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Development Team Member
Posts: 2

Greetings all,
I hope this is the correct location to post my information and experience using SmO2 to monitor the current lifting phase.

Back squats: Phase 3 of 4 hypertrophy period. Lifting four days/week with a full break on Wednesday. Monday and Thursday are heavy lift days (65, 70, and 75% of one-repetition-maximum -1RM). Tuesday and Friday are light lift days (60, 65, and 70% of 1RM respectively.) Each percentile level consists of two sets of 10 to 12 repetitions each separated by 1.5 to 2 minutes of rest.
Stiff-legged dead lifts: three sets of eight repetitions each separated by 1.5 to 2 minutes rest
51 year old, male, road-racing since 2009, firm user of periodization plans and quantified, goal-oriented training

Routine: warm-up with 2 minutes of running stairs and no-load squats at the top/bottom of stairwell.

Here's the results:

P1hwk3 squat sldl.jpg 


  1. Starting SmO2 level (~50-70%) appears as expected at the left vastus lateralis location based on other workouts
  2. The recovery baseline was met in all squat lifts except after the second (~8:19:21) 
  3. The target, or depletion baseline was met in all squat lift attempts
  4. SmO2 re-stock seems to replenish sufficiently, although the trend slope is steeper/quicker during intervals on the bike trainer comparatively
  5. Stiff-legged dead lifts (SLDL) follow the squats after weight change on the bar
  6. The current weight level of the SLDLs do not appear to produce the same SmO2 depletion rate as the squats previously
  7. The SmO2 SLDL re-stock rate seems rather slow compared to the squats rate
  8. Weight bar/rack clean-up occurs after the last SLDL (~8:39)

Monitoring format was based on the guidance from "Moxy Strength Training eBook." Full recovery was used between lifts as a starting point. Unfortunately, my device does not expose the tHb metric, although the text mentions using this metric as a performance indicator. (Would love to have a Moxy device of my own.) 

Warm-up and bar setup ends at about 8:16. One difficulty was the inability to observe the real-time measure of SmO2 during lifting by use of the Tablet software application. The squat rack is outside and exposed to the weather, which in the current Seattle, Washington weather, would likely render the device unusable. Between-lift breaks are controlled with a stopwatch. I think in order to use the other recovery protocols, I would need to observe the SmO2 measures in real-time, or use appropriate stopwatch durations based on re-stock trends for like workouts.

It's likely that I didn't rest long enough after squat #2 in changing weights to the next level (65% 1RM,) hence the insufficient recovery level.


  1. I'm not certain that the depletion target (~43%) meets requirements? Is this target sufficient to cause hypertrophy adaptation? Thoughts?
  2. I think that the SLDLs required their own recovery/target baselines since they are a different lift pattern. Thoughts?

I think I'm generally on the right track in order to achieve the plan intent and outcomes. My plan is similar to last year's; and contains corrections for lessons-learned. Your comments and thoughts are welcome! Thanks for reading.



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Development Team Member
Posts: 1,501
Skipper ,
Thanks  so much  for opening a  discussion in this  section of our  forum. I am  surprised this  did  not happened  earlier on, as  for strength workouts  NIRS is possible  a great choice. No please  do NOT  take  anything I  write here and we may have perhaps a long discussion  and ideas exchange on here personal.
 I am getting it completely on what you do with your training ideas as I was brought up in the hay days of periodization's in Europe.  I  like to start as usual very different tan expected.
 Many many years back I asked  myself the question.
 Does it has r  to be really :
No pain no gain 
Could we replace this perhaps  with 
NO brain no gain ?

Now lets'  start  there.
 The fundamental difference  between a  physiological  feedback  live guided  workout  and a   calculator prepared  workout.
 In a  simple picture e it would look like this

Moxy versus  calculator.jpg

So let's  dive into your great  feedback.

Back squats: Phase 3 of 4 hypertrophy period. Lifting four days/week with a full break on Wednesday. Monday and Thursday are heavy lift days (65, 70, and 75% of one-repetition-maximum -1RM). Tuesday and Friday are light lift days (60, 65, and 70% of 1RM respectively.) Each percentile level consists of two sets of 10 to 12 repetitions each separated by 1.5 to 2 minutes of rest.

