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Registered: 1380484167 Posts: 1,501
,I like to offer a physiological " cook book " to try to help the readers to easier understand on how we look at physiological interpretations and based on this how to understand physiological guided workouts.
Please take it apart or help to add with questions and suggestions or where I need to clarify some of the ideas. Pictures can replace thousand words. 1. The different way of looking at a person ( athletes, patients or anybody ) Ask yourself what classical testing ideas you and I may use or have used are in the above picture. What information do we get form this ideas. How do we apply the test result when we try to target a specific system. Example: You find your LT ( using one of the +-25 different ideas to find an LT. Lets' take a very common LT idea. The 1 mmol increase in lactate in 2 steps in a row. How do we know in what " zoning " or intensity we may overload respiration for example. 2. If we translate the above ideas into a race or a workout we may have the following picture. I hopefully get the idea over with the above idea. You can win a race but you do not know why. You may loose a race but you may have an idea why. It is all about the team and how they support each other. Physiological example. Muscle weakness may create an early occlusion direction with a outflow restriction or even a complete occlusion. This create a lower return of blood to the cardiac system and as such SV will drop due to lower pre load and to try to maintain the needed CO we have to increase HR. Now an increase in HR will change CCT ( cardiac contraction time. CCT is the multiplication. of HR x LVET ( left ventricular ejection time ) LVET is measured in ms. From hundreds of Physio flow test we did we got a trend , where better trained a athletes ( endurance athletes have longer LVET than less trained athletes or people. The LVET will drop with increase in HR. Untrained person example. HR 150 LVET 200 ms so CCT = 30 sec. Trained athletes HR 150 LVET 230 ms so CCT = 34.5 sec CCT means the time during 1 min where the cardiac muscle itself is getting limited to non O2 as the cardiac system is getting blood during diastolic and not during systolic actions .. Hope you see, where we can go with this situation. Longer ejection time more blood for locomotor but less for cardiac system. Risk of m CG reaction to protect the pO2 in the heart . reaction see later. Second example Respiratory VE l/min limitation. Your push an intensity, where the VE needs to be 150 l/ min to maintain H + balance and to get rid of CO2 to achieve this. Your current VE peak is 120 L / min. So you are short of 30 l and will accumulate CO2 rapidly. Reaction. O2 diss curve shift to sustain the performance somewhat longer ( fight an flight ) and better utilization of available O2 due to the problem that in take of O2 will be limited now. The increase in CO2 will enhance RF but in a weak respiratory system may drop TV. / problem increase of dead space and so on. Question. Is your favorite test system giving you any feedback on this potential performance limitation ? Your or our body has a clear priority list to try to stay a life as long as possible. This pyramid is the base from the fight and flight concept ( survival) Easiest example of this concept is the survival mode in cold or hot temperature . If we go further to the idea, that cardiac and respiratory systems are much more important to survive than your leg muscles , you can see, why , when we reach some critical intensities the CG ( Brain ) may redirect energy from less important body areas, like for example leg muscles , to the needed vital organs. So the earliest feedback , that wee start to " guide up " loco motor performance shows up in the little or non-involved muscles if we have a vital system limitation. or will show up in the involved muscles when we have a loco motor local limitation. This than may look like this . Example of a THb functional reaction. Vasoconstriction ( Drop in tHb ) to protect BP due to a cardiac limitation. Functional SmO2 reaction. Drop in SmO2 due to a respiratory limitation during a game . Holding breath like in wrestling ) Example structural change in tHb. ( Andrews hint ) increase in tHb at 1 min rests or end of a step test far above resting tHb. ( most often due to a much bigger vascularisation in this athletes muscles Example structural change in SmO2 reaction. Very low SmO2 plateau in certain muscles but sustainable performance. Indication of a very optimal utilisation ( mitochondria density.) in this muscles. See Ruud and Daniele's VL reaction compared to their RF reaction. This leads us to the ext. step. Each team member ( heart , respiration and muscles itself has some additionally team members. They are all interlinked with each other. Example . A higher TV in respiration will change the HR and the SV of the cardiac system. This ultimately will show up in a difference in SmO2 and tHb trends. A better intermuscular coordination will show up as a different SmO2 reaction in a main contributor. Example Ruud and Daniele. Their VL is the main contributor in cycling. To keep the VL as efficient as possible in a high intensity they will try to add additional help fur example by activating RF. Now this only works if delivery systems are strong enough as an additional sue of O2 due to an additional muscle help will create higher O2 demand and if this is not achievable from delivery ( heart ) or the additional CO2 production overrules the limited VE from respiration, the performance increase can not take place. This is one reason why in top athletes VO2 peak ( max ) does not increase and some times actually drops ( Racliffe) but actual performance in their sport improves. A limitation of vital delivery system will not allow a further O2 use from super trained locomotor muscles ( Sleeping giant ) A beginner where delivery is not problem will have it easy to increase VO2 peak as he simply adds to a weak coordination even more muscles to keep balance and what ever he needs to keep going. Exercise physiologist from top endurance teams all see that ( no further VO2 improvement.) if the substitute additional O2 than VO2 can go up as well as performance. Result delivery is a limitation, solution prop up delivery . How ? simple find a substance who allows a higher delivery. EPO , plasma expander a.s.o all what we see. Did you ever asked your team doctor or coach how you could increase your respiratory system to improve CO2 output. Or in other words you have a VE l/Min tested in a VO2 peak test of 150 but you like to be able to move 250 L ? Is the practical approach to improve personal training ( stimulation ) planning completely lost in statistical zoning calculations and absolute test ideas based on performance. do we gap the ideas form a lab with the option for coaches. Summary : Short overview on how we approach thoughts , when looking at physiological feed backs.
