| Author | Message | ||
     Juerg New member Username: Juerg Post Number: 129 Registered: 04-2006 |
Vo2 an old issue with an new wave in the fitness industry. Before you go and purchase any of the now relative cheap available VO2 testing equipment , inlcuding ours. please ask the question , : What do I do with it , what does it change in the service I provide to my customer , besides a nice computer printout with a scale , who tells you , you are bad / good excellent. Ask more questions on how you can improve the service to your arthletes and clients in the fitness center. Our big issue is less , how do I improve first the client , but more , how I can control my job , my suggestion to the client, and can I see trends in different reactions on the clients system caused by my suggestion for training. Yes , you are right we don't like to see , that the lack of improvement is due to a wrong idea of a program. Smile Here just for interest , if you still believe the max VO2 is valuable for your training suggetion. You may think twice and perhaps more and than you come back with some questions. The fact , that we may see a plateau at the end of a graduated test of VO2 is a nice theory, never proven and rarely seen. There are different reasons why. There are a lot of different factores on which VO2 max is dependant on and which may influence VO2 max. Before I list them below , think , that VO2 max can be changed very little with training and using VO2 max to show improvement is difficult , with exception your client is 100 pounds overweight and you take his food away and 50 pounds later you test . He is "much " fitter thanks to VO2 max / kg body weight. Yes true you may be able to use VO2 max for "genetic " profiling . so how many clients do you have for that ? and how important is that for the majority , who just like to improve their personal best. Okay here a list of some of the factores where VO2 max has a connection: 1. Internal factores : Ventilation Diffusion in the lungs HMV ( heart minute volume ) arterio - venous O2 difference ( peripheral utilisation ) Blood volume Hb ( total Hb Nutrition Some external factores. Type of activity ( upper body / lower body both together ) technique in the tested sport % of muscles involved Body position O2 partial pressure in the inspiration air Temperature, humidity, So as you can see lot's of factores , who create a question mark to the maxinal value and my reduce the value to the maximal tested value at a given day. With this in mind we move basically back to where we started . Maximal heart rate or 220 - age as values to designe intensity zones. Than we may have to add as well Karvonens thought of resting HR and deduction of this . so how about resting VO2 and deduction of that value ? Hmmm how many thought about that ? Differents between using maximal heart rate and 220 - age and using maximal VO2 and % of that number ??? 7'000 -= 8'000 dollar. Hmm lot's of clients to test. So perhaps a point where we should sit back and consider the value of a VO2 equipment. Yes there are lots of values , using your equipment different and you will be surprised , that you can change the use of a max VO2 test to a very smart way of using the equipment to find out much more about the different reactions during a graduated test. See for some inputs and ideas under FaCT IRIS. I will come back here some more to try to explain why VO2 max has less values than relative VO2 datas by given intensities and other given points, like LBP or certain respiratory frequencies and so on. All the above factores we listed here will give you a hint , where we can see improvement over time in trying to see whether we can go a given physical performance ( Watt ) by a lower VO2 value , as signs of more efficiency. Think about and come back with questions . Juerg I know you just payed 150.- dollar for a VO2 max test and you are above average but you still loose against your neighbour who was just average in the test. Take this as a small help. VO2 of Armstrong Lance 85 ml/kg/min Marathon time just under 3 h Grete Waiz ( norway ) VO2 73 Marathon time 2.25 Derek Clayton VO2 69.7 Time 2.08 well the predicted marathon time with 85 VO2 is around 2.04 Just some interesting thoughts and some questions to ask your tester when we give you predictions and feed back. If you are really interested , on how long it may take you to run a marathon. Well run one and you have the answer. Have fun. Juerg | ||
| Juerg Senior Member Username: Juerg Post Number: 1052 Registered: 04-2006 |
Understanding VO2 ? Here a follow up on the "interval discussion" by shifting some info over to VO2. Basic ideas of many : As higher the VO2 as better the performance ? Or : an athlelet with a higher VO2 is "better " than an athlete with a lower. Remember: We think : VO2 is just a summary of all the O2 which is udsed at a certain intensity. So we know how much O2 is used for example to push 240 watts. Now here the question to our readers. Do we know , who uses the O2 ? How much is going to the working muscles , how much is used by the cardiac system ( heart ) , how much by the pulmonaery ( respiratory system ) Just to name some of the potentially main users and "demander" of O2 . Here to think about this : 240 watt workout . 3 versions : 1. always 240 watt but different RPM 55 and 110 2. 240 wattage but different respiration rate 15 + 50 + RF. 3. Subjective most efficient biking with 240 watt load. Here some test info: Work 1/2/3 VO2 3. "efficient 240 watt 2574 VO2 1. RPM 110 240 watt 3198 VO2 1 . RPM 55 240 watt 2964 VO2 2. RF 15 240 watt 2722 VO2 2. RF 45 240 watt 2956 VO2 Now assuming the 240 watt for the extremity muscles always ask for app. the same amount of VO2 we may be able to speculate where the other O2 consumers are. Here the speculation in the RF workout. 