Development Team Member
Registered: 1380484167 Posts: 1,501
First again thanks for the great feedback and input.
Allow me to go perhaps step by step so it is not a dialogue between you and me, but hopefully we can contribute to some additional thoughts for more regular and new readers here. As you will and all readers see : What I often get is the question: Can you not make it simple as a number or formula. Answer sure we can do this . We can just look at a specific trend in a step test and than assume ,where ever there is a clear optical drop in SmO2 there is your critical point and depending on what we like to sell, we name it what is easy to sell, like lactate threshold or VO2 max as most people phoning us for testing ask for a VO2 max test or a lactate threshold test. I than try carefully to tell them , that this is great for my bank account as it is easy to do. The software spits the " magical " point out and the software makes the % calculation , you pay and go and the deal is done. ?? We all do this and we all sell it. On this forum we try not to sell anything but rather open a fair discussion or debate. Now in debates when absolutely perfect we have an opinion, we try to back it up and if good enough we may have a positive debate and add to each others idea. That means including for us, that when the debate shows, that the opposite ideas have a much better foundation, that we are willing to look at it and in some cases we may have to give up our own what we thought strong point. A debate is as you stand naked here and you show all what you have. the risk is that you have to give up sometimes and sometimes you gain. This is what we like to do with MOXY. Not a desperate defending on our ideas and equipment but a fair open debate in the hope that we can give up our own EGO in many cases, where we still lack information. So not a shouting match but a decent debate on what we like to show with NIRS. The shouting debates are in full swing here in Canada for election and looking once in a while south than they have the same "debates" no space for discussion but senseless story telling with a basket full of empty promises. Hope we do a slightly better job here. Most regular readers , or thinking readers who show up regular here know by now , that we have more questions than answers as there is no such thing like a magical statistical number. I am absolutely convinced that earlier than later some companies or somebody will come up with this magical point and will make lot's of money ( For a while at l least). There was a great article in the early 1990 in the journal of Chest on what I describe her. If you read it very very carefully than you see , what NIRS may actually achieve , what the classical ideas where at that time not able to achieve. Chest. 1997 Mar;111(3):787-95. Dangerous curves. A perspective on exercise, lactate, and the anaerobic threshold. Myers J 1, Ashley E. Author information 1Cardiology Division, Palo Alto Department of Veterans Affairs Medical Center, Stanford University, Calif, USA. Abstract
A number of general observations can be made from these recent studies. Lactate is a ubiquitous substance that is produced and removed from the body at all times, even at rest, both with and without the availability of oxygen. It is now recognized that lactate accumulates in the blood for several reasons, not just the fact that oxygen supply to the muscle is inadequate. Lactate production and removal is a continuous process; it is a change in the rate of one or the other that determines the blood lactate level. Rather than a
specific threshold, there is most likely a period of time during which lactate production begins to exceed the body's capacity to remove it (through buffering or oxidation in other fibers ). It may be appropriate to replace the term "anaerobic threshold" to a more functional description, since the muscles are never entirely anaerobic nor is there always a distinct threshold ("oxygen independent glycolysis" among others has been suggested) Lactate plays a major role as a metabolic substrate during exercise, is the preferred fuel for slow-twitch muscle fibers, and is a precursor for liver gluconeogenesis. The point at which lactate begins to accumulate in the blood, causing an increase in ventilation, is important to document clinically. Irrespective of the underlying mechanism or specific model that describes the process, the physiologic changes associated with lactate accumulation have significant import for cardiopulmonary performance. Thus, any delay in the accumulation of blood lactate which can be attributed to an intervention (drug, exercise training, surgical, etc) may add important information concerning the efficacy of the intervention. A substantial body of evidence is available demonstrating that lactate accumulation occurs later (shifting to a higher percentage of Vo2max) after a period of endurance training. In athletes, the level of work that can be sustained prior to lactate accumulation, visually determined, is