Not personal remember.
 But how  do we know  we can  do another workout tomorrow just  from using  numbers  and days ?
 Do we know  whether you  recovered. what's happened when your muscle  after a workout looks like this  here.

eccentric muscle dammage.jpg 

As you can see  from the date  1984 no new  question. This is a  muscle biopsy after an eccentric  overload.
 Straight leg  dead lifts  for example are eccentric  loads  at least  for you hamstrings   and  other muscle groups.  So  timing of  repair  between loads is a very important part of   performance improvement or more important     injury prevention.
 So the timing  can be  figured out  with using NIRS  in combinations  with some other  tools  like SEMG  and  some blood markers  as well. Using this combination  help us to get some ideas, how  to use  NIRS feedback , when we  can not afford all the other goodies.

 So  this  the point of  how often  as a  number versus how often as   physiological feedback.  Next  up :
hypertrophy period

There are  as usual different ideas  on how to load  to create hypertrophy. The common discussion is   done in %  calculation, as we all do or  id  based on 1 rep max load. As  all  max loads  1  rep is  a very mentally  changing  number and highly depends  on  daily motivations. And much more
Where most agree is  that the load  should bee  65 %  and up  from your  1  rep  max. The hyper trophy  takes place  so  empirically this seem to work inmost of us  .

 The  one reason , which seem to trigger hypertrophy is  HYPOXIA

  Here a great   short   info  on this

Hypoxia increases muscle hypertrophy induced by resistance training.

Nishimura A1, Sugita M, Kato K, Fukuda A, Sudo A, Uchida A.

Author information

  • 1Department of Orthopaedic Surgery, Mie University Graduate School of Medicine, Tsu City, Mie Prefecture, Japan.



Recent studies have shown that low-intensity resistance training with vascular occlusion (kaatsu training) induces muscle hypertrophy. A local hypoxic environment facilitates muscle hypertrophy during kaatsu training. We postulated that muscle hypertrophy can be more efficiently induced by placing the entire body in a hypoxic environment to induce muscle hypoxia followed by resistance training.


Fourteen male university students were randomly assigned to hypoxia (Hyp) and normoxia (Norm) groups (n = 7 per group). Each training session proceeded at an exercise intensity of 70% of 1 repetition maximum (RM), and comprised four sets of 10 repetitions of elbow extension and flexion. Students exercised twice weekly for 6 wk and then muscle hypertrophy was assessed by magnetic resonance imaging and muscle strength was evaluated based on 1RM.


Muscle hypertrophy was significantly greater for the Hyp-Ex (exercised flexor of the hypoxia group) than for the Hyp-N (nonexercised flexor of the hypoxia group) or Norm-Ex flexor (P < .05, Bonferroni correction). Muscle hypertrophy was significantly greater for the Hyp-Ex than the Hyp-N extensor. Muscle strength was significantly increased early (by week 3) in the Hyp-Ex, but not in the Norm-Ex group.


This study suggests that resistance training under hypoxic conditions improves muscle strength and induces muscle hypertrophy faster than under normoxic conditions, thus representing a promising new training technique.

 So  here is  where we   now  with live feedback  of  NIRS have a great step forward.
 a)  do we  create a  hypoxia
b)  how  do we know  the SmO2   value  shows  hypoxia  or  the muscle will have to go hypoxic  with the load  I apply ?

 Here a  case  study  from our  own  kitchen  done by a student  from UBC ( university of  BC)  during his summer break in my office  . Nick Mc Lean.