3. 240 watt RF 27 VO2 2574 by RF of 15 we seem to use more O2 2722 and by 45 even more 2956. Question: Do you think the more O2 ( higher O2 ) was due to more O2 demand caused by the not "natural" and therefor not very efficinet respiration rate : Now here more info . 1. VE in efficient 240 is 73 liter/min VE in 15 RF 240 is 66 L/min VE in 45 RF 240 is 95 L / min Now here the next step . O2 in ml moved per heart beat. in 1. eff. 19.3 ml / beat in 15 RF 20.4 in 45 RF 22.2 No next O2 per watt used : 1. eff 10.7 ml / watt 15 RF 11.3 45 RF 12.3 Now her O2 moved per breath 1 eff. 102.9 15 RF 170 ml 45 RF 73.9 Question : Where and what would be the goal . Short info : In this subject the most efficient RF 4 years ago in tests was 36 RF / min . Now it is 27 RF / min. VC 4 years ago was 4.8 L now it is 5.5 L TV at LBP 4 years ago was 2.1 L now it is 3.2 L Compared with another athlete , who did not work on the respiration sysrtem in 4 years nothing changed in RF and VC or any of the above values. The changes may be realy related to a minimal 3 x / week specific respiratory training integrated in teh workout schedule. Now can we use VO2 perhaps to find possible changes in some specific areas, who contribute to VO2 max levels. 2. Does a drop in VO2 at a given wattage level may actuall rather show and imporvement ( efficiency ) rather than a drop in performance. 3. Should we use VO2 rather at a level like LBP or at a fixed wattage number below max wattage to see potential change in O2 usage for that particular intensity. 4. Could it be , that testing for VO2 may be far to much depndent on motivation at that specific day to really push all out. Similar like searching for max heart rate or max wattage. This and other questions leaves us with the idea, that VO2 and other biomarker levels at LBP may be a much more objective way of assessing physiological changes over time as they are not based on mitivation to push all out, but rather show physiological limitations. Juerg | ||
| Juerg Senior Member Username: Juerg Post Number: 1211 Registered: 04-2006 |
Now as we go along with more critical view on VO2 we have learned so far: The VO2 max in amny people , who train regular over years may not change to much or nothing anymore due some known and some overlooked possibilities. What we know for sure is , that advertising for regular Vo2 max test for athletes may be only good for one person. Which one ? Here a statement often seen in many training consulting Websites : "Incorporating additional VO2MAX tests every few months is a great way to track your progress and measure your health as it improves." Is it really great top track VO2 max or what would make more sense ? Another very common statement we see, here from the same Website : "A properly conducted VO2MAX test will last only between 6 and 12 minutes. The test begins at an exercise intensity that you are comfortable with, and gradually increases in intensity until you are working as hard as you can." Here the question : As we know now : VO2 max = CO x (a-v) O2 difference. Now if we look first CO as SV x HR we know by now from many of the publsihed research on our different Forum areas, that time is very individual and in some cases the Stroke volume may reach very early on a individual max , and in other cases it is much later . By limiting a test as so often on a time like 6 or 12 min will miss many of the potential physiological reactions. A very often used argument is than : We let the people "warm up " before the test. This is done very subjective and without any control. We loose with the warming up many interesting informations like HRV, change in SV, SpO2 changes and even respiratory rate changes. By limiting the test to 6 - 12 min we often make far too big steps ( 40 - 50 watts ) and when you take an average cyclist with a max tested wattage of 260 - 320 wattage and you make 40 - 50 watt tests you actually increase every time by 15 - 20 % performance, which in any case will trigger an oxygen independent energy surge in any of the steps and if you keep the steps donw to 1 min and even shorter like in old test we did with Wingate, Conconi , MAP you really only find out how much watt the person can push in this stress stummulation with very little or even wrong physiological infos. Lactate sampling during this short tests steps will always give you some wrong numbers, as the readings you see may be lactate accumulations produced 1 or 2 or even more steps back. Same will happen if you look at FeO2 and CO2 as well as SpO2 as all this readings have a lag time of at least 30 seconds and longer. FeO2 can have a lag of up to 1 - 2 min. This is, why in any FaCT assessment we have to tell the client , that the test will go at least 30 min but very often 45 - 60 min.( Just some thoughts, as many centers, who offer testing are often very un-critical to their own testing protocolls. Any test has strenght and weaknesses in it and the key is to try to optimize the testing to the client, and the clients goals and nees on information. | ||
| Juerg Senior Member Username: Juerg Post Number: 1455 Registered: 04-2006 |
