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     Juerg Senior Member Username: Juerg Post Number: 1625 Registered: 04-2006 |
Look at the classification and give it some thoughts on wattage as a guidance to some physiological ideas as a guidance. Check the top 10 by the half way mark and teh end result. Our final update on the times... Intermediate standings 7.5km 1 Alberto Contador (Spa) Astana 0:11:22 2 Tony Martin (Ger) Columbia-HTC 0:11:27 3 Bradley Wiggins (GBr) Garmin-Slipstream 0:11:28 4 Cadel Evans (Aus) Silence-Lotto 0:11:29 5 Levi Leipheimer (USA) Astana 0:11:30 6 Roman Kreuziger (Cze) Liquigas 0:11:30 7 Vincenzo Nibali (Ita) Liquigas 0:11:31 8 Andreas Klöden (Ger) Astana 0:11:32 9 Lance Armstrong (USA) Astana 0:11:39 10 David Millar (GBr) Garmin-Slipstream 0:11:43 Finish times 1 Fabian Cancellara (Swi) Saxo Bank 0:19:32 2 Alberto Contador (Spa) Astana 0:19:50 3 Bradley Wiggins (GBr) Garmin-Slipstream 0:19:51 4 Andreas Klöden (Ger) Astana 0:19:54 5 Cadel Evans (Aus) Silence-Lotto 0:19:55 6 Levi Leipheimer (USA) Astana 0:20:02 7 Roman Kreuziger (Cze) Liquigas 0:20:04 8 Tony Martin (Ger) Columbia-HTC 0:20:05 9 Vincenzo Nibali (Ita) Liquigas 0:20:09 10 Lance Armstrong (USA) Astana 0:20:12 | ||
| Juerg Senior Member Username: Juerg Post Number: 1630 Registered: 04-2006 |
Now here a nice "interview" section, which shows you, how much is coach and how much is athlete and how much is knowledge and or experience with no background. Yours to enjoy . " "I knew on the first uphill portion I should take it easy and not give it everything, not take in too much lactic acid till the top of the climb. [Directeur sportif] Bjarne Riis told me at the casino that I already started really strong, and then I rode my own pace and made the difference on the flatter parts." The director Sportive was in his olden days more interested in some outside help and missed the idea , that athletes could be developed as well over training ideas. Let's hope there where some training ideas in this victory and not the Olden days ideas. | ||
| Juerg Senior Member Username: Juerg Post Number: 1651 Registered: 04-2006 |
Well let's add another very nice comment from a top cyclist. From the comments you often wonder, how much this athletes really understand from their own body besides the feeling. This is a very common fact. IN a recent presentation I asked some cyclist some very basic questions: a) how heavy is your bike ? b) What gear ratio do you use. c)What wheel do you choose for a ITT. All without exception had the perfect and clear answer. Than I asked: a) How big is your Vital capacity ? b) what is your respiration rate in a ITT c) By what intensity ( watt or HR ) do you have the most optimal or biggest EDV ? d) by what intensity in Watt and or HR you may switch to a more O2 independent energy delivery. All , without exception had no answer or only some suggestion as a guess on what would take place n their own body. This is not just surprising but for me shocking. The main tool for this profession is their own body. So you have a carpenter who knows all about his body , but nothing about his work tools. Would you hire him ? The biggest problem really is , that many of this "pros" give daily interview with answers like the lactic acid one or other myth or ideas, and the reader of the magazine just simply gets' the same low information , as the athletes level is on its own. Here another nice example : " Armstrong confirmed that he is climbing better than he was at the recent Giro d'Italia. "I have a lot better legs than at the Giro, that was to be expected." Well if he works mainly with wattage and genetics and experience , than he can make this statement, but it tells a lot of how much they actually put time into learning the reasons and their own body. Why does his legs feel better: Is it , that thanks to a certain intensity he was riding at the Giro he functionally increased the cardiac hemodynamic. Is it , that with some altitude exposure at the Giro and the long stages on a certain intensity including the training he still did , his respiratory system improved and he just simply make the statement of his legs due to the phenomenon of the "Breathless legs "( Boutellier ). This statement again show the weakness of "classical " testing , where only the improvement of wattage counts. So if the legs feel better you are happy but have no clue why , if he would go not well they would have no clue why. With a proper Physiological testing they could actually assess and see why certain trainings and racing will in fact imp[rove performance in some athletes and certain races and trainings may for an other athlete not work with the same Benefit. Compare Armstrong and Menchov - Giro D'italia and Tour de France. Does the Menchov team knows , why he is so behind Armstrong , or does the Armstrong team physiologically knows , why they are so much better. Or is all based on experience and great personal body feelings ?. This is, where the challenge starts , as we improve testing tools we may have to accept that test ideas will change and that performance tests are a part of the past , with exceptions I test in the actual activity > So I race 5 km if I like to test the performance on 5 km . I do a 40 km TT if I like to know my performance for the 40 km TT. I swim 1500 m if I like to know my actual possible swim time at the current moment. Why would I do a Conconi Test for running and hope the theoretical time based on the test is the real performance. Why would I do a Wingate test on the bike to estimate my 40 km TT. Why would I swim 3 x 200 m and take lactate to estimate my 1'500 m time. Testing is here to find physiological parameters to establish basic information's and answers on how the planned and executed training I planned or my coach planned really may change important functional or structural situations in my body to have a better baseline for the upcoming race and or performance I like to see on a race. | ||
| Juerg Senior Member Username: Juerg Post Number: 1653 Registered: 04-2006 |
Here another world class athlete with the same "problem". "Premont was gracious in defeat, and philosophical. "The national title was not as big a priority for me this year, and I just have come off a big three week training session as I get ready for Mont Ste Anne. I knew this morning that my legs were heavy, and that it would be very hard to the defend the title. " Legs where heavy. One of the common answers of athletes and coaches. The question is why.? The answer is simple as well: 3 weeks training block. Our question: What was the aim of the training block ? was it to get heavy legs ? A possible answer could be yes. If this was really the case to just train the musculoskeletal system than the coach really has an incredible nice ability and knows what he was doing. It is not easy to just train the musculo skeletal system, without straining the card and pulmonary system and in t needs a lot of very smart planning and exercises. Straining the musculoskeletal system over three weeks would have some major implication and to control this stressor it is nice to use ammonia and urea to get a handle on. It would be nice to see this results from premont. We did this in preparation for the 1984 olympics the first time with some 1'500 and 5'000 m runners and it is fascinating to see the very individual responses. My speculation in the above case is, that they really have no idea why the legs where tired if they look specifically . This seems to be answered with the word " 3 weeks training period ". Based on Hans Selye the father of the modern stress research they did the following : They used the training as a stress. Stress or training this way is very unspecific and the result is very unspecific and based purely on hope and experience . The unspecific stress will be hopefully resolved at the right time due to unspecific respond by the bodies own homeostatic build system. The beauty again in this case of three weeks training would have been the FaCT CLR. What did we stress so we move from a stress to a specific STRESSOR. Once we know the STRESSOR ( for example a cardiac training ) we can try to define the goal we like to reach with that STRESSOR. By assessing with FaCT CLR the pre Stressor situation and follow thru with short assessment during the planned block we can see, what and how the body reacts on that very specific STRESSOR. Is he reacting and when at what rate and timing and how strong and what are the results ( for example tired legs ). Remember Boutelliers / Dempsey and the metaboreflex which can produce "breathless legs" One reaction a big portion of athletes have, when exposed to altitude training is exactly the breath less legs. This are as well the same athletes , who are named in the research the so called "altitude non responders " with the outcome, that we have no answer why. Our opinion is, that when the respiratory training is the limiting factor and we go up top altitude we stress ( Stressor is altitude and pO2 change ) again the already weak system. The Stressor hypoxia low pO2 ) with the goal to create more Rbc ( epo ) is not the limitation and even if they would create more Rbc it actually does not help as a way of a better performance, as the limitation is to actually bring the O2 into the system. If the respiratory system is the limitation ( like in COPD or in certain type of asthma and or in pulmonary sarcoidosis the limitation are not the red blood cells. In fact they don't have to go to altitude at all, as in any intensity workout even on sea level the SpO2 is or will drop very easy down to 90 sand even below 90 % so they are constantly in altitude of at least 2'500 m and up. The system will not respond to altitude at all as they stress the EPO system steady. So before any attempt is made with a group to make some altitude studies they would have first top be properly assessed to find out, what is the limitation of their performance and what system and than the coaches can make a good based decision , which athlete would benefit at what time from an altitude camp. So let's hope in the above case from Premont , that their experience was well timed and the result is the way they hope but they don't know. In case of a good result we loose the "discussion" in case of a failure nobody would care about our ideas any way , so that's why we have fun to work as a small group on some very interesting ideas. Have a great day and hopefully not too heavy legs. By the way the legs could be heavy , because we are sitting too much on our butt and than the legs muscles are really the limiting factor . In most of the high performance athletes this is never the case. so limitation of legs are very easy to find out why. Do a 100 m frog jump workout today and check your legs tomorrow . have fun | ||
| Juerg Senior Member Username: Juerg Post Number: 1654 Registered: 04-2006 |
Here a comment from an athlete , who can use Mc' Lean's brain systems from the human Brain over to the mammalian brain and to the reptilian brain in a nice mixture at the right time. " "I was surprised that it held together so long," commented Kabush. "Derek and Max kept making these little surges, but it wasn't enough to really split it up, so i was just hanging in behind them. Max was the guy I was worried about the most, because he has been riding really well this year, but I was also concerned about Seamus because he was hanging out at the back, and I didn't know if he was saving himself for a big attack." The reptilian Brain kicked in after a short precise decision from the human brain : " It turned out that McGrath was at his limit, because when Plaxton jumped, only Zandstra and Kabush could respond. The trio stayed together - with Zandstra and Plaxton making small feints - until shortly before the singletrack climb, when Kabush launched a huge attack that no one could respond to." Races on that level like a Canada cup and a Canadian champion ship are watch on , who is winning and not how much ahead you win. So a comment like this : ""I decided to race it a little differently, to be the pace setter," explained Zandstra. "Geoff and I raced together for the entire Canada Cup in Canmore a few weeks ago, so I knew that I could stay with him." shows , that he forget to watch the time difference at the last few races where the win for the Canadian champion is not easy , as he has stronger competition and has to go to his personal and over his personal limit as well. If you race on and above your own personal comfort zone you have a much harder time to let the human brain make the decisions as in this case. The result will be just to survive. "It turned out that McGrath was at his limit, because when Plaxton jumped, only Zandstra and Kabush could respond." As you can see a very nice report from this journalist and sometimes it would be fun to actually have individual data's prior to the race to see, whether physiological numbers end up in a explanation of the race. I will show you some physiological numbers from a race going on just now in north America, where one of the competing athletes was heralded as a pre race favorite and I thought to myself as I have some physiological data's, if that is really true if he not looses at least 10 - 15 % of the time to the winner I have to go back and review all my crazy idea. Lucky for me the time he looses is pretty much what I expected . I may show some of the data's perhaps , who for myself confirmed, that the "dream " of the athletes is far of to reality of the bodies ability and structure. But having fun seems to me still a very important conditioning factor. Depending on the amount of time you but in and the time investment can be justified with the result. | ||
| Andrew Senior Member Username: Andrew Post Number: 243 Registered: 04-2006 |
Another quote...this time from a 16-year old athlete, regarding a recent discussion on a drop in performance by one of his team mates, who is a 40 year-old age-group triathlete. He has experienced a drop in performance at all levels of intensity, and I will try to attach the graph demonstrating this below. Enjoy the reading...Joel's conclusion match what we have written for "training" for this week, with the plan on retesting next week to watch the effect. "I believe that with a loss of coordination it would only affect a portion of the test (low end or high end). This does not explain the even drop in performance everywere... However, I have found that when I rest for a couple of days I notice that my numbers are worse at the bottom end and better at the top end. You have claimed the oposite with your results in the past. This may not be an issue of coordination. This either reflects the diferance in our training or mabey our bodies... I wonder if I might be stressing my oxygen dependant systems more than my oxygen independant systems, thus my lower end does not have time to recover but my top end does have time to recover. This would explain my and Thompsan's reacent platue of our bottom end systems. This is why I feel it may be benficial to maintain our lower end and adding 1 or 2 high intensity sessions per week. As long as we maintain what we have built we have nothing to loose! This change in my training may also make room to focus on my respiratory training as well. It may take more effort to solve your problem which has been developing for such a long period of time. Possibly a loss of coordination combined with over training. Rest plus nerological training until a change occurs." Joel  | ||
