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Development Team Member
Posts: 1,501
As promised here a  rare inside view  in a  practical  example of  using NIRS  for  rehabilitation or  workout  control.
 It is as well an additional   idea or feedback  to  one of the great seminars  on BFR  ( blood  flow restriction )  and how we  handle  this topic in the real world .
 I will focus on the actual section, where the client  uses  NIRS  for live feedback during the session and how  the  live feedback  will guide  the BFR  workout  in duration  load   length, recovery  length  and   how many repetition on the   actual workout  day.  Nevertheless  as I know  that many rehab specialist  visiting our  forum I will  make an overview    to show it iss not a cook book  and what we involved  till we reached the BFR  stage. The pictures  will  tell more  than words. 
 Stage 1:

Stage 2  most important  stage and step.

Incredible  job  done by  the  orthopaedic  surgeon  and now  the  task  shifts  to get a perfect  physiological rehabilitation  done.


Problem 1
 After  any of this  extreme  accident  the activation or the recruitment of motor unit is a  big challenge.
 There are different options  and each person depending in the trauma  and the post  traumatic stress will  react differently in the way  of finding the  confidence  and ability to  contract the  involved muscles. IN the past 30  + years back we where hoping that electrical  stimulation is  the solution
( Compex). Today  it is one options  but  it is as so often the difference how we look at physiology.
 Electrical  stimulation is  a local  fixed  idea  to contract muscles  and  losses the connection to the Brain.( see  EMS on paraplegic  people ) it  works  for muscle contraction but it  does not help  for   actual muscle control)
So  personally  I  do not use  this in the first place  as I like  whether we have  an actual ability  to trigger  the contraction  form the CNS. In this  case I used right  arm PNF  pattern (some may be this days more familiar  with DNA  pattern or with Spiral pattern )
 This client  reacted best with right arm PNF pattern to overcome the problem of motor unit recruitment. As  feedback  for the client, I use either SEMG  with acoustic signals or MOXY /NIRS  as optical feedback.

Problem 2.
 Motor unit recruitment is one  part and  after we had this  somewhat in control the  next step is  physiological  ability to actually use  O2. Interesting is  that we  have often a decent  SmO2 level  but we see a huge problem to actually desaturate .Same in this case. So  next  step is stimulate  desaturation but  due  to the problem  of  lack of  actual  contraction strength  and non weight bearing situation we have to do this  first over systemic  desaturation. Feedback over  NIRS on  priority  leg muscle  and  any upper body  muscle.

Problem  3.

Now  we start BFR ( blood flow restriction )   with the idea  to  stimulate   O2 utilization  as well as  the well documented  physiological reaction.Tool I use is NIRS and sometimes  SEMG  with acoustic feedback for motivation.

Task  1.
Classical  V BFR  as  you can  see in the webinar  is :
a)  use a  pressure  cuff  system  to   look at  compression pressure. Use a certain  pressure  to  believe or hope  we  actually create a  venous occlusion only  as this is needed  for the  stimulation. For this  we learn cook book pressure  and simple  hope  .
 b)  look  for 1  max  Rep   weight for  100 %  max  strength  and than  use a certain %  of  that  depending on school  20 -  30 %  of  max rep strength.
 Easy discussion on here.   It  can 't be done    and even if we could  find a  1 max  rep   there is  some interesting questions to that.
 So we  do not   find a  20 +- %  load  as well  even if we would find this   how  doe we know  that in this client  this load  really   creates  the  needed  stimulation  and we do not create an  arterial occlusion .
 Than  how  long is  the  load  duration. how long is the recovery duration when we base  the  workout on physical  information ? Even more  questions come up  when we  use BFR  as we see in many gyms  simply  use a  cuff  elastic  and close it off and hope.

So here what we  try to  do as an individual  BFR  workout. We use a simple  cuff  belt  with a  fast release. Than we  sue a NIRS on the  priority  muscles   like in this case  on the  quadriceps  and some times   we may use a second  NIRS on the lower leg like  calf .
 In this case we  simply used one on the hamstrings for this  workout  and  than  some days on the quadriceps  mostly rectus
lets start  and I  try again to us mainly graphs  to show  you the  feedback  and  the workout.