Here a nice summary from a Website. : After you have reached your peak level of oxygen consumption, a two minute cool-down period will begin to assess how quickly your cardiovascular system recovers." After 8 month of daily assessing "recovery" I just can say , taht the idea that the "cool" donw in 2 minutes suppose to tell you how much your cardio vascular system may recover sound for sure great in or on a Website , who offers VO2 testing . What the really can read out of teh datas collected with a VO2 equipment on cardiac recovery is a big question mark. Even bigger the answer they can give you on vascular recovery. None of the dats they collect with exception of HR will give any close hint on any of the promised recovery. Even HR is a question mark , as their VO2 equipment they use would work as well and would spit out as well the same data without any HR collection. The fact that the HR may drop fast has no clear information on cardiac , nor on vascular recovery. The VO2 data tehy collect may have some indication on the gas and pulmonarty raction after the VO2 max tests. This is never used in their discussion , as they never look at the real changes or not changes of FeO2 , nor on the VE/ RF frequncy ( TV ) reactions in the "recovery" zone. The fact is really , that we not real recover in 2 minutes anyway , but rather shift ATP production back to the vital organs if possible to sustain "life". There will be a major shift in the way we use traditional nice wordings with very little meaning s but good sound to impress the not yet educated population with doing tests with relative little effect besides our bank account. We hope with the On line courses for students to make an open thinking course with some critical look at established ideas with very little foundation of reality and practical implementation. Cheers and please shoot back with critical and constructive feedback and discussions. Juerg | ||
| Robh Senior Member Username: Robh Post Number: 445 Registered: 12-2007 |
Hi Juerg, I've never had VO2 test and will most likely not have one unless like you say it's free. My question is being in the UK and with no one offering FaCT IRIS testing I was wondering when the Fitmate demo CD is avaialble would a tradiotnal VO2 tester be able to follow the CD and being able to test me using the FaCT IRIS protocol? The next step then would be convincing someone changing their way of working but I think I have a contact who knows people who might be able help me out seeing I've tested 7 of his athletes using the FaCT level II test. Cheers Rob | ||
| Juerg Senior Member Username: Juerg Post Number: 1461 Registered: 04-2006 |
Here some VO2 info, for all the people arguing about the VO2 plateau and that we can proof that the idea of a CGM does not work. Here what this direction claims. If we do a step test as usual and we find the VO2 max lets say 45ml/kg / min Now the next day we go and stress the same person but with a wattage which is 25 % above VO2 max from the day before than we can do that , but if the CGM works this should not be really possible. Now here some data. real test : 320 watt all out in a 3 min step test VO2 45 Than as suggested 400 watt all out VO2 38. Some points here to think about. In some training suggestion they use 120 % above FTP for developing of VO2 max??? Well where do you think VO2 max is more stressed by 320 or by 400 ? Why the difference : Here some numbers. 320 Watt RF 29 VE 125 L TV ??? FeO2 16.4 % 400 Watt RF 38 VE 126 L TV ??? FeO2 17.6 % Duration possible 320 full 3 min . Duration 400 watt 1min 24 sec. The 400 watt just simply will not trigger the CGM, as the ability to produce ATP is from the beginning O2 independent, so there is really no O2 delivery stress to the heart or even the lungs, as the local " survival " sensor of dropping to low with the ATP and potentially some Ca++ delivery problem is so fast so high , that there is no danger nor need for the CGM to kick in, as the energy delivery problem is far faster than the reaction on the cardiac system. We see in this cases on the cardiac hemodynamic as well a lack in "time" to actually try to increase EDV and SV and we just see in some cases a in crease in EF %. But we for the moment at least had no case, where we could see a good and clear response form the cardiac side, The time of the stress is simply to short. You can see this even in the HR reaction : 320 HR 169 400 HR 155. So this will leave us again with the question , what stress do we really apply by doing short 1 - 2 min interval from a physiological point of view. ? What do we stress and what does not react at all. Some may remember Miha's and Robs "Training zoning sheets you can use as a cook book if you use FTP as your guidance in training zoning. So what we learned or discussed now since than may help you to understand, why it is easy to make a cook book , but it is hard to proof and explain , that the expected changes really are happening with the suggested zoning. Yours to think through | ||
| Juerg Senior Member Username: Juerg Post Number: 1464 Registered: 04-2006 |
Now here a typical "research " were the groups , respective the intensity for the test groups is based on % of VO2 max. Now this is really a normal procedure and fully accepted. Any "research " paper you will read or nearly any , will be based on % of VO2 max. Our big questions are " 1. Are we sure we hit VO2 max ? 2. Is in a group for 10 people 70 % of VO2 max really the same physiological intensity or just the same mathematical percentage. There is ample evidence, that some people can use 70 % of their VO2 max very nicely in the oxygen dependent zone and can run a marathon or a TT on a bike easy at 70 % of their VO2 max. On the other side there are people , who can't sustain 70 % of VO2 max for one hour. We see that on the LBP testing , when we compare the LBP HR and or watt level with the VO2 % of VO2 max. during a FaCT IRIS test . If we add the FaCT CLR version we see , that some people by 70 % VO2 have a CCT of far above 30 seconds and they have no chance to go for 1 hour. Other people are nicely below 30 sec CCT and have no problem to sustain that intensity for 1 hour. So you see what I mean , when we draw a conclusion form a research based on 70 % VO2 ,as we have in the same group of people different reactions due to