| Juerg Senior Member Username: Juerg Post Number: 1664 Registered: 04-2006 |
Here some additional thoughts on the overlap test picture above. Let's just take only the blue line. This is for us a typical so called " double test line. " Meaning , that we see this type of tests when you start on a treadmill a test and the speed is first too slow for running so you walk and than it is too fast for walking so you run in the middle of the test. You actually still move on the treadmill , but you do two different sport . In cycling it is less common but as well , if you do test and the person starts firt with a different RPM and finally moves either in a higher or lower RPM. This one could suggest the RPM dropped by HR 140. ( Coordination problem ? Now as I don't had the exact HR numbers I estimated it based on the squares and produced a performance line with the estimated HR +- 1 accurate I assume. Now here some assumptions resp. some hints as well when we test. - Check the RPM and mark down should you see a clear change in RPM +- 5 perhaps as some ideas. - _ because we don't "warm up" some coordination fatigue may take some time to be under control and you see a change in the performance line. If the test was done on a taxc trainer than the unit needs some 4 - 8 minute to get a regular resistance. When ever you do a test check if you have the ability and assess RLX or HRV. This will help to see, where the LLL ( lower linear limit) may start as well it may give some additional information , how the cardiac system may have recovered or not. If you look on the three tests above you can see , that the LLL is on the blue line the highest , based on the discussion on the line. This , if true would suggests a better HRV as the other two tests. As we are not completely sure , whether the LLL is accurate with the HRV we now take always the HRV and it is just fun to compare.. Now here two ways we could look at the test.  You can see clear the "double " test performance line. Something clearly "shifted at 140. The correlation here is an incredible 0.999. Now the following is speculation , as we don't have the HRV and other biomarkers. If the LLL really would start by 105 and the HRV is by 105 than we would have to ask some possible question on some cardiac changes. Now by 140 HR area we see, that despite another 20 watt increase, which at that moment is over a 10 % increase n performance we have really no increase in HR ( 2 beats ). So an increase in over 10 % would ask potentially for some additional cardiac output. Cardiac output is HR x SV. As HR does not increase there must be an increase in Stroke volume. Now what we see in some "fatigued cardiac situation is a certain time of "warm up " for the heart itself. At that stage we are about 15 min n the test and if you compare some of the printouts from our running without "warm up " you can see a steady increase in SV over teh first 15 - 20 minutes. So the question here is : Was it lack of warm up of the equipment. \ was it lack of warm up of the cardiac system was it lack of "warm up " of the CNS coordination system. And last but not least we don't know from a performance line alone , whether it was perhaps a lack of "warm up " on the respiratory system. Now let's look at the second performance line:  Same points , but the line is discussed from 141 to the end. correlation 0.994, still better than the discussed line on the overlap. Interesting here really is , that the two point at the beginning are actually perfect on the line, and if you take point 3 to 5 out you have in fact a ).999 correlation. This is an interesting result and agin the performance line does not tell us why and some possible reasons are up there. The problem with the FaCT test in the overlap the way we have it is the same , as when we take wattage or speed, It is as we name it a simple performance line. Like any performance test the performance line is a summary of the function of all involved system at that particular performance wattage. What we don't know is the question on : who or what system contributed how much at that particular point to the result. So what we do is we add, when people do just performance line comparison additionally all easy to collect bio markers to it . This would be RLX ( or HRV . If you don't have a polar watch with HRV use the start of the Own zone test.. You take the Fit test into account. You take the respiration rate in account. and you watch as I am sure was done in this overlap , that you have the same situation like ( equipment warm up or not warm up) and so on. If the test where always done the same , than we can eliminate the 5 % of teh variables the equipment may bring and than it is easier to see possible reasons of the different performance lines. The beauty of the performance line for athletes, like in this case, that there is some changes going on. The beauty of a FaCT coach is, that this cases are what makes coaching so much fun. So as an athlete will sent to you overlaps and we see some changes in performance we are ahead of the game to any other testing system , by now follow up not with a performance test , but rather with a FaCT CLR test. So in this case , when a coach get's a picture like that the next step could be a full assessment and see, what system by this 140 +_ HR is working clearly different , compared with a previous test we had, as we have the performance lines from three tests here. The simple version is to make a FaCT HL and see the change in LBP. A revers deflection ( The opposite we see here ) often goes together with a muscular fatigue and lack of coordination , as the cardiac system can follow the demand but the muscular system not so we have a big increase of HR versus a small one we have here.. So If we add the HRV and it was lower than the previous tests and we have the same deflection as here we are closer to potentially thing cardiac limitation. Now you add simple respiration rate by counting and this is the same as usual you are even closer to cardiac possibilities. Now you add the Fit Mate and have accurate info on the respiration system and you have all the same as before in RF and TV but you see a change in FeO2 and VO2 you have to start eliminating the respiratory system as a potential factor. So you are back on the muscle versus heart. Missing reverse deflection ? now we have to look at the FeO2 % higher would mean less O2 used by the same wattage. either because more efficient or less ability to extract from fatigued muscles Or lower MVO2 by the same wattage which would mean better efficiency. The next step here may be to keep the test going to the same wattage as the last test and see, whether you really could go 20 watts higher with a good feeling which would indicate the better efficiency or you can't reach the same wattage or only with heavy work , that would mean your performance really is worse and the lower VO2 is due to lower performance ability. So you add the info into the recovery sheet and you can see where the recovery looks okay and where you may be far of. With the FaCT CLR you than have the full picture. Here a print from a full recovery assessment . The first number is the number on the way up ( Performance test , the second number is the Physiological FaCT test part. Now when we have to tests like in the overlap than we have the same in the recovery sheet. You use both performance information as we have here and you can see, where there is a difference. In this case you can find out on your own , what system recovered how much and what system may be not recovered by the same wattage.  Summary : This is not a critic on the above tests nor is it the truth on what I write. It is just simply an add on and for me a critic on our own ideas, and an additional example, why performance information is lacking a lot of substance. In case the performance line would have moved up towards the left hand corner we would not even discuss, despite the fact that based on the performance line alone we would have no clue what was shifting the line towards the left corner. In case there is a right corner drop , which could indicate a loss of performance or fatigue, we start , as we do here to discuss. Unfortunately we are not better than any other test , if we only use performance as the info. This is the very weak point of the FaCT H system. as we line up with any other performance test. The idea behind the overlap is to see trends in overall performance and than go back and assess with a physiological test to find the weakness and the strength the previous weeks of the training may have produced and we than can go from there. That's and this example is great for me, is the motivation behind looking for additional help and assessment ideas to eliminate guess work and speculation , and even once we think we have more we still have many unsolved questions , which can change performance lines. ( Nutrition , hydration, mental situation during the test and so on ) So have fun to take FaCT apart as any positive critic and ideas will help us all to go to the next step.  | ||
| Andrew Senior Member Username: Andrew Post Number: 244 Registered: 04-2006 |
Brilliant as always...in fact we did record HRV and resp rate for these tests, but did not report them to keep the discussion at a more introductory level at first. The test was done on a TAXC trainer, and the "warm-up" data was recorded at 100/120/140 watts before the unit was calibrated, and then repeated, with the second time up being recorded for the blue line in this case. When you take the extra data of HRV and resp rate into account, the first interpretation by Juerg makes more sense, as the HRV was down to RLX=4 at only a HR of 105, meaning the LLL was not the 125 as shown in the original overlap. The "feeling" of the test was of heavy legs, and just more difficult than the athlete is used to. We did not have access to the Fitmate on the day of the test, but have planned this for later this week, and will post the results again. If we consider the "double line" with a relatively poor performance up until 180 watts, and then a somewhat better (but still depressed) performance up to 260 watts, we might see a reason to consider the argument for cardiac fatigue. We will add the lactate and FeO2 data to see if our theory on the cardiac fatigue can be confirmed with a drop in LBP. Of course, the Physioflow would be the best way to confirm our belief that the cardiac system is having trouble, but we will do our best to assess this with the equipment we have. Thanks again Juerg, for your interpretation. | ||
| Andrew Senior Member Username: Andrew Post Number: 245 Registered: 04-2006 |
To follow up on the previous post of overlaps showing some sort of system failure. The athlete chose to participate in a Half Ironman last week-end, but used it instead as a training stimulus, rather than as means to test his system which was already under stress from work, life, and lack of sleep. Today (three days post event) we repeated the step test, with Fitmate, and lactate measurements. If you look carefully, you can see there is improvement over the range where we had previously predicted a problem with "cardiac fatigue", which I had attributed to some problem with ability to attain or sustain SV, either due to a drop in EDV, or due to a drop in EF. Without physioflow, we have no idea. However, the athlete feels more rested this week, despite "racing" on the week-end. He was given instructions to do nothing to tax his range where we expect SV to be maximized (predicted to be just below LBP in his case). So, during the "race" he swam well, and then did two types of riding on the hilly course in Osoyoos...short hard efforts to climb the hills, with HR well above LBP, or slower steady state work well below LBP. As expected his bike split was nearly 15 minutes slower than last year, and though he felt good on the run, he stopped after 8km, to allow his body an easier time to recover. Since the race, lots of rest, and only two short easy swims for flexibility and balance. Here are today's results...  From the data list, you can see he went to 260 watts three times. Each time was only slightly less well-controlled as the first. His VO2 data confirmed this, as he actually was more efficient (lower VO2) at 240 watts on the second and third attempt, despite the slightly higher HR. And here is the overlap comparing the results form last week before the race to today's results. Blue line (last week) Pink line (today) Green Line (May-2009) Looking very closely, you will see there is hardly any difference in performance between last week and today, with the exception of the few points between HR=125-140, and a slight difference at the top end. The big difference was the "feel" of the day, and the ability to maintain constant wattage with very little change in lactate on the second and third portions of the test. Breathing and O2 sats were maintained easily up to HR=158, which corresponds very well to the LBP in this case. We are going to make an assumption for this athlete, that the heart is beginning to recover form the stressors that had previously caused some problems, but keep a close eye on this to ensure there are continued improvements over the following 3-4 weeks in preparation for the big race he has planned for October.  | ||
| Juerg Senior Member Username: Juerg Post Number: 1668 Registered: 04-2006 |
This is a very nice test picture . Before we can actually get some closer ideas on the lactate trend we need some more info, as in any test. This is where many organisation ask for the "protocol" As we don't have a standard protocol it is helpful, if people use a FaCT type of an idea to just simply show they individualized protocol. Here an example for the above tests. 1. Performance line : Step tests of 3 min or how long ?. FaCT Physiological section with lactate : how long on each of the different steps. 3 min 5 min or ?. For all classical lactate users: Watch the not uncommon numbers, as by the last step in 260 lac was 3.7 and despite a drop to a much lower wattage and a lower HR the lactate still increased. This will give for the rest of the test some indication of the possible lactate dynamic. So it will be nice to see the individual length of the second part of the test in minutes to actually see the lactate dynamic. Based on the timing and the trend we have some indications. If available it would be fun to see the Fit Mate print in the second part so we can actually fill it in the recovery excel sheet and than compare easy as in Duncan's example the different systems ( in this case the respiratory system in the performance situation and the recovery situation. Plus the heart rate on its own in the performance and recovery situation. Thanks Andrew for that nice example and we can use it nicely to show different ideas and possibilities to answer some open questions with this combination of equipment. | ||
| Juerg Senior Member Username: Juerg Post Number: 1671 Registered: 04-2006 |
I will try to come back this weekend with some interesting graphics from the data collection of the above test, as I got all the VO2 information as well. This is very interesting , as we have on the VO2 info some very clear trends, which may conflict initially with the lactate trend but when we look closer back to the FaCT printout above you may already see what I may have done differently to find out the LBP trend. Check in on the FaCT thread, where we look from our point the test results of some short version FaCT tests. Stay tuned, as I like to use Herb's excel sheet to print out a variety of comparisons from the above VO2 testing. | ||