We  assessed maximal  contraction force using SEMG  and NIRS. Than we loaded  different %  of   max NIRS  activity to find out   how Rhonmerts idea of   reduction in  blood flow due to muscle compression really looks in reality. So by  what % of  contraction force do we see a reduction in blood flow  due to  muscle compression.
 Here the result  by 67 % of  maximal  contraction force  and what we see in NIRS
67 % iso.jpg 
The vertical line is where he  quit( his decision)
 Green is  as usual SmO2  %.
Blue is  HHb  (  deoxygenated  Hb /Mb)
Red is O2Hb  so  oxygenated  Hb  /Mb
Purple  kind is  thB   ( total hb /Mb)
You can see  SmO2  simply indicates, that he used   immediately  O2  . (  which  asks the critical question of  " anaerobic"  versus newer ideas of O2 immediately involved in any activity )
More   fun is to  follow tHB trend.
 Look carefully. Do you find
 a)  compression outflow  ?  Or  as we discussed perhaps  better  reduction of tHb  or  reduction in blood volume.
 I like from a visual  point n of view the wording  outflow ( but it may bee wrong )
b)  thb increase.  " outflow restriction  due to  higher compression force  form outside /muscle contraction , than vasodilatation effect  form CO  and other vasodilatation options.
c) complete occlusion  situation. and  already   motivational  problems  or  brain protection  and early  release of  complete  occlusion till hee gives  up.

 In a  subsequent  forced occlusion test he was able  as he  had  no choice  to drop SmO2   down to 0 %  so very low.

 Was he  hypoxic ??

We  will  get  back to this perhaps But  first  stay  in general.  NIRS:
 SmO2  alone  can give some indication but it is not a great way to control  strength loads as  suggested.
What we know is that trained  people  working on these idea of  hypertrophy  can desaturation  very low. meaning that they really  go very low on O2  content  so  hypoxic. Now  as in the article  you can do this  very local on a muscle group  or you can do it systemically.  a) locally . You have to   see, how your workout  improves the drop in SmO2. The bets way to  force  SmO2  to drop is  to be able to create  an occlusion.  To see, whether you are able to do this you can use tHB trends.

See below  an example of  squatting.

3 squatting smo2.j thb pg.jpg 
Green is  SmO2  , yellow/brown is tHb trend #  sets  and  than the body  told us , that's it. 
Extreme  version.
 Numbers versus  physiology.

 Physiological guided   workouts  are mentally  hard  to do. You do not know  how many sets  you will have to  do, you do no t know how long rets in between you do not know  how often during the week.

You really know nothing.
  Now   workout based on numbers. You know everything  what  concerns  the  operation organisational   plan. How much do you know what really goes

on ? Why  10 -  13 2  reps , why  1 min break    and so on. Physiological guided workouts  are  very short if the gaol is  to deplete as low as posisbel and as fast as possible. They  can be very  long if you do not push yourself  and than change the idea of stimulation. What we know is , that   stimulation of GH  growth hormones  are  not based on  number of sets  but intensity of load. and possible  % of  muscle mass involved in  total body  workouts  versus isolated  body workouts.

GH hprmon and intervall.jpg 

So this leads  us  to a first summary.
 Strength workouts  are  based  when you use physiological feedback like NIRS on your goals setting as usual.

1. Do you like to  keep   delivery somewhat open  so tHb  may  drop only.
 2. Do you like to  keep inflow going but create a  stop in outflow   than tHB will increase  till you quite. Immediately after you quite you see a  drop in thB  as a sign of a  outflow  after occlusion or  outflow restriction.
3. Do you like like in your case to create a  Hypoxia  for triggering  hypertrophy   you can do that over  a local  reaction or a systemic  reaction.
 No  you have to create a  stable tHb  ass a feedback of an arterial occlusion. or you  have to be able to  drop  SmO2  not just locally  but systemically as a sign of a  hypoxia  generated  in the systemic  circulation. For this you can sue  one  NIRS  and one SpO2  sensor.  or  2 NIRS one on the involved  muscle group  and one on a minimal involved muscle group.  At the end the workout  would look.
Squatting to exhaustion  weight unimportant . As  heavier  as faster you may desaturate  as you can easy  cravat an occlusion but as faster you may cheat as well and get injured.

How many sets.
 : depending on the goal. Do you like to  recover back to baseline. ( complete recovery
do you like to over compensate
 do you like to incomplete recover
 Below  2 of the three options  :
 what is what ?

Both  examples    from NEXT Level  coaching Brian Kozak  One  form a  swim workout  in thee water  using NIRS  and one  from an ice hockey  ion ice  workout. Simply  looking  at metabolic recovery

3  loads SmO2    decrease  low end.jpg 

swim ipahr.jpg 

What  does  NIRS  SmO2  tells us in metabolic feedback ?