different metabolic needs to sustain this intensity during a workout. Nevertheless let's see this study here : " Time-course of adaptation in cardiorespiratory fitness with exercise training in older and young subjects." J.M. Murias, M.D. Spencer. J.M. Kowaluck, D.H. Paterson :School of Kinesiology The university of western Ontario London Ontario. " Endurance improves cardiorespiratory fitness, however comparison of the amplitude and time-course adaptation in older and younger adults yielded conflicting results.Thus , this study examined the time -course of training adaptation for peak oxygen uptake(VO2 peak) and estimated lactate threshold (OL)in response to a 12-week training program in older and younger adults. Fourteen older( 8 men and 6 women 68=-7 yr) and 16 younger( 8 men and 8 women 24 +-5 yr)healthy, recreationally active subjects participated in the study.An incremental ramp test was performed on a cycle ergo-meter to determine VO2 peak and OL pre training, and at 3,6,9 and 12 weeks of training.Pulmonary gas-exchange was collected breath by breath using a volume turbine and a mass spectrometer. Training was performed on a cycle-ergo-meter three times per week for 45 min at a power output corresponding to 70 % VO2 peak.Training intensity was adjusted at 3 week intervals to reflect changes in fitness level. After training, VO2 peak increased in younger ( 19 % from 3.23 to 3.84l/min ) and in older adults ( 25 % from 2.05 to 2.55 L/min ) The amplitude and rate of increase in VO2 peak was similar in both groups, ).13 l?min ever 3 weeks) OL in creased in both younger ( 20 % from 2.01 to 2.41l?min ) and older adults ( 29 % form 1.33 to 1.71 l/min ) The amplitude and rate of increase in OL was similar in both groups ( 0.10 and ).)9 l/min every 3 weeks ). The main findings were that : 1. The time -course and amplitude of adaptation in cardiorespiratory fitness( as indicated by change sin VO2 peak and OL were similar in older and younger subjects. 2. Twelve weeks of training at 70 % of VO2 peak did not induced a plateau in adaptation of either group. " A few thoughts here. a) When we take the study as it is we see, that a relative low intensity 70 % of VO2 peak actually showed a very nice improvement of VO2 changes. 70 % of VO2 peak and the ability to train for 45 min indicates for us, that this was below LBP intensity and would support our notion , that to increase endurance you have to train below LBP. However there are some open questions: a) They never actually tested VO2 as you may remember that VO2 is CO x (a-v) O2 difference. They only tested respiratory gas exchange and than used a lactate idea to estimate a potential lactate level , they termed OL or lactate threshold. They never actually tested the CO part of the people ( cardiac output ) nor do they ever used any cardiac information like heart rate for any readings nor training intensity. The " VO2 improvement is a speculation based on a higher respiratory reading and could be based on an improved respiratory situation due to the regular work out. We have no information on the cardiac reaction after this 12 weeks. Not even the basic idea of a potential HR change on a certain intensity . So CO is HR x SV . and we have no clue , whether the cardiac hemodynamic actually changed EDV up and therefor SV up by the same HR or whether they just simply showed a functional reaction with same EDV after 12 weeks, but higher EF % ( Stroke volume up or HR up only or both ) This would be a very interesting study , if they would have collected in the same testing all the possible reactions : Lactate trend LBP , cardiac changes over Physio Flow and pulmonary respiratory adjustments with the VO2 equipment. This what we could see, whether older and younger people with the same type of a workout , but based on LBP intensity would respond with the same physiological reaction , or whether one group or very individual people would adjust by improving their weakest links . So some would react over respiratory adjustments, other over cardiac reactions and last but not least some over metabolic changes. With our "smallest " lab of the world Lactate Pro , Fit Mate and Physio Flow we easy could do that now. Interesting is , that this type of the above study always find sponsors so ,if there are sponsors out there , who like to have this done in the way we suggest ,you are welcome to sponsor people from our groups and FaCT NOC centers. ( Smile ) | ||
| Juerg Senior Member Username: Juerg Post Number: 1466 Registered: 04-2006 |
Thanks for the feedback from Switzerland, and it is nice to see you guys are reading our Forum. True I had a window seat during . my English classes with free view on the ski hill. The mail I got is understandable, as they take my "critic" very serious . The critic , that I think many of the research done with VO2 max or VO2 peak and than use a percentage of this values to determine training intensity during a study are not a good idea and ,in fact give potentially wrong study results and therefor a wrong conclusion. I like to share a part of a presentation done by Dr. J.Helge, Dr. G. Van Hall and Prof. BG. Saltin from the Copenhagen muscle research Center in Denmark. The reason why I Like to use this as the answer to the above critical statements may be clear . This three researchers have much more knowledge and information than potentially many or all of the research institutes in this field, as they are potentially the worlds leading center in this direction. Okay here word by word the section concerning percentage and VO2 . "Skeletal muscles have three to four times greater mitochondrial enzyme activity after extreme endurance training compared to those seen in sedentary people giving type I and II a fibers a