| Juerg Senior Member Username: Juerg Post Number: 1678 Registered: 04-2006 |
Let's start here with the most common review n a VO2 test. Remember. This is a combination of a FaCT HL test with a FaCT R test. Above you see the lactate dynamic of the athlete as he is basically repeating three "tests from 200 / 220/240/260. The update data's I got from this test is , where I now use to assess the Respiratory system and to a certain ability the Cardiac system . HR Here first some ideas, where I would have done it different. I would not run three times the test from 200 - 260 . Possible problem. 1. As we got from the info before this test person uses 3 steps at the beginning to warm up the taxc trainer system. Than he did this test with 3 min steps duration so all in all above 1 h testing. In some cases we see a drop in glucose , if teh test is going that long and we use blood sugar back ups in any test close or over 60 min to be sure , that the lower or dropping lactate trend is not due to a low glucose storage situation. At the following spot I would have waited 1 additional minute for a re-test at the same intensity. a) After the 260 watt the first time we had 260 watt HR 157 3.7 lac ( Which with 157 was considered his LBP ) Now he dropped to 200 HR 142 Lac 3.9 This after 3 min. So with the HR still at 142 and as it seems the LBP from previous tests close to 160 +- I would add another 1 min 200 watt and check HR trend and re-test lac. . Than go up to a HR somewhat higher 145 +_ we have that here with 144 and 220 watt. Now based on the performance line it was very easy to predict in this case the HR trend , as the 260 seemed to be not that hard for this person, despite the fact that the feeling was not good or great. More important for me would have been the following area.: As he reaches the 240 watt area and a HR of 153 than we know , that in the performance test the lactate was by a bit higher intensity and a slightly higher HR 3.7 So as three minutes are very short, and we have with the 142 and 3.9 an indication in this person that at that stage his lactate dynamic was out of what every reason slow. , I would have stayed after the three minute lactate sampling by 240 for one more minute to see the trend as the 3 and 4 min timing would have given a trend in that stage. Now for sure the next stage of 160 HR and 260 wattage I would have taken a three and 4 min or longer sample to really see the trend. This way I have a shorter test time and less question on possible low glucose situation with lower lactate readings as a consequence. Now when we add the Fit Mate info it is getting very interesting to see certain trends. Here I like to start with HR ? VO2 and you see a very interesting situation with an actually ( rarely seen ) VO2 plateau . Here the graphic .  Red and Blue show a clear perfect plateau and this are the Performance line ( Blue ) and the red line is the first time repeat of 200 - 260. The green line is the third time repeat 200 - 260 , where we as well ahve a lower Lactate info. Now interesting is , that if we move to a low glucose situation we see often a lower lactate level and an increase in VO2. Very nicely to observe in Diabetic I people. The question here i s, whether the lack of glucose as a source of O2 dependent ATP production will cause a more intake of FFA if the intensity still allows it but on cost of a higher O2 need at that level. So if the VO2 is not at its max this could be possible. The way to proof that in this case would be to check the FEO2 trends and see, whether the FeO2 in the green line was on fact potentially lower than in the red line. Or if you have a CO2 sensor the CO2 will drop as you switch to FFA. But again the FeO2 % can often give some info as well. Otherwise we have to do more thinking. Now next up may be to assess what happened with VE and HR resp we can see what happened by looking actual watt performance.  Same colors for the same steps and it shows HR and wattage situation. | ||
| Robh Senior Member Username: Robh Post Number: 451 Registered: 12-2007 |
Performances at the Tour 2009 By: Michele Ferrari Published: 19 Jul 2009 On the ascent to Verbier (638m of difference in height at 7.5%) Alberto Contador (62kg) climbed at 1852 m/h, equal to 6.73 w/kg, developing an average of 417w. Lance Armstrong (72 kg) climbed at 1720 m/h, equal to 6.25 w/kg, developing 450w. The difference between their VAM's is 7.4% in favor of Alberto, while Lance, whose body weight is 16% heavier, pushed 8% more watts: a suggestion that in the upcoming time trial in Annecy it could be a very close and uncertain duel. In Arcalis (751m of ascent at 7.1%) Contador climbed at 1671 m/h, equal to 6.18 w/kg, with Armstrong and all the other best riders at 1649 m/h (6.10 w/kg); but in the last couple of km Alberto had already showed a power that was 7.2% superior to his rivals'. | ||
| Juerg Senior Member Username: Juerg Post Number: 1679 Registered: 04-2006 |
Rob , this is great and pretty much shows, where the researcher has his focus. There is not much of a help in this numbers, besides we know , that the stronger or faster rider is pushing a better body weight to watt ratio. That's pretty much it and I think to speak very open really pathetic , that you need a Ph.D or Dr . titel to be able to rewad out this numbers from a screen. It would be much more helpful, if we had information , what system work so much more efficient or better, that the winner can go that much better of a performance. What limits the one to develop the same wattage by using the energy production in what way. Does the second guy may have a better wattage output , but not in the O2 dependent energy delivery. Testing of the power out put has really nothing to do with exercise physiology. It is exercise physic or mathematics , but not will contribute to a better understanding on improvement or limits of physiological systems. Tests and publications like this numbers feed to the already wrong idea, that we can use power as teh way to define exercise intensities and people like you and me will go out and throw wattage number around on Forums to show how good or bad we are, will go out for workouts by pushing wattage numbers, without understanding that the wattage is the summary of a whole lot more than the power on the pedals and any workout based n power and not based on combination of bio markers at a certain power will be pretty much worth less. The power readings are nothing other than what we see at the finish line the first guy passing the finish line will push the best or highest body weight to power ratio in an uphill race and in a flat race the idea will shift towards the heavier rider, depending on the setup of the flat stretch. So my question really is, besides showing the clear info in clear numbers: What do we really gain from this readouts for future consideration on this athelet towards his strength and or weakness in his physiological system. Just very personal thoughts in a world where absolute numbers dominate. As a last critical question: Where did teh author spent all his time to try to develop real better performance. They can see, that the athletes has to work hard and therefor needs some "help " to recover. What help ? | ||
| Juerg Senior Member Username: Juerg Post Number: 1680 Registered: 04-2006 |
The above is really what shows us , that the current testing is based on absolute performance and maximal performance of a full physiological system. Why would we test for that in a lab. Just let the client race and you see, who is the best. Testing in this day and age has to focus on identifying strength and weakness in teh different system , who contribute to this overall performance. I would like to know , what system allows a winner to push this watt ratios and what stops him from pushing perhaps even more.? That is where physiology comes in , the rest is close to horse racing . I bet based on some ideas, that this guy is winning . No clue why but nevertheless I have some numbers. I get many emails from people asking : Why when I can push over 5oo watts and have a VO2 max for example of 85 I am not able to even stay in a Cat 1 race at the front. ? So what answer do we give him , after he just pushed a higher Body weight ratio at his University Lab and has an equal VO2 max as L.A ? You as teh regular reader answer this question. | ||
| Juerg Senior Member Username: Juerg Post Number: 1681 Registered: 04-2006 |
The above and now follow up info will show, why I responded to Rob's great info as I did above. The printouts are from a Triathlete and we have his FaCT HL info , as well as his FaCT R info from the fit mate. Now let's stay in a practical approach. If L.A has some respiratory restriction prior to a flat TT and A.C is in great shape . What happens with the Watt calculation. What, if there is some cardiac fatigue in one or the other competitor and they just hammer a fixed wattage. I am sure they from their feeling would not do that , but rather will adjust pacing with feeling . Problem : They may have no clue what went wrong . We may get an answer as we have above as we started that thread and The "researcher will tell us the watt ration at that day with no explanation why. So let's go to more physiological information in our above case discussion. Here now some additional info from the assessments : See already the difference in watt ratio in the two time they tested it . Contatdor : 6.73 and 6.18 so nearly 10 % by the same athlete. ( Motivation urge to push and so on ? Or perhaps some special ingredients from ????\  This shows the HR and Tidal volume in the three "tests " as we started out above. Now watch when we compare as well the VO2 / breath with the HR and you start to see some trends.  | ||
| Andrew Senior Member Username: Andrew Post Number: 248 Registered: 04-2006 |
Juerg, I appreciate your time picking apart the different aspects of the three "tests" done with the Fitmate last week. For those who are not used to these discussions, it might all seem a little overwhelming, but stick with it, we might be able to make some sense of it all in the end. First off, let me remind everyone, this was not a FaCT Test. It was not meant to find LBP, nor were we using our brains when we did the lactate samples, as we would noramlly do, even in a simple Level I "protocol". In FaCT testing, we examine the trends and repeat samples when the trends are not obvious, and we challenge a system for longer periods of time to help show greater trends. This is what we teach at the FaCT-Education courses and camps, and that is what we encourage all coaches to do. In this particular case, we decided to stick with 3 minute intervals, to see how the body would respond, when not given the time to fully recover from an intensity slightly higher than perceived LBP. And then we repeated the same steps again, and again, to view the differences in Respiration and HR dynamics, as well as VO2 and pulse oximetry. As Juerg points out, this does not always give us clear answers, but does start to show which system might be limiting the athlete under stress. The reason we tried this was to see first whether the athlete was recovered from a recent race...when comparing Performance Lines overlapping, this certainly seemed to be the case. See the green line compared to the pre-race blue line, and to the better line form May.  This simple look at performance of course only reveals that the athlete's global system is only just as good as it was back in May...nothing more, and certainly no better. So the question remained, is there still ongoing cardiac fatigue, respiratory fatigue, structural damage as a result of racing and "detraining"? The excellent graphs that Juerg has displayed show some clear trends to help answer these questions. In each of the three step tests, there was a clear drop in Tidal Volume above a HR of 152, and not surprisingly a drop in VO2/breath. In the watt/VO2 graph, what we actually see is HIGHER wattage at LOWER VO2 in the 2nd and 3rd step test, and this raises the question of "efficiency". Did the athlete actually get better as the test went on. Certainly he began to use the lactate produced in the first part of the test, which might have given him a more efficient fuel source for subsequent steps. If he had required FFA as a result of a low glucose situation, we might have expected a higher VO2 at each of the given steps. Another possibility, is the first step test allowed him to "warm-up" his CCT to allow more efficient cardiac dynamics? This is impossible to tell without Physioflow data of course. When looking at the HR/watts data, his efficiency seemed to remain stable during the initial recovery, but was subsequently worse in the third round. However, although the HR did not recover initially, as soon as the respiration rate came under control, so did the HR. It is clear in this simple case study that there is a close correlation between respiratory rate, tidal volumes, HR and VO2. From our point of view, it continues to be a question whether the cardiac system remains the limiting factor as we suspected, with an inability to sustain stroke volume, as the overall system begins to fail. The respiratory system recovered on each subsequent test, though it took a little longer to do so each time. The HR was higher with each subsequent test at any given wattage, owing we believe, to the dropping SV. And despite a more "efficient" energy source, and lower VO2 in the final two step tests, the athlete was found each attempt at 260 watts more taxing. In two weeks, we will repeat a similar test with some High Performance athletes, to examine whether they respond in a similar manner to a short SV challenge. | ||
| Juerg Senior Member Username: Juerg Post Number: 1682 Registered: 04-2006 |
As usual Andrew makes some great points and here some add on to his observation. 1. VO2 plateau . What does that mean or could mean. Well as in any plateau it means , that despite the increase in physical performance, where you would expect a higher O2 demand, we can't see that in the graphic. Why ? There are different explanations. Here not an explanation , but a question: O2 moves from the outside over your lungs to the blood and than to the heart and than to the muscles, to make a simple explanation. If the lungs are the limitation we see often a drop of SpO2 ( we don't see that in this test ) If the RBC count is down we see as well often a drop in SpO2. When the cardiac output is not optimal we don't see a drop in SpO2 but a plateau , as the heart seems to have a limitation in itself to move blood and with the blood the amount of O2. So as it moves less blood out ( SV it as well "feeds" less blood to the cardiac circulation. This ( T. Noakes ) will trigger the CGM and with it a "tired" or strenuous feeling in the working muscles despite a low or lower than usual watt level. To finish the above assessment I like to show you some of the left over graphics and you see in all a trend by 240 watt and or 150 +- HR a change in the ability to perform. The interesting part in this case would have been to actually have a LBP trend as suggested and see, whether LBP may in fact drop as a indirect info on cardiac or respiratory fatigue. If we can see that , than we as well can see this , as in this case with Fit Mate and lactate , as we clearly see here , that the respiratory system reacts but not as a "fatigue situation , but rather as a possible reaction due to cardiac "fatigue ". Here the rest of the "story " without interpretation yet .  } | ||