A brief review of the use of near infrared spectroscopy with particular interest in resistance exercise.

Pereira MI1, Gomes PS, Bhambhani YN.

Author information

  • 1Departmento de Educação Física, Universidade Gama Filho, Rio de Janeiro, Brazil.


There is growing interest in resistance training, but many aspects related to this type of exercise are still not fully understood. Performance varies substantially depending on how resistance training variables are manipulated. Fatigue is a complex phenomenon usually attributed to central (neuronal) and/or peripheral (muscular) origin. Cerebral oxygenation may be associated with the decision to stop exercise, and muscle oxygenation may be related to resistance training responses. Near infrared spectroscopy (NIRS) is a non-invasive optical technique used to monitor cerebral and muscle oxygenation levels. The purpose of this review is to briefly describe the NIRS technique, validation and reliability, and its application in resistance exercise. NIRS-measured oxygenation in cerebral tissue has been validated against magnetic resonance imaging during motor tasks. In muscle tissue, NIRS-measured oxygenation was shown to be highly related to venous oxygen saturation and muscle oxidative rate was closely related to phosphocreatine resynthesis, measured by (31)P-magnetic resonance spectroscopy after exercise. The test-retest reliability of cerebral and muscle NIRS measurements have been established under a variety of experimental conditions, including static and dynamic exercise. Although NIRS has been used extensively to evaluate muscle oxygenation levels during aerobic exercise, only four studies have used this technique to examine these changes during typical resistance training exercises. Muscle oxygenation was influenced by different resistance exercise protocols depending on the load or duration of exercise, the number of sets and the muscle being monitored. NIRS is a promising, non-invasive technique that can be used to evaluate cerebral and muscle oxygenation levels simultaneously during exercise, thereby improving our understanding of the mechanisms influencing performance and fatigue.



Development Team Member
Posts: 168
Skipper / Juerg, hi. I second, it's great to read some activity from the ST topic.

I do a little MOXY guided ST at my gym and usually process like this:

15 min. Client warm up period for calibrating individual oxy/deoxy levels

60-75 min. Client is coached within live display of muscle oxy/deoxy range


1. Load to the minimal SmO2 level achievable, try to maintain for a rep or two at most and move to recovery (usually see a deflection of SmO2).

1. Recover back to highest SmO2 or 'warmup level'.
2. Recover briefly to stay below SmO2 'warm up level'.
3. Recover longer to see if we can "overshoot" the SmO2 'warm up' level.
3a. Load as soon as we see an "overshoot" of the SmO2 'warm up' level.
3b. Load after the SmO2 "overshoot" decreases and again client reaches the SmO2 'warm up' level.

Volume for each ST exercise:

Move to next exercise/lift when no longer can reach SmO2 'warm up' baseline level within a sensible reload period... 


Move to next exercise/lift in sequence when no longer can reach greatest DEOXY level, despite best effort to maintain proper/safe lifting.

Inter Set / Intra Workout Variations:

Explore both break down sets and progressive loading increases with limited recovery to further decrease SmO2 Level

As mentioned in other topics... we now try to move the focus of lifting exercises from intermuscular - intramuscular.

Juerg mentions below that hypoxia is one of the main mechanisms associated with hypertrophy outcome.

I'm curious to discuss this idea of hypoxia-induced hypertrophy a little further from a perspective of tHb trends and wonder if the hypertrophic effect will be best from a series of workouts using an increased tHb (muscle pump) load OVER a series of workouts using a decreased tHb effect (muscle compression outflow) load.

Thoughts ?       

PS, I mostly work with non-athletes and generally see the tHb drop 9 of 10 times during most lifts when we first get started.

Development Team Member
Posts: 1,501
As mentioned in the article  and as we  do since many years. we choose two option.
 1. Local hypoxia
2 systemic  hypoxia.