similar mitochondrial respiratory capacity. In this light, it could be anticipated that muscle fiber types would not matter in regard to the metabolic response to prolonged exercise and endurance performance. Coyle et all have studied this particular problem with intriguing results. In cyclists with a VO2 max of67 ml/kg/min the blood lactate response to sub-maximal exercise was used to divide well - trained cyclists into either low or high lactate responders to cycle exercise. Endurance performance was markedly different in the two groups. The high lactate responders could only cycle half the time at 88 % VO2 max compared to the low lactate responders. Leg muscles where studied for mitochondrial marker enzymes, fiber types and their size as well as capillaries. and no difference was found between groups with regards to muscle enzyme activity and capillaries / muscle fiber. . Thus neither the lactate response nor the performance could be related to these indices of muscle adaptation. Both variables are easily affected by changes in physical activity level and are proposed as a link to a more efficient muscle metabolism. The two indices differed : Those with poor performance and a lower lactate threshold had less type I muscle fibers (47 % vs 67 % ) than the good performer , and had 15 % larger mean muscle fiber size. : So let's go in short through what we read : 1. Mo enzyme difference. 2. But muscle fiber type different. Well unfortunately for some we may have to go back and talk here again about functional and structural. Enzyme reactions are functional reactions and fiber type are structural adaptation. Muscles with a higher % of Type I fibers can deliver ATP longer over FFA and oxygen dependent energy production. Type II a fibers work earlier with glucose and oxygen dependent. So one of the limitation is the "gas Tank " as type I fibers can go much longer , than type II a fibers, where the glucose storage may be o a big limitation. Type IIa fibers can work very well with glucose and may show that as well in a much higher lactate trend reaction if we go with high intensity . Type I fibers may produce as well lactate but may be able to use them already in the fiber and therefor the actual lactate level in the system may always stay lower. With the FaCT test idea we can easy see the lactate trend and can"speculate " on the potential situation on Type I and Type II a fibers as we observe the trend in lactate in the second part.3. Interesting is the part , where Coyle proposes a link to a more efficient muscle metabolism. As you can see it is just what it is a PEROPOSAL . Here some on the edge thoughts from what we see as we use the Physio Flow now besides the lactate and the VO2 information : Read again and I will give you some potential answers to that section : "Leg muscles where studied for mitochondrial marker enzymes, fiber types and their size as well as capillaries. and no difference was found between groups with regards to muscle enzyme activity and capillaries / muscle fiber." Now here what we see in some small cases studies over the last 1/2 year. High lactate responders reach much earlier a CCT of 30 seconds and once they reach that the move very quickly lot higher and easy up to 35 37 seconds. Low lactate responders reach the CCT later in % of VO2 max or peak and even when they reach it , they can stay very long close to the 30 seconds with a very slow drift higher. They seem to be able to adjust the LVET by dropping LVET nicely , respective have overall a much lower HR. But with the lower HR we see a much bigger EDV and as well as much bigger SV. This fact would support T. Noakes idea of a CGM, as with 2 athlete with the same VO2 max the one with the better cardiac system will be able to keep the O2 situation for the cardiac muscle much longer in a sufficient region, . That would as well fit with the explanation of a higher Type I fiber situation in this people, as cardiac development and type I fiber development go often over years of structural changes.. Now summary. As we can see the same % of VO2 can in fact stimulate 2 very different metabolic reactions, shown in low or high lactate responses based on either different structural fiber composition and new form us as well different cardiac structural situation. Why do we never discussed that before or still are not ready to discuss. Answer is simple. 99.9 % of all the studies done with VO2 and percentage of VO2 do not 9 NOT ) test the VO2 as proposed everywhere with VO2 = CO x (a - v ) O2 difference. Their test or test equipment only assess the second part of the formula . the ( a- v ) O2 difference. and therefore two equal VO2 max tests can't give this testers any answer on the above proposal of the CO as the other 50 % of the VO2 testing . FaCT CLR is the only and first test idea form tee moment , who can give you now this info. C = cardiac info L = metabolic lactate info R = Vo2 respiratory info. So any of the existing test center , who really like to make a difference in real assessment will move earlier or later to a FaCT equipment base. Whether they use the FaCT CLR test protocol is not important . What is important is the situation where they no can assess the situation why 2 equal VO2 athletes will have very different outcomes, depending on the race situation and nature of races they do. What that tells us is exactly the answer where we started out. Studies with percentage of VO2 max are most likely of very little values in the way of telling us anything about the outcome. They still have values, as it is interesting to see what the individual result of each of the tested person did. The problem is, that the study ends up with statistical results so the individual results is getting lost and the conclusion is often meaning less. Please come back as this is a fundamental question on how test are done and results are "manipulated " Juerg | ||