| Andrew Senior Member Username: Andrew Post Number: 249 Registered: 04-2006 |
Thank-you Juerg for helping confirm some of my possible conclusions based on how I have felt, and what you have taught me through your work with the Physioflow. I will retest this week with doing repeated LBP tests in a single session, with similar steps to last week, but with a "smarter" approach to actually looking at trends, rather than just challenging the system. I believe we may see a small shift upwards of the LBP in the second or third test, as the heart moves to a more efficient CCT, even as the SV begins to falter. I will not have the Fitmate this time, but will repeat that test again on my return form travels to the North...much farther North than even Quesnel. We are reviewing some of your recent work with some athletes in Yellowknife this week. So your wisdom and questions are being shared all around the world. Even where the sun is shining 23 hours each day. | ||
| Robh Senior Member Username: Robh Post Number: 452 Registered: 12-2007 |
Some more analysis on Contador's VAM figures on the Verbier. Source :- http://www.sportsscientists.com/2009/07/tour-2009-contador-climb.html The anatomy of a climb: Contador on the Verbier - its place in Tour climbing "history" Well, the response to the post yesterday describing Contador's climb has been overwhelming - being in SA, I slept through most of your emails and woke this morning to a deluge of comments and analysis of the climb. Thank you to everyone for your input. It would be wonderful to do a more detailed breakdown of the climb, but that would require accurate information regarding the profile and the specific gradients per kilometer. Unfortunately, there is little chance of consensus on the actual figures for the climb. Many of you have commented in the last post and referred me to profiles, breakdowns, specific kilometer-by-kilometer gradients, and thank you very much for that. However, not a single person's input agrees with anyone else's! For example, on the Tour website, the climb is listed as 8.7km at 7.5%. However, the profiles many of you provided vary quite a bit from this. The Tour profile indicates a 9km climb with a total rise of 638m (a gradient of 7.1%). Other websites were saying it was 8.8km at 7.5%, or 7.1%, or 8.3 km long. There was even a suggestion that it was only 7.2km long! Finding the real profile seems a mission impossible! This has obvious implications for the calculated wattage and VAM on the day. I believe that the distance of the climb is 8.7km - I base this on the fact that at the bottom of climb, as the peloton turned left, the banner signalling the start of the King of the Mountains "competition" very clearly indicated 8.7km to the summit. I can believe that the Tour website might be incorrect, but I find it difficult to believe that they would also err on the actual measurement of the route. Also, one of you said that an SRM from a Tour rider showed the length of the climb to be 8.74km. So I think it's a safe bet to say that the climb is 8.7km long. In terms of the vertical rise, it is more difficult. It seems that most are saying that it rises 638m. A few commenters said this, and it was also the assumption used Dr Michele Ferrari in his own analysis of the climb at 53x12.com. Finally, SRM data from yesterday suggests that the climb is 640m, which differs from the 653m that is inferred from the official Tour guide and even from the mapmyride.com route, which has a 653m rise over an 8.7km length. As a result of all this "disagreement", doing a detailed analysis on this kind of data is fraught with assumptions and therefore possible errors. As it is, Contador's climbing rate is either 1858m/hour or it is 1900m/hour. A small error - 2%, but still, going into more detail than this makes that error even greater. So unfortunately, a detailed breakdown of the climb is not possible until one knows the altitude and distances with greater certainty - at the moment, the figures just don't match up. The mere fact that there is so much "disagreement" from one profile to the next, where the climb begins and ends, and what the gradient was means it's pretty speculative to try to work out power output per kilometer. I was really hopeful this would be possible, because it would have been fascinating to track how Contador's power peaked and then stabilised as he first followed, then attacked and built his lead. Comparison between Contador and the history of the Tour Nevertheless, it is still interesting to compare Contador's climb to those of riders in the past. I said yesterday that Contador's rate of 1900m/hour (based on the 8.7km @ 7.5% assumption, recall) was a record in the Tour. I know a lot of people have said that VAMs alone cannot be used to compare one climb to another. If you do so 'blindly', I agree, but provided you acknowledge that length of the climb and its gradient influences VAMs, as you'll see below, then this analysis is still quite intriguing. It will reveal, for example, that Contador's high VAM was achieved on the least steep of all the top 10 climbs in the history of the Tour. Therefore, on a steeper climb, it would be even higher. Yes, it was also a short climb, but more on that below. If we go with the more conservative climb of 640m (as per SRM data), then the climbing rate is lower, at 1864m/hour. That is still a record in the Tour, mind you, as the graph below shows. This is a graph of the twelve highest VAMs ever in the Tour de France (click on it to enlarge if it's too small):  So Contador surpasses Riis' climb of Hautacam 13 years ago, as well as those of Pantani, Armstrong, Leblanc (a surprise name on this list!) and Ullrich. Just as an aside, Pantani's form in 1997 was astonishing. VAM and relative power output, and influence of gradient VAM (or vertical ascent in meters per hour) is a measurement popularised by Dr Michele Ferrari (yes, that one) as a means of comparison between riders and climbs, because it can be used to calculate relative power output. It is important to understand that VAM is affected by the gradient. According to Dr Ferrari himself, the higher the grade, the greater the VAM at a given power output. The relationship between VAM and relative power output is defined as follows: Relative power (W/kg) = VAM (m/hour) / (Gradient factor x 100) This gradient factor ranges between 2.6 for a gradient of 6% and 3.1 for a gradient of 11% (The gradient factor is equal to [2 plus (% grade/10)]. You can read more on this relationship here) Implications for the Contador climb This has implications for Contador's climb. For Contador, the relative power output can be calculated by taking the VAM (1864m/h) and dividing by 275 (the constant for 7.5%). This gives a relative power output of 6.78 W/kg. (Ferrari calculates 6.73W/kg, but he uses a VAM of 1852m/h, because his ascent is 638m, not 640m. This shows again the discrepancies in measuring this Verbier climb!) The point I have to make is that on a steeper climb, the same power output would produce an EVEN HIGHER VAM. Therefore, if you look at that graph above, Contador's record VAM would have been higher on any of the other slopes - Alpe d'Huez at 8.1%, Hautacam at 7.7% and Joux Plane at 8.5% would produce higher VAMS. For example, had Contador been on an 8.5% slope, producing the same power output, his VAM would increase to 1932m/hour. In other words, Contador's climb was a record IN SPITE of the more gradual climb. Confounders and explainers There are a number of things that have to be factored into all these performances, particularly that of Contador. I touched on some yesterday, but here are some other contributing factors: Wind It's been reported that there was quite a strong wind blowing up the valley on the climb. Alex very helpfully calculated what impact a wind would have on the required power output on the climb. It turns out that with NO WIND, the power output required on the climb is approximately 422W. A tail-wind speed of 3m/s (10km/hour) reduces the power output required to 387W, which is a pretty sizeable difference. Of course, the climb cannot have had a tailwind all the way up - it had hairpins and so there will have been headwinds and tailwinds. However, this is an average tailwind, and it seems reasonable. I tried to watch for signs of strong winds on the climb, but must confess it was not noticeable. Also, in the graph above, there is no controlling for the wind. Perhaps LeBlanc had a mighty tail-wind on Hautacam in 1994? Perhaps Pantani faced a head-wind in 1997 and could even have been faster? It's impossible to factor that in, which is why it can be risky making judgements in isolation! That is why averages over longer time-periods provide more meaningful information than once off events. The average power output on climbs over the course of a Tour tells you more than single climbs (but more on that in other posts). However, it's safe to say that wind can have a substantial impact on climbing power calculated from ascent time. Climb length Many have been quick to point out that the climbing rate should be higher, given that Verbier is a shorter climb than most of those done at the end of Tours. This is certainly a factor, since most of the climbs in the above list are 35 minutes long (Hautacam) or even longer (Alpe d'Huez). Soler's climb in 2007 was short - 22 minutes, but the difference in length is certainly partly responsible. Therefore, Contador's record VAM is at least partly due to a shorter climb. I say "partly", because I don't believe that the effect of length is as great as many seem to believe. It's certainly a factor, I don't wish to dismiss it, but not as large as one might first thing. For example, when the Tour did the time-trial on Alpe d'Huez in 2004, the climbing times of all the main riders was only just marginally faster than when the same climb was done at the end of a 200km stage (all the other times in that list above). Similarly, long climbs like the Tourmalet and Mont Ventoux are climbed only a few percent slower than the shorter climbs, and so while length plays a role, and would account for some of Contador's record ascent rate, it's not as simple as saying "shorter equals faster". Race situation I will say that the way this Tour had gone, the first big finish was always going to be spectacular. The Tour was effectively dormant for 8 days, and the Pyrenees were done with minimal attrition. Therefore, given the situation and the way that the race had developed, the climb was always going to be fast. This again illustrates how isolated climbs can't be taken out of context, and is the reason one should look at a collection of climbs to reduce the impact of these confounders as much as is possible. Doping? Finally, I did mention in yesterday's post that given the change in pro-cycling over the last few years, one would expect a drop in climbing rates, not new records. People will wonder about what this record ascent means - it's only natural given cycling's history! I've hopefully managed to explain some of the other factors that must be considered in the Contador climb, but this question remains, without a doubt. It would be naive to dismiss it out of hand. I will say that performance analysis of single performances does not constitute proof of anything. In fact, it's a weak method of inferring doping. That was never my intention in yesterday's post, by the way (in case it came across that way). The better approach is to look at all climbs and work on averages, as I did for Tour winners from 1989 to 2001 in a previous post. Why? Because doping has an effect on the repeatability of the performance, just as much as it affects performance acutely. Many will think only of the acute doping effect, but in fact, most of the doping products exert an even bigger effect on recovery, and hence the ability to produce this level of performance over and over. Think testosterone, growth hormone, cortisone, insulin - all are used to reduce stress response or improve post-exercise recovery. Even EPO would have this effect. Therefore, one cannot infer too much from a once-off performance. Rather, you have to look at a collection of performances, which also partly addresses variability provided by wind speed, temperatures and race situation. In time, however, this performance will be placed into context - one of perhaps 10 climbs in the 2009 Tour, just as there may have been 10 climbs in 2008, 2002 or 1996. At that point, one will get a better idea of what is happening, and hopefully the analysis we did of the Tour winners 1989 to 2001 will be comparable to what is happening now. Conclusion That's the short analysis of Contador's climb. It was spectacular, without a doubt - a record in the Tour, even factoring in wind and climb length. There are too many unanswered questions regarding wind, absolute power, gradients and distances, however, which is a pity. Hopefully the discussion and the great debate it produces is worth the absence of a definitive answer! Certainly it has generated a lot of discussion, for which we thank you once again! Bring on day 2 in the Alps! Ross | ||
| Juerg Senior Member Username: Juerg Post Number: 1686 Registered: 04-2006 |
Of teh 9 top results in the climbing analyses 6 where done with drugs as we know today with poof. Some more comments on that ? | ||
| Robh Senior Member Username: Robh Post Number: 454 Registered: 12-2007 |
From the google wattage forum :- "Just saw LA interviewed pre the stage today. He said AC's VAM on Verbier was 1852 and then said that his own best ever on Aple D'Huez was 1790, he said he was never as good climbing as AC "back in the day". " | ||
| Juerg Senior Member Username: Juerg Post Number: 1687 Registered: 04-2006 |
I really like the last part of the article. Unfortunately as he is a cycling fan he misses the consequences of other sport organisations like track and field as one of the examples or cross country skiing as the other. Cyclist and cycling fans claim , that their sport is the most tested one , which may have some truth to it. nevertheless Track and field for example avoids very clearly using former top results like Ben Johnson or Marina Jones to be listed as "achievements" in retrospective analyzes, as they where tainted with some additional help. So using Pantani's or Rhys information in a summary just moves Contadors result even closer to the open question on how come , that most of teh top climbing results where done in the Festina time ( Willy Voet ) and now here is one , who suddenly moves to the top of the list without drugs. ( How can he so much faster without drugs , than guys , who where using a lot of them ? ) Again this article is great and again it misses the opportunity to explain the mathematical numbers by having open access to the physiological abilities of these athletes. This would be interesting and than any cyclist can compare his physiological structural situation and will understand the difference in wattage performance. Here just a very small inside view in one of teh athletes , who wrote a part of this Verbier stage history . His limiting factor is for sure not the respiratory system. Here for all Hobby racer like we are e. VC of that racers is 8.2 liter. In a hard effort his TV is 4 liter and his respiration rate up to 50 which gives him a respiratory minute volume of 200 liter and more by an extraction of FeO2 % of just above 14 %. So for any person , who ever did a FaCT test in a FaCT certified Center . ( Certified by www.fact-education.com) or on any FaCT NOC center will have information on his respiratory structural and functional ability and will have a first glimpse at teh structural difference between a top athlete and a hobby athlete. Even more extreme is the information , once we look at cardiac hemodynamics and than we understand why there is so much more overall performance in this athletes besides hopefully a healthy and smart nutritional intervention ( not chemical altered nutrition ) . | ||