an accurate predictor of endurance performance. Presumably, these concepts have implications related to vocation/disability among patients with cardiovascular and pulmonary disease, but few such applied studies have been performed outside the laboratory. Blood lactate during exercise and its associated ventilatory changes maintain useful and interesting applications in both the clinical exercise laboratory and the sport sciences. These include metabolic acidosis, impaired muscle contraction, hyperventilation, and altered oxygen kinetics, all of which contribute to an impaired capacity to perform work. However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science. The red section tells you what I mean , looking for " acidosis " so O2 diss curve shift influence of SmO2. Impaired muscle contraction looking at tHb reactions Hyper ventilation looking again on tHb reaction and SmO2 due to O2 disscurve shift. altered oxygen kinetics due to all what we talk about when we talk about limiter and compensator . However, the mechanism, interpretation, and application of these changes continue to rely more on tradition and convenience than science. Perhaps not anymore or at least not as much as it did in the past thanks to combination of cardiac , respiratory, muscle contraction and other feed backs, which can show up sometimes very clear sometimes more hidden in NIRS data collection. So let's stick here with our own critical interpretations with sometimes more than one option to work on , but than we can go and try and test and see live, whether the idea is a good one or whether we have to reassess once more. So in this way we go through your many great points below. So do not be surprised if more questions show up than we had before we started this. Point A. have re-read through the posts a few times now and I feel like I have a much better understanding now about the theory of looking at the cardiac limiters/compensators, I think the concept is clear but just to be sure. . We do NOT look for just a cardiac limitation or compensation, This is one possible limitation of many. Here some pictures from the ide a of feed back loops and we may for sure forgot some. A as I can recall critical voice form UK from a cycling coach gave some great hints in that direction. He argued with right, that we can not blame the limitation just ion cardiac respiratory or muscular reasoning. Absolutely true and you can see that there are many more feedback loops. Interesting enough the same reader ask to make it much easier so SmO2 goes up it means this and down it means that. Well you see, where we have our own contradictions and that is good. We can start easy but have to accept , that there may be much more option which have to be discussed. So therefor let's go back with this in mind to the easier model . Now I use this here due to : I am somewhat stuck on the differentiation between muscle limiters as in your isometric biceps example. Are these different limiters or are these just description of the 'phases' during muscle limitation? Absolutely great point. We will have many great feedbacks here. We can always look at it from different directions. Let's see whether I can get that clear through. In your feedback Isometric muscle contraction. LIMITER: a) could be the delivery system really and not the muscle contraction, as the contraction is so string, that it overrules the pressure from the delivery system. b) in fact when looking form a muscle contraction quality point o f view, than a perfect arterial occlusion would be a perfect good muscle contraction so strong , that you close up in and outflow. tHb will be stable. The bad story from this stable tHb is , that it means either no flow ( occlusion ) so blood volume does not change due to no inflow and no outflow. or perfect flow !!!! Where do we see what is what : NO flow means that no matter what you do like nothing ( occlusion test ) or a hard load SmO2 will drop. In case of nothing no activity it will drop slow , in case of high intensity activity if will drop fast. Unfortunately that could be the case as ell when we have flow in cases, where delivery is lower than utilization. So we have to look at either when we let go the load and hope for an occlusion outflow. There is one rare but possible situation, where the re is minimal or no clear out flow ??? What situation is this.??? Now when we look a " general " reaction than when we look at art occlusion created by actual very intense contraction the SmO2 drop is very rapid compared with a drop in SmO2 due to lower delivery than utilization. We are talking in the range of 10 - 15 seconds to end the load versus minutes to end the load. So are there different LIMITERS : Yes and you can see how we look at this question. Again form a different point of view in the isometric contraction of the biceps. question : delivery limitation , when looking from a point, where we hope we can go for a while, so when we create an occlusion than we have not enough vasodilatation to overcome the