| Andrew Senior Member Username: Andrew Post Number: 221 Registered: 04-2006 |
We have seen some interesting reactions to "training" again at our camp in Mallorca again this year, and I thought it might be interesting to show some people a real world example of soem of Juerg's theories. Our first athlete is 55 years old, and very good Masters cyclist. Has completed our Transalp on a few occasions. He experienced a dramatic drop in HR during his third day at the camp. Some have called this HR depression, and some people think this is a sign of good training. I think it signals some potential cardiac damage, and it would be really nice to have seen the Physioflow results with regard to CCT. After 4 hours at steady pace (25km/h), and a feeling of very controlled intensity, he recorded HR average of 98 beats/minute. Even when he was "pushing" his HR never climbed over 110 on that day. His last LBP in March=135. So, we made the observation, that possibly his heart was in fact contracting not only slowly in terms of beats per minute, but that it was also contracting sluggishly with each beat. Juerg describes this as a prolonged CCT. We convinced him to take a full day of rest, and on his return, he was able to achieve significantly higher HR, with less effort, and felt much stronger on the bike. HR average 112 on that day, without the feelings of fatigue at the end of 5 hours of riding. This was a demonstration of what we are learning about individual differences in cardiac response to exercise from different people. This athlete was the only in the group to respond with drop in HR after long training days. And, it was a recognition of the possible cause of the prolongation of CCT that allowed us to adapt his program to best fit his response to training and recovery. | ||
| Juerg Senior Member Username: Juerg Post Number: 1471 Registered: 04-2006 |
Thanks Andrew and it is a very interesting situation. Some may remember the discussion we had with the CC skier from the USA ( Diabetic I ) and his very low HR . As a reminder. CCT is our definition and is the product of HR x LVET ( left ventricular ejection time. What we see n healthy top athletes is the situation , that LVET in a step test is steady dropping from 230 - 250 ms down even under 150 ms. Now ctt is HR x LVET. so if out of what ever reason LVET is not dropping ( perhaps cardiac overload and as Andrew describes it as sluggish, that the only other way to "survive " is not increasing HR. The traditional idea was that the lower HR is because of a bigger heart and a bigger SV. I am not convinced , that this is that of an easy answer. at all. Once we reach CCT of 30 plus we see the increase in lactate and it may be , if this 55 year old person had pushed higher to 110 1 15 Ht he would have been surprised that he already had lactate despite his resting LBP of 135. | ||
| Andrew Senior Member Username: Andrew Post Number: 222 Registered: 04-2006 |
I agree with you Juerg. The athlete is very used to LBP testing, and the "feeling" of LBP-10 to LBP-20, where we were focusing most of our training in the first three days of the camp. By holding the same "feeling", he was having much lower HR, which was the reason we made the conclusion about his "sluggish" contraction, and the need for more rest. I believe his LBP would have been 112-120 on Day #4 of the camp. So, his perceived training at LBP-20, gave him a predictable average HR of 98. After the full day of rest, he was able to ride again at HR=115, with a very good feeling, and in fact pushed to HR=144 trying to "race" with one of the German Pro riders who was joining us for a few days. He had fun, and took the following day off, knowing that he had pushed his limits, but was an experience he did not want to miss. I rode with the "tourist" train, and have been able to maintain stable Fit Test (Polar Trademark) numbers each day, and have therefore been able to enjoy my own preparations for Kona, with the two other athletes who have not experienced the same drops in HR or performance over the past 8 days. The sropping HR and performance is the same feeling that both Ginny and I had after racing in Ironman New Zealand in March. Low HR, but a feeling that we had not truly experienced full cardiac recovery. Our LBP proved this, with post-race LBP HR nearly 10 beats lower than pre-race, even after two weeks of "recovery". They took nearly 4 weeks to fully recover. We would like to set up a pre-race post-race Physioflow assessment to see the effects of racing in Kona on our hearts, so if there are any Physioflow users looking for test subjects, we have at least 4 athletes in BC attending Kona this year, and it would make for a very interesting study. Much better, than using VO2 max as a means of measuring the effect of long course racing on the heart, as Juerg has pointed out in a different thread. If we do not have access to Physioflow, we will post our Fitmate/LBP pre/post numbers for others to see here. In fact, we could do the same for the Half Ironman Nationals in July (Osoyoos) with the group of 8-10 athletes that will be competing there for BPR. One day, we hope to be able to provide real numbers to go with our on-road observations. | ||
| Juerg Senior Member Username: Juerg Post Number: 1472 Registered: 04-2006 |