Below is   one workout. In this case  actual pain is the  point  when we stop  in case the physiological feedback  would allow  for more reps Here   the client  stopped  due to  physiological, feedback  after 4  loads. The circle is a closer look  at what happens.

smo2 thb biceps  all  4.jpg 
smo2 thb biceps  closer look  wiht explanation  thb  smo2.jpg 

Green. The client pulls  the occlusion strap on  and  than waits  to see, whether the   pressure  actually  starts  to create a venous occlusion. tHb  is the  trace we look  first  so we  have to see a   slow increase in tHB  due to pooling  as blood  flows in but  nothing  or less goes  out.
 Now  why  do we see a drop in  SmO2 ? despite no activity ? 
Red shows  the  section  of actual  activity of the  target muscle  and we can see the  increase in tHb  goes faster up as well  SmO2  drops. Duration is  till we se a hesitation in tHb   so risk of  actual  arterial occlusion. Here a perfect reaction and wee see an  occlusion out flow in tHb You can see the  immediate reaction of tHb as it is a mechanical  reaction ( in contrast to systemic  reactions  we will   perhaps discuss  once we look  more into depth of priority and non priority muscles.)
 The  delayed  reaction  is a O2 disscurve  reaction  due to  the accumulation of H +  due to lack of  the ability  to get rid of  it during the venous occlusion. For  critical readers.  yes we id  blood test  in the occluded  extremities  to see  how  lactate  but as well pH  and H +  reacted. Than we see the  sharp  increase  delayed in SmO2   as a sign of reloading ability  due  to normalization of the inner  O2   disscurve  situation. Again   easy to   get feedback over    same blood sampling and comparison  on the non involved  side. Blood sampling in  legs  over the  toes.  Summary. We use  the NIRS feedback to see   whether the occlusion tape  has the individual needed  pressure. than we  use   NIRS  to see how long we  can  increase  venous occlusion and  avoid  arterial occlusion and than we    use NIRS  to decide , when the next     load  can start again  and  or  whether we  still do another load.
The  picture  of  an occlusion in a  MOXY print  graph  is  below. As we have no outflow we s will see an accumulation of  HHb  which is higher  than in a free flow where O2Hb and HHB  will be equal. but here we will have  an increase in HHb.

bias  closer look  zones and arrows.jpg

Now imagine how  Biased  or   real  HHb  and O2Hb  races will look  , when we  have  instead of  an integration of  nonpriority  muscles into an activity we actual  have  blood flow regulation  away  from a non priority  muscle.?


Development Team Member
Posts: 1,501
Here  one feedback  t one  mail I got. The  question as a summary  was,  why it  would be crucial  to know , whether we  have a venous occlusion  and not an  arterial occlusion ?

 This is a great  question  and it is not  just a  crucial  question in BFR   training  but possibly even more  important in  any strength  or  HIIT  workouts.

As  so often mentioned.  Any   muscle activity  will need  energy  and in Contreras to earlier believes  we  will  activate  any possible  option to maintain  critical  pO2  as well as defend  a  critical ATP level.  BUT we  will in  a high intensity   load  use  fast  and a lot  of CP ( creatine phosphate ) . Now  CP is   important  as well for a  fast re store  on ATP.  BUT  CP  can only be   resorted   as such , when we  have blood flow  (  so not  under occlusion  situation )  and  when we have a decent controlled  intracellular pH  value. As we have  shown  before  SmO2 is a great indication of  CP   recovery  and we have the  2  section of  fast recovery, if  we have  an optimal blood  flow  or  a  delayed   SmO2  ( CP ) recovery if we  have a respiratory limitation  with a   high CO2  at the end of a  severe load . This s  why respiration  has  often in short loads  less a  function of O2 intake  as more a function of CO2  out put.

 But to have it  better formulated  here  in words  of he  great studies in that  field.

U You can see when you look the  science  behind , why we   look so much on tHb reactions   and less on SmO2  alone.

Resynthesis of creatine phosphate in human muscle after exercise in relation to intramuscular pH and availability of oxygen. Sahlin K, Harris RC, Hultman E.


After exhaustive exercise the muscular store of creatine phosphate (CP) is almost completely depleted. The resynthesis of CP during recovery normally occurs rapidly, but is totally inhibited if the local circulation to the muscle is occluded. The limiting factor for CP resynthesis which could be a low intramuscular pH or availability of oxygen has been investigated in the present study. Biopsies from musculis quadriceps femoris of man were analyzed for pH, ATP, ADP, CP, creatine, lactate and pyruvate. It was shown that resynthesis of CP only occurs when the blood supply to the muscle is intact. From this it was concluded that the creatine kinase reaction is at a steady state or at equilibrium during the period of recovery. The influence of oxygen on the resynthesis of CP was investigated by incubating muscle samples taken after a fatiguing isometric contraction in atmospheres of oxygen and nitrogen, respectively. During 15 min incubation in oxygen CP was resynthesized from a starting value of 4% to 68% of the normal value at rest. No resynthesis was observed when parallel muscle samples were incubated for the same time in nitrogen. It is suggested that the initial fast phase of CP resynthesis is limited by the availability of oxygen whereas the subsequent slow phase is limited by the hydrogen ion transport out


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