compression, so it could be a cardiac limitation. But if we have a great cardiac system and we still see an occlusion trend or a very strong compression trend , than we could have a muscular strength limitation . So an increase in absolute strength ( max strength w) would reduce the % of maximal contraction force by a given load and the cardiac out put may have better chance to actually keep blood vessels open. Rhomert and other we showed somewhere but here just as a rep. Very old overhead from a presentation I gave in Spian ice ages back ( wow I am getting old ) So as you can see we can take limitation form tow or more areas. If we have a occlusion trend than it can eb muscular maximal strength weakness for example or it could be cardiac output weakness but they feed each other . A reduction in blood flow due to muscular compression educes back flow for a good preload and as such the SV will drop and as such CO. How can we look at this. A ) HR If HR can go up we can maintain CO ( HR x SV ) . or possibly better with the 5/1/5 idea. I If the CO is great, than at rest we see a great overshoot of tHb as it opens all compressed blood vessels due to no existing contraction at rest. If we have no overshoot just base line than we may have a vascularisation limitation or a CO limitation ( or as in some cases an athlete who dories not relax Now additionally we can look at trends in less involved muscles . So a cardiac limitation wil, show up as a drop in tHB at rest in minimal involved muscles as the e weak CO can not maintain the BP.. We will back here many more times. Summary. Yes different limiters but look at what you lie to achieve and what question you have. Isometric biceps and good or bad to have an occlusion . Here is where you add performance. Same contraction strength a few weeks late r and no occlusion than you know you made progress as you now have a delivery ability and will be able to maintain the same grip strength over a much longer time. Yes in some cases it sounds crazy . Example motocross or MTB downhill forearm pump or rock climbing. More strength more contraction . Yes but by the same strength in the grip less occlusion if the h maximal strength is higher. Hope it makes sense Next up we go further down in your feedback but ask back here so we not get lost.
Development Team Member
Registered: 1380484167 Posts: 1,501
Part 2 of some additional add on or better trying to explain it hope fully better. Here the section I try to address
" I can see that as the subject starts the contraction the increase in tHb indicates a pooling due to the overwhelming peripheral resistance from the muscles which I connect to a venous occlusion. However I donâ€™t quite understand your other terminology. Are you saying that during the first rep the compression of the muscle forced the blood that was in the muscle out, creating a drop in tHb . I think we are looking here at the biceps contraction. I hope it is this section you had your feedback and questions on " terminology" Let's see whether I can add some more feedback as your explanation with the garden hose as mentioned is exactly what we try to use. 1. Time 860 green down arrow green line This is his first biceps contraction.. We see very often , that the first contraction is of a different " quality " than the follow up contractions. Same with SEMG and that's why we are relative confident we can explain what happens. The SEMG activity in the first contraction has very often a lower amplitude than the follow up contractions. The same interesting picture in NIRS with a much easier to identify initial drop in tHb than the following contractions. Our explanation is a not optimal intramuscular contraction the first time around and than the second time a much better one. Meaning the first time it took some time before we had a the full availed muscle contraction which than is strong enough to initially stop out flow but still has inflow. ( venous occlusion trend or outflow restriction.) To use the garden hose example. The first reaction is a push or pressure on the garden hos e which reduce blood flow due to the compression. tHb drops. Now we have and I will explain this in our hurdler topic , a situation that: a) we maintain this contraction force of o so much pressure we may see no a stable tHb if we have a balance between the compression form the muscle contraction and the pressure from the cardiac out put. So in a start of an activity we will see first a drop in tHb due to this contraction compression and due to the fact , that cardiac out put is very low and it will take some time to increase HR and with that CO. Below a very close look on a running test in the start phase You can see out of a "cold " start the initial drop in tHb as a compression outflow by 0. Than approximately 30 +- seconds later you see an increase of tHb. In contrast to the biceps example, where the increase is due to compression of the muscle contraction, which increased above the venous BP level and therefor slowed down reduced or completely