1. local hypoxia 
  is used  when we  do rehab on specific  target muscles . so  little  coordination is involved. This is a great idea  for rehab, as we often can do  full muscle  slings  or muscle chains  yet due to  restrictions like  weight bearing  or   other forces  which may be not  applied in that stage.
It is not  a great  idea of strength  for health  but as well as  for sport, as it  completely misses the neurological as well as  dynamic  motion pattern.  Sorry  big  fitness chains, but I  believe the development of  this huge   gyms  with  this huge  equipment collection  is doing minimal  to nothing besides being a good business  for   overall health  and prevention in our population. It may not even be true  that it is better than nothing  (  Smile ) I  just  can't see the physiological value of a biceps  curl  equipment for a few thousand dollar  to make a single  joint single  movement pattern as a    progress in our  health  and fitness promotion.  Movement  have to be  as soon as  possible full patterns  of  natural  motions  to actually benefit    from the workout. We name it DNA  as a  pattern  which  shows up in any movement  with a natural  idea  and will run in a  kind of a  spiral motion like a DNA  pattern. So I do not think a  cyclist  benefits  relay  from a double leg  squatting for his  sport that great.  He needs a DNA pattern.
 Same with many other sports.
 The interesting part is that  the sport  where we  see thee most amazing strength  development and  ability to move the  body is  gymnastiques.  Non of this world  class  athletes  ever sets a  foot in a  gym  to lift  weights. Exception again if they are injured you may  have to make some exception  for  some time. So  when we do local  hypoxia  wee  initially trry, whether the contraction force in the  target  muscle  can create arterial occlusion  so that we   can  deoxygenate  down  so we have a  hypoxic reaction. Now  I have two option if  I can no yet create this  contraction force  like in beginners.
a) I  add some restriction  in delivery  to it  and monitor.
b)  I  create a insufficient  bio availability  for  O2

2. Systemic  hypoxia.
 This is used, when I work in our  DNA pattern.
 I  can again have tow  options.
a)  create first a hypoxia  and than immediately follow  with the  exercise
 b)  create the hypoxia  during the exercise.  Now  I  can create hypoxia  two  way's
1. By  really  stimulate  utilization  so I  drop SmO22  as far as possible  .
2. I  reduce  the bioavailability  of  O2  so SmO2  will actually increase during the load

 So  many options   to  do that.  I often  do  2   sets  +-  sometimes  just one set  for one DNA pattern.
 Sometimes  two  just to confirm  really that the first one  did its  job  and overloaded.

So  therefor I  often  do not use the recovery  of SmO2 but I often use the tHb  trend in recovery. Occlusions  tend  to  create  an increase in tHb  after each load.

occlusion reactions.jpg

Now this is the case, when we  do  an actual  occlusion   artificially. In a natural  created  occlusion  we have a different reaction after we let go  with a much more pronounce  occlusion  outflow  due to the integration of a much higher CO.

 The  small problem is , that lab  work  and studies  have  to  do this  as of yet  as  in the pats  there are very few studies  looking  at the  blood flow  or volume reactions  besides  what we  do  practically. There is  one nice  newer  study   recognising  some problem  with blood flow.

Too bad  that they  did  not look  at tHb as they  had all there to  see it.

Evidence for restricted muscle blood flow during speed skating.

Foster C, Rundell KW, Snyder AC, Stray-Gundersen J, Kemkers G, Thometz N, Broker J, Knapp E.


University of Wisconsin-LaCrosse, 54601, USA.



We have previously hypothesized restricted muscle blood flow during speed skating, secondary to the high intramuscular forces intrinsic to the unique posture assumed by speed skaters and to the prolonged duty cycle of the skating stroke.


To test this hypothesis, we studied speed skaters (N = 10) during submaximal and maximal cycling and in-line skating, in both low (knee angle = 107 degrees) and high (knee angle = 112 degrees) skating positions (CE vs SkL vs SkH). Supportive experiments evaluated muscle desaturation and lactate accumulation during on-ice speed skating and muscle desaturation during static exercise at different joint positions.


