Development Team Member
Registered: 1380484167 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: accident. 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. 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. 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
Registered: 1380484167 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