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Registered: 1380484167 Posts: 1,501
Thanks for the interesting responses and one questions people had in common.
How does NIRS fit into VO2 and lactate ? We may be able to ask the question different. How does VO2 and lactate fit into NIRS. Here a super basic explanation I use for my students in the high school. In other words , they have all a connection as they all deal with energy situations during rest and performance. All have one goal for coaches , Finding the critical intensity , where utilization and delivery just may loose a balanced situation. So using VO2 is one indirect method to do it with some as often discussed disadvantage to apply it in the field or during a race. But it is a great equipment allowing us to create a great feedback and when combining with NIRS it is getting even more fun to use. There is a reason why one of the top VO2 equipment companies . COSMED Italy added direct SmO2 and tHb feedback to their new VO2 equipment by combing feedback form MOXY to their VO2 data. So lets look first VO2 and MOXY / NIRS. Now we discussed this before . VO2 = CO x a - v O2 difference. as a very basic formula. The content of this idea is somewhat more complex. but let's start simple first. Remember the black athlete. Than what we hope to get as message/ the team in the athletes. Here a picture of the main team members in a different way. Each member can be assessed with some different points and you can see NIRS is nearly in all available with as usual some restriction and some needed combinations . Here when we look at NIRS just in combination with systems and VO2 alone. Picture is out of Holmbergs great cross-country presentation. Now as mentioned it is somewhat more complicated and let's look at a different view. So VO2 - CO x a- v O2 diff. I showed this slide for sure before but perhaps after all this time it may start to make some sense and it is a summary on what we used prior to just moving down to MOXY only. But as well it shows , that we sometimes may make conclusion with MOXY , which we may have to review and than we go back and combine all the tools we have. It shows as well that VO2 is an end result of a very big team all creating demand for O2. That explains why two people with the same VO2 max ( peak ) result may have a very different performance outcome. Most discussed example is Paul Tergat and Lance Armstrong before NY marathon with both 85 +- VO2 peak both running the same race and having nearly 60 min time difference at the end of the race. VO2 is a great equipment which when we look it at that outside the box can give a great additional feedback and confirmation to when we use MOXY. As soon I have time I will show some rowing VO2 MOXY test result and how they go nicely with each other when combined. So here when we just look the idea with the view of delivery ) CO and VE and utilization a-v O2 difference. One problem we had with VO2 is time lag and therefor we made some different conclusions. As VO2 did not reacted in the first 30 + seconds we assumed there was no O2 used. So there was a deficit create and the rest is history. NIRS and even better technology showed us that we did not had the full picture yet. This is what we learned. Now you add to the historical testing ideas lactate sampling, where we have as well an unknown lag time for a summary of possible lactate in the systemic circulation with no idea, when and where it got used as buffer or predicted and not needed. And you end up with a very logical but not up to date idea of anaerobic alacticid. Due to lag time of sampling reaction and lag time of VO2 sampling reaction. So a similar load in NIRS showed up like the below picture. and when we now overlap this you can see , where we have some confusion if we do not allow to objectively look at all the sampling ideas. Now this confusion is even bigger when it comes to combined lactate and NIRS. Historic reminder. Any current LT idea or lactate discussion was originally based on the assumption , that lactate is a bed and ugly substance and the resin of many bad reactions after a hard workout or race. So we had to learn to tolerate this substance and had to get rid of it as fast as possible in between intervals' or after training and races. Cool down is one of the reason we did it, getting rid of lactic acid. Today we would love to actually I inject lactate so we can go longer and faster when pushing it to the opposite spectrum . ( see g BROOKS INTERVIEW.) So there is this idea, that lactate trend and SmO2 trend move together. Example In a three minute classical step test we see an increase in lactate and a drop in SmO2 . So search for a break pint and than you have the LT and as you will have a BP in the NIRS curve than you have LT by using just NIRS. Now we will have again go back to history and see that lactate can change its trend by different step length and different situations like diets and so on. I like to get back to this in a great data collection from a 6 min double dip lactate sampling idea combined with MOXY in the MLSS section later. Here just some questions: a) you do with the same athlete a wingate test and a 3 min VO2 max test. a 1 ) is the max or peak VO2 value the same in both tests ? a2) is the lactate value at the end of the test taken the same in both tests. a 3 ) is the drop in SmO2 and tHB the same at the end of both tests. b ) in which test is the end test lactate higher wingate or VO2 max. b1) In which test is the SmO2 lowest level lower ? In the wingate test we see a fast drop in SmO2 , cane we see a fast increasein lactate.? . On the other side what happens when we end the wingate test and SmO2 goes up , which direction is lactate going ? So does a drop in SmO2 can show an increase of lactate or could it be that the increase of lactate shows up as we see an increase in SmO2. ? c) how do we know , that the lactate we can measure in the finger is from the muscle we applied the NIRS. And many more critical questions we should be able to ask, when we allow us to ask the same critical questions when using NIRS.
Development Team Member
Registered: 1487308118 Posts: 91
i dont see pics