decision based on the bio marker   on what  wattage level you will  go  with. Than you simply observe  SmO2  to stay stable  and you look at tHb trend as well for  tHb  drift  and HR  drift in combination. We  can  explain later    on how nicely you actually can see physiological reactions by looking at tHb  and HR.  Try  to  think  through what and how the trend in tHb  and HR  will correlate  to each other by a stable  oxygenation (SmO2 ) trend .
 Here a great example sent to us  by Mark  form South Africa, who soon will  have one of the most advanced  cycling centers ready to go.
mark workout thb smo2.jpg 

See the interesting trend of tHb. What  may  be the explanation behind this trend ?  Now  before you look at the  below graph. Think what may happened  to the HR ( CO  ) when tHb is dropping  and why is tHb  dropping ? It  could be  some insight  information in the so often discussed HR  drift?

Mark workout HR SmO2.jpg 


2.  You as well  can use a very different location. for your MOXY. You may out of what ever reason  not like to have the MOXY on your leg muscle.
  You can  even move it on a non involved   muscle location.
 If you do this  always make a 5/1/5  first  with this preferred location plus an activity involved muscle.
. You will see, that for  stable   SmO2  workouts, but as well for HII workouts  you can mount your MOXY  nearly anywhere. There is an interesting  " reflex"  working  in this combination
Like in many other reflex  ( feedback loops) we  need a trigger  to  create a reaction.
  One reflex  we talk a lot is the metaboreflex  where the trigger is a  critically low PO2  situation for the respiratory system ( leg muscle  may steel blood  and as  such O2  )  from the vital  systems  and the metaboreflex  will create a vasodilatation  to  reduce  blood flow to working areas.  Now  when placing a  MOXY on a non involved muscle, we  can get an information on the situation in your working muscles.
 A great  and  optimal supply on O2   in the working muscle  will as well show an optimal supply in the nonworking muscles.
 If we reach intensities, where the O2  supply is getting  somewhat  closer to a limitation for  any physiological system looking for O2,  the  body's ECGM  will have to make some kind of a priority where O2 is needed , respectively where we  can afford to drop  O2  delivery  as it is not needed  and not a  survival  reason to have O2  there.
 So in an non involved muscle group, when O2  delivery to the involved muscle groups  is getting  harder to maintain , as vital system may start to get  somewhat picky  with delivery,  we will see a   vasoconstriction  (tHb  drop )  and as well a  drop in SmO2  ).  the SMO2  drop is  not due to O2  utilization, as we have no  or very little activity in the non involved muscles, but it is in fact due to reduction of  blood volume delivery paired with a  reduction in O2  supply as well.
 Before we see this we see the change in the involved muscle. This than triggers a reflex  situation ( O2    demand in working muscles )  before we get a reaction ( reduced  blood volume  and O2   to the non working muscle. [wink] We  got  an interesting feedback on this  topic 
  :

Thank you. Fascinating that the trends were almost identical, but slightly delayed in the deltoid. I would have thought the deltoid might have changed first in an attempt to shift blood flow and energy to the working muscles.  

 So  as usual  when you get a different opinion  we have to go back and see how our ideas  may be backed up  form existing  studies . In this case  it seems that we  first need a trigger  before  a non involved muscle  will  change tHb  and  reduce  the SmO2  due to less delivery  rather  than that the delta  would  kind of "voluntarily"  decide  to  reduce  tHb  and  SmO2  in case the main muscles  may ask  for  more O2  . It seem : Trigger  first than reaction  as well in this case.
 First here the  picture  of  a n involved  and non involved    muscle moxy assessment.( Case study ) tHb 1  as well as SmO2  1  are   involved muscle  (  Quadriceps )  and  tHb 2  and SmO2  are   non involved muscle  ( deltoideus pars  acromialis )

involved  and not nvolved.jpg 

 Now here some back up from different  studies  supplied  to  us  for reading  by:

hokaido.jpg

"

When the Vo2-power output relation is extrapolated into higher power output, measured V o2 is higher than Vo2 estimated from the relation (Zoladz et al.1998). The higher Vo2 is called excessive Vo2 or slow component of V o2. Ventilation also linearly increases and then exponentially increases with higher power output.