Thanks Andrew for this very interesting summary and observation. I will put together some practical test examples over the next few weeks to show exactly what Andrew points out here. 1 .! will be a cyclist after a 2 day stage race on the road all out . and the effect this had on the cardiac hemodynamic. 2. will be a pre and post marathon run from a master runner. 3. will be an example post training cam and recovery after the training camp. We have now approximately close to 100 test done in the different situations and start so see some very clear trends , which helps us to keep working in that directions. As we have now other groups using the physio flow in Quebec and Ontario we will be able to collect over the next 1 - 2 years many more information and can than start to develop new ideas with a strong foundation. Frank from Manatec France has organised a meeting where the different physio users world wide will meet and exchange ideas and directions where we would like to go for more practical application and I am just preparing over the next few weeks my presentation for that event in May. I will keep all updated on the direction we decide to go and where new FitMate and Physio flow users are stationed , as we now have daily requests for info and instructions form different parts of the US, as well now from BC and Alberta. ( Ice hockey coaches ) as well as some fitness testing centers. So we will keep you updated on new NOC test centers as they show up. Cheers and have a great weekend or what is left over. Juerg | ||
| Juerg Senior Member Username: Juerg Post Number: 1476 Registered: 04-2006 |
Hallo Doug here your answer and it is a very common question as you can imagine : VO2 is the total amount of O2 during 1 min. The True O2 is the % of O2 used from the 21 % in the inspiration air. and measured breath by breath . The connection is as you guessed exactly that without FeO2 % or True O2 there is no VO2. The VO2 is a calculation based on True O2 ( FeO2 ) and the total air we breath VE. That is exactly , why VO2 testing is so dependent on respiration. You breath deep and slow your )2 extraction is much better and you VO2 is going up, but your performance may actually go down , as the deep breathing at that moment is not very efficient and you may need too much O2 just for the respiration ( Dempsey and the metaboreflex ) . That's why respiratory training is better for altitude than any short term acclimatisation . It is not NOT a question of red blood cells only . EPO only works , if (IF ) the O2 transportation system is the limitation. If the cardiac system is the limitation or the respiratory system EPO does not help at all, so that's why we have positive responders on altitude or EPO and negative responders as well. With the FaCT CLR we finally see, where the limitation is and where we have to focus our time to improve the weakest link. What we see is that VO2 has to drop by a given performance ( intensity to show a progress in training as we need less O2 for the same work intensity and this is a sign potentially of a better efficiency from the whole body and now we can see , which system works more efficient. See efficiency sheet in the excel program from Herb | ||
| Juerg Senior Member Username: Juerg Post Number: 2015 Registered: 04-2006 |
Reaching a VO2 plateau in testing . As we discussed with the Conconi test and or other max test we see as well that in a VO2 max test often not even 1/3 of test will show a plateau of a VO2 max. The regular reader on our Forum will see and understand why. In this particular group of sedentary women's the likely hood that the muscles where so great trained, that they simply could not convert more O2 to ATP and the heart and respiratory system as well where reaching a limitation is most likely very slim. The once , who reached a plateau are interesting ,as it would be nice to see the trend in this people with the SV as they as well reached the highest HR in the relative untrained body . here to enjoy : Full Text: • PDF for printing (119.3 KB) • PDF w/ links (162.6 KB) Noella A. Misquita, MD Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland Dawn C. Davis, MS Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland C. Lynne Dobrovolny, MS Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland Alice S. Ryan, PhD Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland Karen E. Dennis, RN, PhD Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland Barbara J. Nicklas, PhD Department of Medicine, Division of Gerontology, University of Maryland School of Medicine, and the Geriatric Research Education and Clinical Center (GRECC), Baltimore VA Medical Center, Baltimore, Maryland This study examines the applicability of using three standard criteria (age-predicted maximal heart rate [HRmax], respiratory exchange ratio [RER>1.10], and plateau in oxygen uptake [Vo2] for the measurement of maximal oxygen consumption (Vo2max) in postmenopausal women. One hundred eight postmenopausal (60 ± 6 years), overweight and obese (body mass index [BMI] = 33 ± 4 kg/m2), sedentary (Vo2max = 19 ± 3 ml/kg/min) women underwent one exercise test (Bruce protocol), and 71 of these women underwent a second test (modified Balke protocol). On test 1, 69 (64%) women achieved age-predicted HRmax, 61 (57%) reached an RER>1.10, and 16 (15%) achieved a plateau in Vo2 (<2 ml/kg/min change). Women who reached age-predicted HRmax and reached an RER of at least 1.10 had a higher peak Vo2 (p <0.01) than women who did not meet these criteria. There was no difference in the highest V02 obtained between women who did and did not achieve a plateau in Vo2 during test 1 (p = 0.55). Resting HR, HRmax, and RER were similar between the two tests. On average, peak Vo2 was higher on the second test (p <0.01). However, Vo2max was not different between exercise tests in women who achieved at least two of the three criteria on both tests (n = 24; test 1, 19.4 ± 3.4; test 2: 19.8 ± 3.7 ml/kg/min; p = NS). In addition, Vo2max was similar between the two exercise tests in 14 women who reached a plateau on the second test but did not reach a plateau on the first test (19.2 ± 3.3 vs. 19.6 ± 4.2 ml/kg/min; p = NS). We conclude that achievement of a plateau in Vo2 is not a necessary criterion for a valid measurement of Vo2max in overweight and obese, sedentary, postmenopausal women. | ||