Consistent with the hypothesis were reductions during skating in VO2peak (4.28 vs 3.83 vs 4.26 L x min(-1)), the VO2 at 4 mmol x L(-1) blood lactate (3.38 vs 1.93 vs 3.31 L x min(-1)), and cardiac output during maximal exercise (33.2 vs 25.3 vs 25.6 L x min(-1)). The reduction in maximal cardiac output was not attributable to differences in HRmax (197 vs 192 vs 193 b x min(-1)) but to a reduction in SVmax (172 vs 135 vs 134 mL x beat(-1)). The reduction in SV appeared to be related to an increased calculated systemic vascular resistance (354 vs 483 vs 453 dynes x s(-1) x cm(-1)). During maximal skating there was also a greater % O2 desaturation of the vastus lateralis based on near infrared spectrophotometry (50.3 vs 74.9 vs 60.4% of maximal desaturation during cuff ischemia). The results were supported by greater desaturation with smaller knee angles during static exercise and by greater desaturation and accelerated blood lactate accumulation during on-ice speed skating in the low vs high position. The results of this study support the hypothesis that physiological responses during speed skating are dominated by restriction of blood flow, attributable either to high intramuscular forces, the long duty cycle of the skating stroke, or both.



[PubMed - indexed for MEDLINE]

 Here is  an example of  an ACL  recovery  patient  where we  have different levels  of  contraction strength so  occlusion is reached with a  very different pattenr  yet  and he is ready to go back to   high performance sport  when this pattern is  equal.
 If he  goes to early  high riks  for a  reinjured situation



Development Team Member
Posts: 1,501
I had  some  e mail exchange  yesterday  after my comment on here  with some interesting  people. Discussion point.
 How  low  SmO2  should drop  and  how long  should it stay  that low ? Here is  where  many have to understand the limitation in a local  NIRS application  and how  a local respond  connects  to a systemic  situation.
 If you go to the long discussion we  had  on U  shape  tHb trends  you  see what I mean.
 There is a  idea  out there  we all leaned    and that is the   great idea of the Fick equation. What we  as well know  now  is that the  Fick equation  is a feedback  forma  systemic   point of view.
But there  is  more and more evidence, that there is a very   great local   reaction on blood  flow or better oxygenation   ability  build in  our  physiological systems  so that O2  is  getting there  where it  is  most needed.
 Now  there is a difference  when we look at  local muscle strength  with small muscle groups  or individual muscles  involved  as pointed  out  and  systemic    workouts  so whole muscle chain involved  like a DNA  workout.
When we look blood  flow regulation and O2 delivery in  endurance sport  we have to look  at the much bigger picture  than when we look a local biceps  curl. On the other hand when we look  bigger  muscle chain  workouts we  are getting much closer or equal respond  as we  get with endurance  loads.
 Here  as a repetition  for strength coaches  on the systemic  view .

Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?

Calbet JA, Joyner MJ.

Author information

  • Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira s/n, Las Palmas de Gran Canaria, Spain.


In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [approximately 300 mL (100 g)(-1) min(-1)], but the pumping capacity of the human heart is limited to 20-25 L min(-1) in untrained subjects and approximately 35 L min(-1) in elite endurance athletes.

.  This means that when more than 7-10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when approximately 80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure.


So  what I  think  and see form years of  using this idea is, that hypoxia  alone is not  an optimal  tool  as  we may see a  reduction in recruitment pattern  when we  stay too long in a  hypoxic  or  very low  SmO2 situation.
 Now is the SmO2  " good  " or  bad  when low.
 It all depends on tHb. If  I have an arterial occlusion I  will  lower SmO2  due to delivery stop  and as  such  I  may loose  an optimal  feedback on SATP levels  and too long  may be bad on a  low SmO2  level. What as well happens here   is the at we see a  reduction in SEMG activity most likely as a protection to reduce  ATP  use  as long as possible to maintain a  stable mingle needed level  for survival of the cell.
  If I look  low SmO2 levels in systemic   workouts  and I have a  still  normal  or open  tHb  reaction than  I  do not worry  at all. What we often see is a  flat SmO2  a  flat but still  same level SEMG  and we may see  an overall  reduction  or no further increase in performance. But  what we often see if performance is still improving is  an  additional inter muscular    help  form other muscle groups  who  can support this  movement  Now  you can see why I lie to have SmO2  and tHB in the same  picture One  for  metabolic  feedback situation SmO2  and  how much  I have left in the tank   to give me an option  to push more as I may be able  to utilize more  or whether I  simply  are balanced but no  further chance to increase   performance  and tHb  which gives  me  feedback on volume  or  thB concentration change in the   observed  area.