| Andrew Senior Member Username: Andrew Post Number: 250 Registered: 04-2006 |
Another good quote, without any physiologic explanation...maybe one day we can come up with an answer. Sastre may prefer to get going gradually - we have seen that before. The danger is that if any good moves go clear on this climb, he'll be too far back to be involved. And if the bunch splits, he'll have a lot of chasing to do. Also, sometimes riders feel bad at the start and then feel stronger than usual at the end...it's a peculiar physiological thing. Greg LeMond was suffereing hugely in the 1989 world championshps and considered pulling out, but persisted... He said afterwards that he felt very, very strong towards the end of the race. | ||
| Juerg Senior Member Username: Juerg Post Number: 1688 Registered: 04-2006 |
Here some more thoughts: As you can read in the conclusion , really they have no information besides physical information on calculated wattage and speed and speed of tail wind and body weight and so on. You would wonder really how the physiological systems where able to provide the needed ATP production for this effort. Here from a FaCT point of view, what this "Physiological " guys may be able to look in the future. Bio mechanical position on the bike to see the difference in Tidal volume and respiratory frequency. SpO2 drop going up to altitude. FeO2 % as a possible information to understand the metabolic delivery system Even better would be live cardiac information besides the HR like adjustment of EDV due to change of RPM as well as EF % due to change in respiratory work as well as LVET and with it cardiac contraction time. There are very different reaction in the cardiac hemodynamic caused by respiratory changes, as well as caused by upper body positions and it seems to me nobody really has some ideas how that works, in fact I think for the moment this top Pro's really just use their body feeling to adjust naturally to the possible best work ability . If it works they are happy if not they have no explanation. This nice summary above again shows , how over the last few years the efforts went into development of bikes and aerodynamics and drugs which works out side the limitations, but unfortunately very little is done to actually improve the physiological system This is not just in cycling . Another example where we strive for faster times but use technology is the once very equal sport of swimming , where you had some swim pants and that is it . Now you have different swim suits to make your body more water "stream" and one may wonder , whether there is still an even playing field. And if it is , why to spent so much money to swim in this suits , if they really would not make a difference. Do we really have faster physiological looked swimmers or do they just swim faster due to technology. ? Just some interesting thoughts, as we work mainly down on earth with people who may just simply like to stay healthy have fun and improve their own physiological system to the next personal best. | ||
| Juerg Senior Member Username: Juerg Post Number: 1689 Registered: 04-2006 |
Here what I mean in real time words from a top rider: " The day was different to Sunday's stage to Verbier, where Armstrong lost 1:35 to the favourites. He said he made changes to his position on the bike yesterday, the Tour's second rest day. "I certainly felt more conformable on the bike. If I go back and look at the videotape of Verbier I can tell that on the bike I was just like a fish out of water." So with some physiological ideas, they would find out easy , what position from a physiological point offers the best ATP supply and this would give the best feeling as well. So they try and are not sure why it worked or did not work. If you look at the budget of any of this top teams you may wonder where all the money goes ? | ||
| Juerg Senior Member Username: Juerg Post Number: 1690 Registered: 04-2006 |
And here another live info from today with some support on my critical ideas : Are the swimmers that good? Yes. But their suits may be even better. Last summer at the Beijing Olympics, the Speedo LZR Racer gave an unprecedented boost to the athletes in the pool, resulting in an avalanche of broken records. Many of those marks could fall again at the 2009 world championships in Rome, where further advancements in suit design could make the swimmers even faster | ||
| Juerg Senior Member Username: Juerg Post Number: 1693 Registered: 04-2006 |
Now it will be very interesting after the TT , how the "sport physiologist " calculate the explanation of the Watt/body weight ratio between Contador and Armstrong. The prediction was kind of different was it ? Well again there are calculation in physiology but than there is actual; physiological ideas and reactions ( with still the open question on some additional help from some chemical possibilities ) Check out the second placed rider in the Giro and how he managed to be second behind the winner , who is somewhat involved in some ongoing discussions. Interesting as well the incredible drop in Menchovs performance. This would rather be a sign of normal performance at teh Giro and a dramatically overload in the Giro with some very normal physiological fatigue reactions. If there is something ( we believe there is ) a fatigue reaction after workouts, than the idea of using physical numbers like wattage for zoning has again to be seriously discussed. Let's wait for all the power calculation and explanations , why it was a different results than expected. | ||
| Juerg Senior Member Username: Juerg Post Number: 1694 Registered: 04-2006 |
Michele Ferraris "physiological " prediction based on physical information's. You are the judge : The difference between their VAM's is 7.4% in favor of Alberto, while Lance, whose body weight is 16% heavier, pushed 8% more watts: a suggestion that in the upcoming time trial in Annecy it could be a very close and uncertain duel. | ||
| Juerg Senior Member Username: Juerg Post Number: 1696 Registered: 04-2006 |
Here is another example, which shows, that there is very little progress made in the view on VO2 since Costill et all 1971. Why . In the year 1969 Derek Clayton run a world record in marathon of incredible 2.08.34. Incredible as the assumed , that his VO2 max must be 80 and higher . Reality was that Costill measured a VO2 max of 69.7. As an example Joan Benoit run n the year 1992 a marathon for women's in 2h 24.52. . Her VO2 max was 78.6. And a few years back a cyclist L. A run a marathon just under 3 h with a VO2 max of 85. Now over nearly 35 years later they still discuss maximal VO2 values in absurd um to proof what. The only physiological info is the % of VO2 the athlete can use at this high intensity . This is direct dependent on the optimal function of the cardiac hemodynamic with an optimal team work of respiration and musculoskeletal action controlled by the CNS. So here the discussion from the "Pro's " LeMond's criticism arose after former Festina team trainer Antoine Vayer calculated Contador's VO2 max (his aerobic capacity) at 99.5 based on the Spaniard's time of 20:55 to ascend to the summit. Vayer, writing in Liberation.fr, based his calculation on an estimated 490 watt average he said Contador would have needed to accomplish that feat.. So the discussion is ongoing but of very little value, as the simple task is not addressed. VO2 = CO x ( a- V ) O2 difference, with a big part of the end result depending on the CO and the CO depending on much more than wattage. Remember : CO = SV x HR. The HR is dependent on different situations like LVET for example. SV is dependent on the EDV, preload and so on and EF %. So an interesting part is the RPM where we see, that a slower RPM may have a different influence on EDV. Now you move to the (a-v) O2 difference and you have a big set of variables , which can make a big difference on this side of the equation. As long we are stuck on maximal comparisons of physical information like wattage and maximal VO2 numbers we will have an ongoing discussion on Drug or not drug. The key would be to really assess this top athletes physiologically different to see, what kind of structural difference they really have. Just some thoughts from the Bush in the north of Canada. | ||
| Robh Senior Member Username: Robh Post Number: 456 Registered: 12-2007 |
The article juerg has mentioned :- http://www.lemonde.fr/sports/article/200 9/07/23/alberto-prouve-moi-qu-on-peut-cr oire-en-toi-par-greg-lemond_1221871_3242 .html Translation of Lemond in Le Monde :- What is one to make of Contadors record setting speed on the climb to Verbier? According to Antoine Vayer and his recently published calculations he would need a VO2 max of 99.5ml to do this effort. As far as I know, this is a number which has never been recorded by any athlete in any sport. This value corresponds to the oxygen needs required of many recent Tour de France winners performances in mountain stages and time trials. This is like a gorgeous Mercedes sedan from the showroom showing up for an F1 race and being competitive or winning. It just doesn’t add up, show me what is really under the hood. Could an undoped individual accomplish the speed and power output that Contador produced? Possibly. If Antoine Vayers study is correct, Contador would have to be the first human ever recorded with these values. If we accept that the VO2 max test and our other mathematical equations are accurate and valid, the burden is on Contador to prove that he is indeed physically capable of doing this without the aid of performance enhancement. Given the recent history in our sport we need to remain skeptical. This means we should doubt these extraodinary performances. The skeptic in me looks at this and says prove it to me Alberto. I want to know, what is your VO2 max? If we know Contadors VO2max we would know what to make of this result. The fastest climb in Tour de France history. The future of testing will not be just through individual blood and urine tests but using an evaluation method of the physiological parameters that an individual posesses. This would need to begin when a cyclist starts to compete even as a junior. Much like the long term biopassport follows blood parameters this would follow an individuals VO2 max over time. These values do not vary greatly over time. Even now I just did a VO2 max test and I still take in 6.2 liters of oxygen which is .2 liters short of my values when I was competing. Of course my VO2 max is much lower because I have gained some weight since then! Measuring wattage outputs and Vo2 max would be similar to having the DNA repository available for proof of a crime. I do not know the true values of Alberto Contador nor do I know the weather conditions for that stage. For the moment I would not make any judgement without further data. In the Festina trial, testimony was given that riders with a VO2 max in the 70’s were able to get their VO2 maxes up into the 90’s.This is very important for each of us to acknowledge. The performance increase is so remarkable that no clean rider could even compete with this. We would have known about the extensive EPO use and the blood doping in progress in Operation Puerto had we used these detection methods long before this oxygen transport doping became so deeply embedded in our sport.This is why I remain a skeptic of any performance which seems too good to be true. The Tour de France has been incredibly exciting this year. I loved watching these new young riders climbing with grimaces on their faces. Reaching their personal limits. I am hopeful that this new generation will bring a new way of thinking into the peloton. | ||
| Robh Senior Member Username: Robh Post Number: 457 Registered: 12-2007 |
Juerg, This article was posted on my club site so I posted your response. Here's a reply :- "I wish I understood all of those abbreviations. LVET, CO and EDV etc. One thing I wonder about in Jeurg's article is how can he be certain that the people he is using as anecdotal evidence weren't themselves employing blood manipulation techniques on the day?" | ||
| Juerg Senior Member Username: Juerg Post Number: 1697 Registered: 04-2006 |
Thanks Rob. The answer is actually a very nice one. This is really the question: Who is actually of this top riders out there clean. If we go from this critical and sceptical point , than we have ask our self even more: Why do we as not race cyclist on the Pro ranks even use ideas like wattage zoning and believe this is the way to go , when in fact we work on a very different scale of medical support , as well as with very different recovery ability. So using the ideas and equipment of wattage (SRM ) and zoning for this critical person would be a very interesting discussion. The other part is ( Abbreviations ) This are very common abbreviations in connection with Physiological information's. The point the writers makes shows, that the Physical abbreviations like watt, mph, 52/48/44 or SRAM or BB or dish wheel are very common as a language in cyclists. Most understand gear ratio and tire pressure and so on, but interesting enough very little know their own tool and how their own body works. If people are interested they shall enjoy the thread physio flow and enjoy the reading on this term. The critical question is very well taken and yes it is a big question. This underscores the need to start switching to more info on physiological parameters. Structural changes versus functional reactions. Some may remember the critical question or statement of our former rower from the UK , who does believe functional and structural are just games of words. Well any blood doping manipulation will have a clear functional answer as oppose to a structural change, as Cera and EPO or any plasma expander will work very fast and mainly first functionally. Thanks Rob for this short and critical info. | ||
| Juerg Senior Member Username: Juerg Post Number: 1698 Registered: 04-2006 |