Hyperventilation requires excessive Vo2 (Aaron et al. 1992). However, excessive Vo2 is derived not only from hyperventilation but also from active muscle (Poole et al.1991). At high exercise intensity, it has been shown that muscle sympathetic nervous tone is activated (Victor etal. 1987, Saito et al. 1999). This results in a decrease in blood flow in inactive muscle (Bevegard and Shepherd1966). The decrease in blood flow in inactive muscle may

facilitate an increase in blood flow in active muscle. It means that blood flow into active muscle may be affected by attenuation of blood flow in inactive muscle as well as by an increase in cardiac output. Oxygen supply to active muscle is mainly due to an increase in cardiac output at low exercise intensity and attenuation of oxygen supply into inactive muscle would be added during incremental exercise at high intensity.Finally, maximal oxygen supply to active muscle is associated with both Q max and attenuated value of oxygen supply to inactive muscle. This should determine V o2max. However, the decrease in oxygen supply to inactive muscle has not been examined as a limiting factor of V o2max, probably because it is difficult to measure blood flow even at inactive muscle exhaustion

by a non-invasive technique. Near-infrared spectroscopy (NIRS) is a new method by which oxygenation level in the tissue can be determined. We have examined oxygenation level in inactive muscle during exercise using NIRS (Ogata et al. 2002). We found that the oxygenation level did not change at low exercise intensity but decreased at high exercise intensity after about two minutes of exercise. Since the oxygenation level is determined by a balance of oxygen supply and since oxygen consumption can be assumed to be constant in inactive muscle, the decrease in oxygenation level in inactive muscle can be assumed to be due to the decrease in oxygen supply. Moreover, it has been pointed out that oxygenation kinetics in inactive muscle during exercise is similar to the characteristics of activation of sympathetic nervous system due to exercise. This suggests that attenuation of oxygen supply is due to vasoconstriction in inactive muscle during exercise. "


fitbyfred

Development Team Member
Registered:
Posts: 168
 #2 
Hi, g'morning. The vasoconstriction idea is very well explained and the mechanisms that trip this protective reflex are more easily understood with the tHb and SmO2 graphics you shared. Thanks, Juerg. 

I use this image with endurance clients to help them more easily learn this situation, and thought it may be helpful for others?

photo.JPG

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Fred, as usual, thanks  for the  nice feedback.  Nice  picture  and nicely explained.  Here  another option for the more visual reader. It is a page    from our basic MOXY intro    course  for our local kids here  for the carrier  prep  program.


MOXY metaboreflex.jpg


What is really fun is  to see, that much of what we show here  now as  practical applications  is  somewhere  published as a very theoretical option.
 The main reason is  still the  believe, that we  as  grass root  users  either  are not able to understand the ideas  and or the cost is so high for  NIRS equipment, that it is  just limited  to   research grants  and  studies.  MOXY in fact opens  this  amazing interesting practical application now  to any body  from  individual athletes to  coaches  to small and  bigger test centers  and to teams  and clubs.
 In fact over the last  few  years  we see a   very strong split of  actual real  NIRS / MOXY applications  with realistic use in the field  and in the lab  and a  very  disconnected direction of studies, desperately trying to force  NIRS  information in a crumbling  theory of  lactate threshold  and VO2  max   ideas.
 Instead of  using  all the great  experience  we  collected  over all this years  with  lactate  and VO2  and  looking for  improvement of some open questions the  "classical" ideas  left  open,   we see many studies  coming in  with the same  fascinating idea  to develop a very  healthy imagination to  find a  LT  in combination with MOXY or NIRS.
 Here a very nice  summary form a great group showing in short words  , what we have on this  discussion in  "local ( cellular ) information   and  "global "  systemic  reactions.
  The trigger  starts  at the local  demand  and the potential   compensation may come  from a more  global respond.
   I may show later the above statement in the  attempt to find a LT with NIRS.


Detection of Hypoxia

at the Cellular Level

Laurie A. Loiacono, MD, FCCPa,b,c,*, David S. Shapiro, MDa,c

 

What is the Next Best Thing to Detection of Hypoxia at the Cellular Level?

 

Somewhere between direct detection of hypoxia at the cellular level (ie, biomarkers,

enzyme assays, complex histopathologic analyses) and indices of global hypoperfusion

(ie, lactate, ScVO2, urine output) lies a potentially more practical and economical

method of tissue oxygenation assessment: near-infrared spectroscopy (NIRS).

NIRS is an evolving technology that uses near-infrared light to provide a continuous

assessment of regional, microvascular blood flow and is measured as the quantitative

clinical variable tissue-oxygen saturation (StO2). Biologic tissues are transparent to

light in the near-infrared spectrum, whereas oxyhemoglobin (HbO2) and deoxyhemoglobin

(Hb) have significantly different spectra56 (StO2 5 HbO2/[HbO21 Hb]). This technology

can be used invasively via transcranial or percutaneous catheters, or

noninvasively using cutaneously applied probes.

Hypoxia (n.): a deficiency in the bioavailability of oxygen to the tissues of the body

 

 


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