closed the out flow option. ( inflow still works as it needs a higher compression on the arterial systems ( better hose quality ) than on the " cheaper " hose w quality of the venous blood vessels. So in a venous occlusion it increases due to out flow restriction. See graph from the Artinis group. ( Portamon) Now just to avoid confusion ( hope fully ) the picture is a static example so artificial occlusion idea. BUT even here we will have a small drop in tHB before we see an increase due to the cuff. Look carefully as we have an initial small compression. Green is Thb in this case. Now what is different as well is that when we move so lot's of activity we have the same tHb reaction but not as in this example a increase in O2 Hb and HHb in this nice way as we may use more O2 than O2 is delivered. so somewhat or often different reaction in the way that HHb ( blue goes much more up and O2Hb red goes much more down. Very individual reaction due to the nature , that a muscular created occlusion trend is not that predictable than a lab created cuff occlusion study. Now in the small tHb start load picture ( courtesy of Mary Ann Kelly case study ) the situation is an initial compression outflow. After 30 seconds the cardiac system and the respiratory system kick in more effective and the HR as a simple bio marker will increase. This leads to a higher blood pressure and as such the question is , whether the blood pressure reaches and even balance force like the contraction pressure or whether it will be higher or lower. Higher BP will start to over rule the muscle compression pressure and tHb will increase as we see. Lower BP will not allow a higher blood flow in fact we may see an increase now due to occlusion ( pooling ) effect. Unfortunately it looks initially the same. BUT. If cardiac out put overrules we see 2 possible additional indication. 1. More blood which is oxygenated so O2 Hb goes up and SmO2 can do go up. Above you see the full running 5/1/5 assessment and the thb we had just the start phase again and now with the SmO2 trend. Now you see the "dilemma" again . If we go with ATP Cr.P glucose and anaerobic alacticid ideas we have a hard time to accept the reaction of the NIRS trend. If we go with somewhat newer and interesting research than we have the following fight in front of us. No such thing like anaerobe This are two sections form our MOXY introduction seminar in Boulder Colorado where we had the pleasure as well to have Frank Bour and his genius Physio flow as a presenter with us. I hope this makes some sense. So back to the original explanation biceps now in short. 1. Sometimes initial tHb drop as a contraction compression out flow. 2. If very strong contraction we see a increase in tHB as a pooling due to venous occlusion trend. If very rapid extreme contraction this increase my be very short and will go over into a flat tHb meaning we reached an arterial occlusion so no inflow no outflow so no change in blood flow or volume. Than when the athlete hesitates or looses some contraction force he may create a venous occlusion and has again inflow and he may go up again. If he hesitates and releases more pressure we may have short occlusion outflow and thB drops . If we motivate again he may increase force again and may reach once more a venous occlusion force and tHb goes up as you can see in the last contraction , before he gives up and than tHb drops as an occlusion outflow. Now this interactions between compression and cardiac pressure but as well vasodilatation and vasoconstriction stimulation due for example CO2 levels will dramatically influence the duration an athlete can maintain a critical load. ( question off blood flow or restriction due to changing physiological reactions.)Now what makes it even more interesting is that this balance between this reactions can change from day to day depending on your stimulation you may have done the day before. Example. You did a very specific respiratory workout with a high VE of 250 l / min but you kept the cardiac out put on slightly above resting level as you had a cardiac stimulation 2 days before so rest day for the cardiac system but full load for your respiratory system. So next day the respiratory system is NOT recovered so very easy a problem with CO2 release. By the way the HRV will create some big questions as it is not included in this possibility despite the fact that HRV is heavily influenced by the respiratory system . The blood vessel reaction will be very different and the duration on a critical speed will be very different. This is the amazing and interesting discussion on many forums on the ability to predict or better hope to predict CP duration based on formulas and mathematical ideas. The assumptions are so open on what today may be reacting as a limiter that it is for me fascinating to see , with what security and absolute certainty this groups are able to predict performance. Does it work in reality ? Will be back in the hurdler topic on the tHb reaction n some different details.