Here an add on to Rob's post. This is an example on Max VO2 from one runner ( I am sure not on any Drugs) Local Girl running in a marathon L.A was running. L.A VO2 max 85 Running time in the race just under 3.h Local running girl from here same age as L.A. Running time 2h. 56 minutes so in fact basically same time. Female runner Max. Tested VO2 1 week before 55. Now I am sure the 2.56 runner was NOT on anything . True I am not sure about the other runner. ??? Now here some info on our abbreviation for Rob's responder. If we look at VO2 than the following formula is internationally used. VO2 = Volume of oxygen used in the body during a certain activity. Max VO2 is the amount of VO2 used at maximal voluntarily performance. VO2 - CO x ( a-v) O2 difference CO = cardiac output and it is measured in L/ min CO is calculated by taking heart rate and multiply with SV = Stroke volume. SV = in ml is the amount of blood the heart is throwing out with each heart beat. Now if we look at performance we have to know the ability of the pump ( heart ) to understand, how much blood a person can pump. Next up is to find out how much oxygen is in this blood before it moves to the working muscles and than how much was used in the working muscles. This will tell us how much O2 the person may be able to use to concert O2 together with oxygen dependent energy sources into ATP in all the systems needed to accomplish the 490 wattage. The mistake we do is to believe , that as higher the VO2 as higher the performance. This is not completely true. As VO2 max is the same as wattage. It is the information of the overall O2 usage. It does not reflect how much each system needs to function . ( Systems means your heart , your respiratory sysytem even your brain and your muscles. To move O2 to the heart we need first a great respiratory sysytem. Than to move it from a good working respiratory sysytem to the heart we need an optimal transportation sysytem ( Blood - that's where EPO and other ideas come in ) and than we need a good heart function and so on. let's stay with teh heart . The Stroke volume depends on some additional factors. 1. EDV - end diastolic volume (in ml ) is the amount of blood we have after the filling time. The SV can never be bigger than the EDV, The % left in the heart after the the throwing out phase ( systolic ) will give information on the EF % = ejection fraction. Example. EDV 100 ml SV 75 ml EF % = 75 %. Some athletes increase SV by increasing EF % some not. EDV depends on plasma volume 9 Drugs ) and on respiration technique ( TV ) TV = tidal volume or how much air you move per breath . ( TV = in the lungs is like SV for the heart ) heart rate is like respiration frequency in breathing. Now if you breath very fast and shallow TV will drop. Now when your heart is beating very fast often SV drops as well. LVET = left ventricular ejection time in milliseconds. This is the time the heart valves are open , when your throw out the blood. So if you beat 150 beats / min and you have an opening of 200 ms per beat your heart has a CCT = cardiac contraction time ( FaCT ) for 30 sec. as CCT is HR x LVET. Now your heart is diuring 30 seconds contracted and therefore can't get O2 resp blood for itself. This may cause some changes in the "set-point " like we have a baroreflex and a metaboreflex we may have a " cardio reflex" warning your brain of potential risk of low pO2 in teh cardiac muscles ,which would have bad consequences. Now top athletes have very low LVET so they can afford very high HR resp. Top athletes may have very high plasma volumes ( nutrition and if the have structurally a big heart they have a big EDV therefor and because of a very "elastic " strong heart muscle possibly a high EF % and therefor a higher SV Example. Average cyclist we test. CO 25 l/ min SV 150 - 180 LVET 150 ms - 200 EF 85 % Top athletes CO 35 - 40 L / min SV 220 - 250. LVET 100 - 125 EF 90 % + So Rob hope you can "translate that to your readers as a possible helpful answer. The motor heart is of major implication n a performance like this top riders have to do. | ||
| Juerg Senior Member Username: Juerg Post Number: 1699 Registered: 04-2006 |
Here for Rob's use a real time print during a workout, where we see live the action and contribution of the cardiac sysytem to the performance at a given time. If we combine this with watt as a physical information and add respiratory information to it , as well as some metabolic markers like lactate we see, that there are very different ways a certain VO2 value will create performance . we can see by 200 watt people pumping 25 CO out and another person by 200 watt pumping 20 l/ min CO. All this has a direct influence how effective the O2 used can be put into performance of movement. Here the printout as it is one of the rare printouts and possible the first seen in the UK with this constellation and this test ideas.  Explanation of the picture: Top left is heart rate dynamic during a step test Next to the right on top row: SV = Stroke volume measured in ml per beat and this is during the same step test. Next top row is CO = cardiac output measured in l? min and it is the product of HR x SV next up on the top right side is EF % = ejection fraction . This is the result of SV/ EDV. EDV readings is middle picture lower row. EDV = end diastolic volume measure in ml as well and this is the amount of blood in the heart after filling time or just before systolic action ( throwing blood out ) Left lower row is LVET = left ventricular ejection time in ms is the time of opening of the valve during systolic ( throw out action ) So you take HR x LVET and you can speculate on this pictures , where this person will reach 30 sec CCT. Try to find out on the screen on what level and post it here. Last on the lower row is SVR = systemic vascular resistance or simply put the after load of how much resistance the heart a has to pump against. This are all values, who directly will influence wattage output in combination with respiration and muscular ability to create ATP efficient and than the transportation of the O2 from and too this places. Here is the key to explain performance rather than watt and VO2 max values. | ||
| Robh Senior Member Username: Robh Post Number: 458 Registered: 12-2007 |
Hi Juerg, Thanks for the explanation. The people from sportscientists.com have looked into Alberto's supposed calculated 99.5 ml/kg/min Vo2 max :- Alberto Contador - can he have a VO2max of 99.5 ml/kg/min? I came across this interesting piece on Cyclingnews this morning. It caught my eye because it's an extension of a topic that we've been covering in the last week, analysing Alberto Contador's Tour-winning climb up to Verbier. In the article, Antoine Vayer calculates that given Contador's power output on that climb (which he calculates as 490W for a 78kg "normalized" rider - more on that later), and with one or two assumptions to turn that power output into oxygen consumption, Contador would be riding at 5.55 L/min. The problem with this is that it implies that Contador's VO2max is about 99.5ml/kg/min! Not that VO2max is the be-all and end-all of exercise, mind you (though some still believe it's the key variable), but that value is off the charts. Some would say preposterous. Most elite athletes have VO2max values between 70 and 80 ml/kg/min, with a few above this. For Contador to be approaching 100ml/kg/min clearly raises a flag. And it did, with Greg Lemond calling for proof that Contador is capable of achieving these numbers without using performance enhanching products "assuming the validity of the calculations". And herein lies the catch - are the calculations valid? Well, first of all (and thank you to Seb for pointing this out - my French is hardly 'parfait', so I'm afraid I can't do the original piece justice!), the Cycling News article is actually incorrect when it quotes Vayer as calculating a power output of 490W. In fact, what Vayer has done is to work out a power output and then normalize it for a rider of 70kg and a bike of 8kg, so that different riders can be compared. This value of 490W actually corresponds to an 'absolute' power output of 440W for Contador. This has implications for how one discusses Vayer's subsequent calculations. Just on this note, I still think that this calculated power output of 440W is a little on the high side. For example: * Last week, we looked at Contador's climbing rate (VAMs) and using Michele Ferrari's formula, arrive at a power output of 6.78 W/kg, or 420W. * Alex Simmons very kindly provided some calculations for the climb, given the speed and gradient, and he arrived at a value of 422 W. He went on to show that if you assume even a small following wind, this power output drops to 397W. * Using the same principles, but making more "aggressive" assumptions, I have calculated the power output at around 440 W - this is an upper end, call it the "worst case scenario", because I think Alex has pretty much arrived at the accurate figures using his equations (which match the estimation of the Ferrari equations based on VAMs). The only way I can arrive at this high a power output is to assume a headwind (which is very unlikely), or that the climb was steeper or longer (or that Contador was riding a bike weighing 13kg!). The length and gradient are contentious - we couldn't find any agreement on how long it was or how high it climbed, so Vayer may well be right. In the end, the data from Trainingpeaks.com showed an 8.7km climb and 640m ascent, which seems the safest bet. There are some other assumptions you have to make - the air density, surface area and so on. However, these have a much smaller impact on the power output than gradient, speed and mass - a lot of people wrote in about this, the effect of air density and road surface. They're factors, don't get me wrong, but they're really very small in comparison with speed, mass and grade. So that's the first problem with the calculation. That said, Antoine Vayer knows about power output - he published the book I referred to in my previous analysis of Tour climbing power, and has a library of all the Tour climbs. He, more than anyone, knows how to look at a climb in context, and so his figures deserve more than out of hand dismissal. Converting power to oxygen - some assumptions required Next, you have to convert that power output into oxygen consumption. This also requires some assumptions. I don't know the specific ones made, but an interesting exercise is to go through what might be "reasonable" assumptions and see what happens. First, you have to assume the level of efficiency. The more efficient the rider, the lower the oxygen consumption at any power output. So, Vayer may have assumed efficiency to be lower than the reality for Contador - short of measuring it, you'll never know. Next, you have to assume energy use per liter of oxygen. This is tricky because depending on how hard you are riding, the value varies - if you are burning fat, it is lower than if you're burning carbohydrates as a source of energy. For example, the oxidation of fat provides 4.69 kcal/L of oxygen, whereas carbohydrates provides 5.05 kcal/L. Because Contador was climbing at a high intensity, he'll be on the carbohydrate end of the spectrum, so the assumption would probably be around 5 kcal/L. If you do this, and assume 23% efficiency (which is in the normal range, and I'd assume would be where Vayer would go), then you arrive at a VO2 of 88.6ml/kg/min on the climb. Next, you assume that this is 90% of the VO2max, and you have the estimated VO2max of Contador - 98.4 ml/kg/min! (note the small difference is because I don't know what assumptions he's made - if you assume even slightly more energy from fats, then the VO2max rises to 99.4 ml/kg/min, for example - I'm just using some assumptions for illustrative purposes for now) The problem - the starting power output is calculated, not measured The problem of course, is not necessarily these assumptions - they can be made to be conservative and work out a "worst case scenario" as I did for power output. Then they are actually very instructive, because if you are conservative and still get 'unphysiological' values, then you have a real problem! The problem is that missing one assumption can create a misleading picture. First, you have the power output of 440W. You must remember that this is a CALCULATED power output, and is therefore the result of performance. Any factor that improves performance (like a following wind) will cause an overestimation of the power output if it is not taken into account in the calculation. In my analysis of the climb, looking at the VAMs (which are also contentious, but minimize the requirement for assumptions to calculate power output), I went to great lengths to explain all the factors that could have contributed to the record climbing speed of Contador. These included the shorter length of the climb, the suspected following wind, the race situation (and of course, the possibility of doping, which is now receiving the bulk of the headlines in this article). Given the shorter climb, the following wind and the relatively conservative riding up to that climb, perhaps the climbing performance was expected. On the other side, one has to also acknowledge that Contador's VAM (and hence estimated power output) would have been even higher on a steeper climb, as I tried to explain (unsuccessfully in many cases, it seemed!). Of course, this assumes you use VAMs, which is not the best for this kind of interpretation. However, on balance, it was clear that you can't take this single climb and read too much into it. The impact of wind For example, just to illustrate the impact of the following wind, for every 3.6 km/h of following wind (and that is a very gentle breeze), the required power output drops by between 2 and 3%. The result is that by the time the average following wind speed reaches 10km/h, the estimated power output has fallen from 422W to 387W (8%). By all accounts, the general wind direction on the Verbier was from behind or the side, so I think it's fair to assume the wind helped the climb. Therefore, Contador's "real" power output may have been substantially lower than what Vayer has calculated. If his assumption is 440W, it is conceivable that the following wind may reduce it to around 396 W (with an average wind speed of 15km/h from behind). Suddenly, the estimated VO2max drops to 89 ml/kg/min. Just out of interest's sake,using the same assumptions for converting power output to oxygen use, and using Alex's calculated power output of 387W with an average wind of 10km/hour, the estimated VO2 on the climb is 78 ml/kg/min, and the VO2max estimate is 87 ml/kg/min. What can be inferred from power output and oxygen use - physiological markers of doping? They are still exceptionally high, but are more in the realms of "normality" (whatever that means). I still have my doubts about these figures - if Contador's efficiency really is 23% (as I've assumed to work that out), then it's highly unlikely his VO2max is that high. We know that VO2max comes DOWN as efficiency rises. So the combination of a high VO2max and high efficiency is unusual indeed. Having said all this, then, I really do believe that Greg Lemond is onto a very important aspect of performance analysis. There are upper limits to what can be achieved physiologically, there are without doubt physiological "impossibilities". Unfortunately, in this case, I think the calculation of the key parameters is too fraught with error to be truly meaningful. What is physiologically possible? If this kind of analysis is to be useful, then every single aspect must be factored into the calculation - the wind speed throughout the climb, the mass of rider and bike, the length and gradient of the climb. Then one might be able to make a strong case for the position that what we are seeing is impossible physiologically. There are people (experts in the sport) who believe that the upper limit of performance should lie around 5.6 to 5.8 W/kg on a longer climb. This is well below what is being calculated for the current Tour, particularly the Verbier. However, if the wind speed is not controlled, then the calculated power output may well fall below that "ceiling". The point is, we just don't know what the wind is doing and so the margins are currently too large. Therefore, you cannot use isolated performances, lacking control over variables, to infer doping. What we should rather do, and I hope can be done after this Tour, is to look at the average of all the major climbs - Arcalis, Verbier, Col de Colombiere, Col de Ronne, and see how the power output goes on average. Why? Because doping's biggest impact may not be on the single performance, but on repeat performances through its effect on recovery between rides. Analysing many riders over a longer period also helps to control the influence of these variables a little better. This analysis would still require accurate estimations of power output, however. A fascinating subject, and one that's sure to get a lot of air-time, but frustratingly, too many grey areas, and "ifs" and "buts" - I look at this type of analysis, and I can see that there is something there, but it's just out of reach... For now! Ross Source :- http://www.sportsscientists.com/ | ||