Development Team Member
Posts: 2
Greetings All,
Thank you for your thoughts and references. I hope my interpretations in the following outline are reasonably correct. The items are in no particular order:

  • Recovery

o    At the system level

§  Quantification is difficult. I know of methods such as:

·         Rated perceived exertion (RPE)

·         Morning heart rate compared to average or baseline

·         Heart rate variability tracking and comparison

o    At the locomotor/peripheral level

§  Possibly subjective, such as “Ouch, my legs really ache this morning.”

§  No other method known to me

  • P1h lifting plan is similar to the Kaatsu test method
  • Dropping SmO2

o    Locally/peripherally

§  Best way to drop SmO2 locally is to produce an occlusion

§  Best way to detect an occlusion is to observe tHb trend

§  Occlusions tend to increase tHb after load

o    Systemically

§  Options to produce hypoxia

·         Stimulate utilization to drop SmO2 as far as possible

·         Reduce the bio-availability of O2 so SmO2 actually increases during load

§  Hypoxia alone is not an optimal tool regarding the recruitment pattern as a protection to reduce ATP use

  • Pituitary gland secretes GH based on intensity of load (>65%? 1RM)

After re-reading your responses and references, I asked myself "What one change can I make to improve my method based on my new understanding?" It appears that stimulating a hypertrophic response can be likely done by producing work at the muscle(s) of interest under a system hypoxia. I thought a conservative test change (incomplete recovery/reduced bio-availability of SmO2) would be to reduce the recovery time from 2 minutes to 1 minute between sets. Reader, please note that my device does not provide access to tHb measures, only SmO2.

Figure 1. The workout before:
P1hwk3 squat sldl.jpg 
We can see that squat SmO2 level recovers to the baseline in Figure 1.

Figure 2. Reduced or partial recovery
In Figure 2, I performed a static, non-movement measurement with my device for 3 minutes, then a warm-up for two minutes before moving to the squat bar outside my home (denoted by "1".) Unfortunately, when I finished and downloaded my data file, I noticed that my device attachment to my left VL was faulty, which produced the "signal loss" areas in the graph.


  1. In Figure 2. I see that the reduced wait-time between sets did not allow SmO2 to recover to Figure 1 levels. So maybe this change contributed to a beneficial, (local) hypoxic condition contributing to hypertrophy?
  2. In Figure 2, should the recovery baseline point be located at the end of the warmup period ("red line")? If this is correct, then isn't my recovery excessive for a local hypoxia to occur?

As always, thank you for your thoughts,

csv NextWorkout.csv     



Development Team Member
Posts: 1,501
Nice  and great summary.
 Not  a lot  to add to the summary.
 There are   different options  you can look for systemic  recovery  and less optimal once  for local recovery as you point  out. I  showed  somewhere in the forum   how we assess recovery  for endurance   sports.

What  can  you do different.
 Well if you are successful do not change anything.
The feedback  form the SmO2  form your squatting is hard  to   analyze as we do not knwo , whether you actually had a chance to be hypoxic  or  drifted  towards  hypoxia.  A  dropping SmO2  indicates a  higher utilization than delivery  at that  time in that muscle.
 So  as the word  says  higher utilization , but u you still use  O2.
 There are  some fun practical approaches  we did in the past  with lactate believers  and people  using a  dropping SmO2  as  an indication of  lactate increase( Boulder  Colorado workshop ).. It is  easy to show , that we  can  drop SmO2  and  when we create this situation we use  more O2  and we  may see  lactate actually dropping and not increasing.
 So a  dropping  SmO2 ina  squatting  ca mane , great O2  use   or it can mean  problem with delivery  and  you move towards a  hypoxic  direction.  tHb  will tell you this  whether you load  that you can achieve a  hypoxia  or whether you load  and   create  perfect O2 utilization stimulation. Depending of your goal you like to see  one or the  other. In fact  I use   often the opposite  situation  to be sure I  can go hypoxic . I  try  during the load  to stop SmO2  drop  by  changing O2  bio-availability in the system  and a s soon this happens I  load  to create an arterial occlusion  either  with muscle contraction if  possible or  with  a  specific  pressure    pump system . With  athletes  I never use a  cuff system always  their  ability to contract.
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