| Juerg Moderator Username: Juerg Post Number: 3493 Registered: 04-2006 |
Here one nice summary of VO2 max. VO2 max testing and Lactate threshold testing where clearly the most common questions over the 2011. Lactate was discussed on this forum now since many years and the outcome is straight forward. If you are successful with any lactate concept , why would you change. The same holds true for VO2 testing. If you have success in the idea of VO2 max why change. Here a critical note on VO2 max testing to enjoy . " The Great VO2 max Myth The Great VO2 max Myth by Doctor Andrew Bosch I often receive telephone calls from runners wanting to know if it would be possible to measure their VO2 max. My standard answer is something along the lines that it is, indeed, possible. However, I then go on to ask why they want to have their VO2 max measured? There is usually one of two replies. Firstly, I am told, by knowing his or her VO2 max the runner will know that esoteric time that he or she is ultimately capable of running for some particular race distance, and therefore their ultimate potential as a runner. Secondly, once their VO2 max is known it will be possible to prescribe the ultimate personalised training schedule. My response to both is that knowing the VO2 max of a runner does not answer either question.It is widely believed that the VO2 max is genetically determined and unchanging and that an individual is born with either a high or low “max”. Someone with a high value has muscles that are capable of utilising large amounts of oxygen and a cardiovascular system capable of delivering this volume of oxygen. The athlete is able to run at a maximum aerobic speed that this oxygen supply can sustain. In this paradigm it does not appear to matter whether the runner is unfit or superbly fit, the outcome of a VO2 max test remains the same. However, it is intuitively obvious that when fit the athlete can run much faster on the treadmill than when unfit. Thus, since VO2 max is genetically determined and does not change (in this model), VO2 max would be reached at a relatively slow running speed when a runner is unfit compared to when very fit, when a much higher speed can be reached on the treadmill. This means that in a totally unfit world-class runner we would measure a high VO2 max (say 75 ml/kg/min or higher) at a speed of maybe 17 km/hr on the treadmill. When very fit the same athlete will reach the same VO2 max at a speed of about 24 km/hr. The problem is that such a high VO2 max is never measured at a speed of just 17 km/hr. This would be almost impossibly inefficient. The theory of a genetically set and unchanging VO2 max therefore begins to appear a little shaky. This concept of VO2 max evolved from misinterpretation of the data of early experimental work. It was believed that as an athlete ran faster and faster during a treadmill test, the muscles needed an increasing volume of oxygen, a process, which continued until the supply of oxygen, became limiting or the ability of the muscle to utilise oxygen was exceeded. At this point there would be no further increase in oxygen uptake. This plateau in oxygen utilisation was regarded as the VO2 max of the runner. If high, then the athlete had great genetic potential. However, in addition to the problem described in the previous paragraph, half of all runners tested in exercise laboratories never have a plateau in their oxygen uptake. Instead, the oxygen uptake is still increasing when the athlete cannot continue the test. The conventional view of VO2 max now appears to be even more suspect. Consider a different scenario. A runner on a treadmill requires a certain amount of oxygen to run at a given speed. When the speed is increased, there is a corresponding increase in the volume of oxygen needed to run at the higher speed. The runner runs faster and faster, with corresponding increases in the oxygen required, until something other than oxygen supply to the muscle prevents any further increase in running speed. The volume of oxygen being used by the muscle when this occurs is at a maximum value, which is then termed the VO2 max. With this theory, oxygen requirement merely follows the increase in running speed, until a peak running speed and therefore peak oxygen requirement (VO2 max) is reached. It is easy to see why the VO2 max value will change as a runner gets fitter and can run faster. Within this framework, the genetically determined limit of VO2 max is determined by the highest running speed that can be reached, or in some instances a true limit in the supply and utilisation of oxygen by the muscle. The inability to use the VO2 max test as a predictor of future performance in someone who can still improve his or her running by using a scientifically designed training programme becomes obvious. A great training-induced increase in running speed will result in a substantial change in VO2 max. Knowing a VO2 max value is not going to assist in the construction of a training programme any more than will knowing current race times. There are, however, some potential uses of a VO2 max test. When constructing a training programme for someone who has not run any races and who therefore has no race times, a VO2 max test will help give an indication of the current ability of the athlete on which to base training schedules.: On add on is the question : Are only working muscles asking for oxygen or could it be that other organs may need some O2 as well ? |