| Juerg Senior Member Username: Juerg Post Number: 1701 Registered: 04-2006 |
Rob thanks so much ; great article. Did you ever counted the word assumption in this article. So here the question . Do we talk here about "sport science" or mathematical assumption. This article demonstrates so nicely , where the sport exercise physiology is going . It is based on assumption and speculation words and possibilities based on statistic and ideas. There is not one area in this article , which talks about real physiological explanations and activities with some very small exception Fat and Glucose as O2 users and the efficiency. Than they use this as a calculation with the assumption , that we seem to know how much FFA and or glucose is contributing to the ATP production . There was no mentioning of O2 independent energy delivery in part during this efforts and the recycling of lactate as a potential energy source. Nevertheless it is fascination how they look for explanations and never look at potential physiological structural changes in this pro riders. Thanks Rob for this feedback | ||
| Juerg Senior Member Username: Juerg Post Number: 1702 Registered: 04-2006 |
After some reading in the nice article Rob sent us I decided to have a reply on our Forum with some inside thoughts: The article is from sport-science .com As mentioned it could come as well from statistical science or mathematical science if you read some of it. Why it is not from a science background is the fact , that every second information is based on assumption and guess and perhaps even hope it may be true. What sounds harsh and very negative the way I put it , is just simply a summary of 30 years of having fun in sport and testing and for a while in coaching. It is not mend to be a critic in the way they look at the results. What I like to discuss here is just simply a very different approach on looking at performance like a Tour or any other performance, even if it is the return of a patient after a heart attack to a very active life style.. To start this out I like to quote 2 comments from Rob's UK groups, as they seem to be nice and very positive critical and help to get as thinking , which never hurts. Quote 1 : " One thing I wonder about in Jeurg's article is how can he be certain that the people he is using as anecdotal evidence weren't themselves employing blood manipulation techniques on the day?" Her a short respond: a) The "anecdotal evidence "is actually backed up by science, as all the example I brought where tested in accepted university labs and science center.For the critical responder here the Lit. Page 40 in Lore of running by T. Noakes fourth edition. So that would give an answer of the comment anecdotal. It does not answer the question , whether all this people on this page where perhaps as well on any kind of drugs, as they did the strong performance.. Now remember for later this point , as our friend in the UK , who made that comment will actually help with this in a whole lot of assumption. 2. Quote: I like this quote as I stopped counting how many times people come with exactly this answer. "LBP-20 will increase blood flow, mitochondria, the amount of capillaries within the muscles but so will higher intensity aerobic training and in fact will increase them more. The latest research indicates that threshold training (approx 85% HR) is the best stimulus, for mitochondria and polarisation. Wikipedia says, "when the energy needs of a cell are high, mitochondria grow and divide. When the energy use is low, mitochondria are destroyed or become inactive." - its as simple as that. LBP-20 may possibly train the body to burn fat at LBP-20 but it is highly unlikely to help burn fat at Road Racing heart rates. A "high intensity" rider will probably notice a larger drop in fitness after a lay off as their fitness is at a higher level (relative to there max fitness level) so will have lost more mitochondria etc. There is no structural difference of LBP-20 Mitochondria and LBP+10 Mitochondria just fewer numbers. 300w x 10% = 30w, 200w x 10% = 20w." There is in fact some clear difference between a muscles with lot's of mitochondria and muscles with less mitochondria. This shows in any biopsy we have , comparing endurance athletes and sprinters. True both have mitochondria with the ability to produce energy ( ATP) There is a fundamental structural , as well as functional difference in both of this athletes. It starts with some basic needed circulation problems and research as far back as Schoen et all shows, that prior to increase in mitochondria density we will see an increase in secularisation. As more mitochondria as more blood vessels. There is already a structural difference. even visible under a microscope. The structure even will maintain the difference for a relative long time as the vascularization may be there even after a pro carrier for quite a while. That's one of the discussion , which never takes place. If we have an athlete using testosterone or Any drug , which can lead to structural enhancement , he can benefit from this chance for a while. Let's take a cyclists like Ricco. 2 year ban for a young rider and he will be back , Rasmussen and others. 1. During this 2 years they are not getting tested on what they do and what they take. So they can abuse many not allowed drugs with some clear structural improvement. Stop a half year before return and still will benefit very strongly from this manipulations. There is nothing done here but many can move very successful back into the Pro ranks with some dramatic help of drugs they can use during their banned time. Oh I lost the actual discussion. Here a question to our UK friend who makes the mitochondria discussion very simple. Here a simple question : You build a house and will start with framing . You decide to frame every 50 cm a stud. You neighbour decides to have every 30 cm a stud. True both will use the same wood 2 x 4 for framing , the one 30 cm apart the other 50 cm apart . There is no real difference as stud is stud. So our UK friend would agree, that both structures are the same and there is really no difference in the structure of this house frames ?? True or false ? Let's wait for the answer before we go further on the possible difference. Game of words: Yes it is true that in sport science we have many game of words. The most confusing once are LT , ANT, AT and IANT to start just one big field of confusion. All contain the problem of aerobic / anaerobic or lactate or threshold. How come we have some many " Thresholds " concepts. Could it be that there is no such thing like a clear threshold in human performance , when we look at the overall performance ?. Perhaps there are individual system limitation which overlap depending on the situations the performance has to take place. Example : Altitude will limit another system , at a certain performance compared to do the same performance at sea level. It could be that in one athlete the altitude will push the respiratory system at its limit, while on sea level his muscular system may be the limitation. Heat : It may be under heat conditions in one athlete the cardiac system may be pushed to the limit , while under cool conditions by the same athlete the respiration my be the limitation ? And many more very clear and often for many readers personally observed situation, but often with no explanation why this happened. Now let's go to the "explanation " on the Tour of Contatdors incredible performance. Why do I do this here. Well after readings Rob's articles I decided, that if Sport science can write this long of a story which is based mainly of assumption , and the assumptions are based on physical ideas ( Wind , road , grade , altitude, bike weight and so on I should be able as well to writhe some words on physiological assumptions. So let's start. UK Help : We assume , as the UK critical responder did, that all of the top 10 Verbier cyclists where under drugs. ( let's hope not ) Why is it a help: Well if all where under drugs for functional improvement , than we can eliminate the O2 transport system : Blood as a limiting factor and get ride of one additional variable in the physiological build up to a performance. . If the second UK responder on ( Mitochondria are mitochondria) is right as well ,than we can get ride of an additional assumption , that they may have had different structural situations as each of the athlete may have different structural muscles to push his bike. So with the help of this UK responders we can set that aside for the moment as well. So we get rid of another possible limitation ,the muscular part of this performance. Now in the sport science article they discuss VO2 needed for this performance. The as well point out, that as more efficient an athlete is riding as lower the VO2 at a given intensity. Well we can get ride of the efficiency as well when we believe the Australian study I showed a few days back , where they believe there is no real efficiency difference in this high trained athletes , but the difference may be in the physiological ability. So this let's us to get rid for the moment on cycling efficiency. ( I believe there are very big differences in cycling efficiency as an athlete will approach a very limiting high intensity as they did in Verbier. and we will see that in the physiological discussion . For the moment let's move that in the back ground. So this leaves us with three main physiological systems we still have in the team approach of a performance. - Cardiovascular ) system - respiratory system - Central nervous system In the calculation to the high VO2 readings ( 90 + ) it seems to me , that they are still stuck in the idea, that all the O2 used or needed is going to the muscular system. ( well according to our structural functional word friend in the UK ) that really does not matter ? or does it ?) Remember : VO2 is used in more than just the legs, in fact there are some systems out there like the cardiac , respiratory as well as the CNS system, which react very rapidly and protective, if the O2 delivery for their own ATP production start to get tight. In fact they not like Oxygen independent energy production at all. Short term closure or low O2 supply to the heart muscles creates very dramatically reaction from AP to cardiac attack or in the brain to some dramatically problems due to closure of a blood supply and no O2 , as well as in the respiratory systems. We know from research like Brooks and others , that in cases, where there is a desperate need of ATP production over oxygen dependent energy delivery , lactate may be the last and very efficient resource of O2 and lactate ( Pyruvate ) to deliver ATP replenishment over the O2 dependent energy flow. So we have lactate in the brain , heart and respiratory system as the main "users" in desperate situation to maintain the survival instinct and stay " alive". So when we look at the end stage of Verbier ,here some thoughts by looking at the cardiac response , the respiratory response, as well as the potential CNS response due to some mental actions. 1. Cardiac response possibilities ( assumptions ! ) What we see now sine testing daily over 1 year cardiac reaction on individual people, that the respond of the hemodynamic can be very different. Assumption. All top riders in this stage where riding together. In all the cardiac system is the limitation of performance. So the one guy may be already close to the limitation. By accelerating again his heart ( Hemodynamic ) can't react any more, in fact it may get worse . Reason: We see in some cases, that the Stroke volume drops as harder they go . It reaches a certain Plateau , stays there, and than it drops at higher intensity. In other the SV will keep climbing. In other athletes we will see, that the LVET will increase at high intensity. As the heart rate still will increase and as well the LVET we will reach a higher CCT ( cardiac contraction time. In simple words, that athlete, with the much higher CCT will have the cardiac muscles contracted much longer. This leads to an O2 supply problem to the heart , which can trigger the CG ( central governor ( T. Noakes ) and create the drop of muscle recruitment in the working muscles. As the athlete will try to maintain the pace ( wattage ) but now has less recruited muscles fibers, the still working fibers have to find the additional ability to replace the faster dropping ATP level with a more efficient energy supply . They can do that by switching over to O2 independent , but this is a time bomb and 5 - 10 sec later they will be dropped. If they "slow" down.( The body forces them over the CG )than the ATP demand will drop and as the switch to O2 independent , they as well produced a lot of lactate , which now in the "recovery " situation can be used by the heart , which in return will feedback to the CG that all is okay , and they can potentially move back if the distance is not to big in the group again. So they will drop and close and drop and close, as long the top guys have the same reaction, just not as bad. Depending on the body surface the one athlete may have to cool the body more, moving more blood to the surface and therefor "missing" some volume in the circulatory system. This will drop the EDV ( end diastolic volume ) and therefore as well the SV and with it the amount of O2 transported in the blood. So a smaller skinnier athlete may have some advantage as he may be potentially better used to heat. The drop in EDV will reduce the preload , which is a free ( energy ) for moving blood out ( F Starling ) This does not need more O2. So the VO2 max is directly linked to the effciceny of the cardiac work, ( MVO2 ) as well on the efficency of the respiratory work and last but not least on the " mind" or thoughts , what may go through your brain during an attack or race. If you are "brain less" no thoughts you safe a lot of O2 , which can be used in the other systems.( Using Mc'Leans reptilian brain ) We did some very stupid basic case studies last week to see, what the VO2 would do under brain activity. The reason is, that we like to make a practical work in our online course for the students. So I tried to bike a fixed wattage to reach a relative stable VO2 number. Than I used very relaxing yoga music and just relaxed biking with no mind as good as possible. My VO2 actually showed a dropping trend. Than I was working on some ideas for the online course by reading and calculating some ideas during riding and my VO2 clearly showed an increasing trend. Now perhaps I manipulated the reactions by thinking or hoping or perhaps even ( cheating with the way I pushed, as I was hoping for that trend.) So I will repeat this on people , who have no clue what I am looking for. Assuming that your brain works with O2 and your think ( ohh I loose contact to my biggest rival and I will loose my Tour de France and my goal and dream can't be reached if he escapes ? ) that may use some O2 to get over this thoughts ??? Summary : Many factores can change the hemodynamic of the heart and therefor potentially push the cardiac system to its own limit. Now if that is the case the whole VO2 max or high readings are gone, as we have first to understand how VO2 is used in the overall situation. A very efficient cardiac reaction combined with a very efficient heat adjustment and combined with a very good respiratory efficiency in a mental controlled situation can safe a lot of O2 so that there is no need for this fantastic high VO2 readings as they like to explain or predict. In fact as more efficient a person can use the available O2, as less high the Max VO2 has to be to be able to show a great performance. Remember Paul Tergat and Lance Armstrong in the New York marathon . Same 85 VO2 max and only 1 hour race time difference so 33 % slower for Lance in that race with the same VO2 max. How come ? May be there is some truth on efficiency between Tergat's running and body and Lance Armstrongs running and body ? But well discussion is open. Respiratory influence. As the heart ,so can the respiration be of limitation . For that let's start tomorrow some ideas. Juerg | ||
| Juerg Senior Member Username: Juerg Post Number: 1703 Registered: 04-2006 |
Here just short a responde from one of the toop five, which goes what we discuss, they know all about bike and weight and wattage, but this answer has at least some questions from a physiological point of view ( Besides teh stronges TT from the 2 day before TT was with him all the time. You wonder , who beat who ? " "Constant attacks were the only thing we could do to drop guys like Lance Armstrong or Bradley Wiggins, time trialists who can keep a steady rhythm " | ||
| Juerg Senior Member Username: Juerg Post Number: 1704 Registered: 04-2006 |
Now here some add on to the physiological work done at the Verbier stage. This are not assumptions but measurements done on cases with the physio Flow. As it was nicely discussed: Contador for example in the TT but as well up to Verbier was pushing a lower RPM as L.A. Now as everybody knows, this was a very heavily debated issue during the Ulrich . and L.A fights at the previous Tours. Now as L.A was always the winner, most agreed that a higher RPM is better. Let's see now , as a guy with a lower RPM is winning. The interesting part on RPM is , that again it is very individual and it depends from our point of view on what the limitation and the weakest link is: Assumption: L. A back at his top time after his seventh win had perhaps the limitation on his muscular system. or his O2 delivery system. Cardio and respiratory system where not limiting. So by using a higher RPM he could reduce the intramuscular muscle contraction pressure and therefor deliver better O2 to the working muscle fibers. A higher RPM will reduce the muscle contraction and therefor the pressure of the capillary bed compared with lower RPM where we have a bigger compression form the surrounding muscles. Now assumption : L. A may perhaps lost some of his cardiac hemodynamic by having a smaller EDV and therefor as well a lower SV. So by still being able to use the same amount of O2 in his working muscles, but a reduction in the delivery system ( lower CO ) the limitation now may switch from muscular system to the cardiac system. I doubt that we have any regular cardiac testing in any of this highly paid pros from any of the highly paid coaches and or "sport- science guys " hoe show nice calculations and wattage numbers on many great web sites and news paper. As we don't have any good testing results from any of this athletes but max VO2 and max wattage and max lactate and some mythical 2 and 4 mmol thresholds we really have only assumptions. Now again if the CO is lower than before we have now with the higher RPM than Contador a potential disadvantage. Why . If you bike with a higher RPM you will see a higher heart rate. A higher heart rate would , based on CO = HR x SV result in a higher cardiac output. This is not always the case, in fact sometimes we see, that with an increase in HR the stroke volume actually can drop so that the CO overall is lower than with somewhat lower HR. The higher HR will switch the energy supply more to glucose and potentially somewhat into O2 independent energy production. The higher energy supply with glucose will increase the CO2 . The additional energy supply over some parts of O2 independent energy supply will produce a higher H+ production. Both CO2 as well as H+ will be of some problems . The short term functional adjustment is to increase respiration. An increase in respiration will demand more O2 from the overall O2 supply , so the higher heart rate with the lower SV will create a O2 demand for the heart with the risk of the CG kicking in. The higher HR over the energy delivery change will increase the respiration work which again will create a more demand of O2 . so less is available for the working muscles. The problem with higher respiration rate is, that most of the cyclist ( as many are not respiratorically trained ) will breath more air but with a higher frequency but a lower tidal volume. The lower tidal volume will reduce the O2 pressure in the lungs , which than will make it harder to move O2 towards the blood , but easier to move CO2 out. The lower O2 delivery will cause again some problems ( fights ) who can use the O2 first for survival reasons. As the O2 delivery is getting smaller we have the risk that some of the main muscle groups contributing to the pedal force ( wattage ) will run into problem and may loose performance ability ) Now the athlete will start loosing a smooth pedal stroke and will start to use some other muscle groups ( like upper body work ( nicely demonstrated with a bio harness ) this now slightly involved additional muscles will work on FFA as their intensity is not that higher but high enough to demand ATP production. This will increase as well O2 use and not to the advantage of the working muscles. Interestingly at that stage is , that , if the heart is NOT the limiting factor VO2 will actually increase in the readout , despite the fact , that the wattage may actually drop due to a very inefficient use of O2 at that stage. The point ) assumption ) they make or our UK friend made, that in race heart rate levels the body will not use FFA is just simply wrong. The body always will use FFA , but just not in the high intensity ( high ATP demanding muscles ) but in many muscle involved as well in the racing motion. A high HR does not mean ( No FFA energy use. ) In fact one of the most used research from High intensity user. Dudley et all. Suggests , that in the very high intensity above 85 % the STF activity kicks in again but they had no explanation why. One of the problem is, That they believe the limitation was due to " anaerobic situation with lack of O2 in the cell. Today we know there is in this stage enough p O2 in the cell. So as we push harder we will integrate more additional muscle for stabilization and additional auxiliary motions. This muscle groups work on a very low intensity , but they work but the ATP demand is slow so FFA and O2 dependent energy delivery can take place in this areas, which will activate SATF fibers again , but unfortunately will take some of the O2 away from the main muscle groups and you can see the circle we turn in. Summary : Assumption : L.A. Three years of missing high intensity racing : Lower cardiac hemodynamic- same RPM due to co=-ordination pattern. Not recognised structural loos of the cardiac muscle- Increase of HR due to high RPM - moves limitation to the heart and away from previous his muscles. Kicks in CG and reduces the recruitment - loss of smooth pedal technique due to loos of muscle recruitment and than the rest is history . Have fun to think this through | ||
| Juerg Senior Member Username: Juerg Post Number: 1705 Registered: 04-2006 |
Thanks for the mail. The Point I got was : Too much assumption. Or is there something out there, who could back up your wild assumptions on CCT ( cardiac contraction time and changes. As so often , yes I can try, as much of the "crazy " ideas we show here is not grown on our own brain but rather collected from all different places outside the often very narrow minded testing and ideas on exercise physiology. I was just lately again surprised listen to a research from a n university where every second word was: I am not interested in this as I focus just on ?????. Well much of the ideas and goals this person has or will have to "proof" something is missed, as the focus is so narrowly and small , that the result may be great but with no practical implication what's however, besides being able to publish another paper with the name on the top and make a presentation to a steady smaller group of highly specialist people with no focus on the practical ideas and implementation for the person on the road. Here the small "back up " on CCT and the "assumption" , that L.A,. may in fact has a longer systolic phase or Contatdor has a much longer diastolic phase. " search for some possible papers I found this. . Vávra1 , J. Sova1 and M. Máek1 (1) Laboratory for Clinical Physiology of Exercise, Department of Sport Medicine and Rehabilitation, Faculty of Pediatrics, Charles University of Prague, Prague, Czechoslovakia (2) Fakultní nemocnice Motol, V Úvalu 84, 150 06 Praha 5, SSR Accepted: 10 May 1982 Summary Measurements of systolic time intervals were obtained by simultaneous recordings of ECG and first derivative transthoracic electrical impedance curves, at rest in the supine and upright body positions and during exercise while sitting on a bicycle ergometer. The same schedule was applied to 70 normal males divided into 3 groups: 20 boys 11–14 years, 25 yound adults 20–30 years, and 25 middle-aged men 45–55 years. Duration of the preejection period (PEP) was not affected by age at rest; during exercise PEP was found to be slightly shorter (NS) in the middle-aged than in the boys and young adults. Left ventricle ejection time (LVET) showed a slight increase with increasing age at rest, and this difference became more marked during exercise. Thus diastole must be shorter during exercise in the elderly than in the young population. The age-related lengthening of LVET seems more likely to be due to some peripheral factor such as increasing impedance of the vascular bed rather than myocardial changes due to aging." As you can see they make as well a "conclusion " with ends a great study with an assumption : as increasing impedance of the vascular bed rather than myocardial changes due to aging: I would assume here, that here is more than just change in the vascular bed, as we see after 1 year of playing around, that different training stimuli can change LVET from day to day and we slowly get a hand on , how or what we have to do to lengthen LVET and or shorten LVET. As LVET is changing , so does the CCT CCT = cardiac contraction time and CCT = HR x LVET. So as LVET increases ( longer contraction of the heart the heart rate can't go as high , before we reach a 30 sec area. Again, if the heart is the limitation than the CCT may have some implication on the CG ( central governor ) by kicking in and this may influence the muscular recruitment pattern positive and or negative. Here a case observation on myself. In the last 10 training units I did I played around with different ideas. - Warm up intense - Warm up slow - warm up only over co-ordination games - no warm up at all. The "wamr up was always controlled over one or the other idea: 1 . Physical intensity control over speed or wattage 2. Physiological intensity control over respiration rate, heart rate, EDV and EF % Now interesting is, and I am sure many runners know that feeling , on what we call "second wind" form the 10 training units I had 3 of them with the "experience of a seond wind, where you just feel great and can move relaxed. In this three occasions I had always a sudden clear drop in LVET from an average of 170 - 200 suddenly down to below 150 ms. The three times I felt this second wind my LVET was below 150 ms. Now the key is to go back and see, whether this specific "warm up" may have contributed to this situation or whether it was just pure luck and other reasons for it. Another interesting situation is the fact , that when I am running above LBP heart rate and or speed my SV is dropping. Problem: If I like to improve my co-ordination and running speed above LBP I have to try to be able to create a stressor , who keeps my SV up despite the faster running speed. Now the last 2 units I tried some specific ideas and I can now run in a clear above LBP speed , but still maintain my SV by adjusting certain cardiac reaction to an optimal time frame. Luck or trend. I need some 10 - 20 units more to see, whether I can repeat that ion myself and than move over to other people and see , whether this is in any person the case or whether this is very individual. So stay tuned, as we will look further in assumption and reality as long we have fun. Cheers Juerg | ||
| Robh Senior Member Username: Robh Post Number: 459 Registered: 12-2007 |
VO2max - Useful? By: Michele Ferrari Published: 12 Nov 2004 How useful are VO2max values to athletes? Is it a determining factor in the competitive results of a cyclist? Some observations... The very first time I got my VO2max measured I was 18 years old: they put a mask with a tube on my face and mouth, tied it to the nape of my neck while having me run on a treadmill, increasing speed and gradient every 3 minutes, until I reached my absolute maximum effort (or so they thought). The result of my maximum oxygen consumption was 4.528 L/min, equal to 72.8 ml/kg/min (my weight was 62.2 kg). I was told it was a good result, but my impressions back then were that running that test was totally another thing from running in the track or on the road. Indeed the gesture of running on a treadmill is really different, and in any case it requires a lot of specific training in order to be able to use exactly 100% of the muscles just like with the natural gesture. The mask (or mouthpiece) is always very annoying and hinders the respiratory flow, seriously stressing those muscles involved in respiration. Furthermore, the mask is not always perfectly airtight, it hinders movements and stiffens up neck and shoulder muscles. In years of experience in measuring the VO2max, I obtained results that differed a lot from each other quite often; discordances that consisted in different effort protocols, but mainly in measuring instruments of diverse concept and accuracy. How useful is the VO2max for the athlete? Surely this test gives a valuation on the maximum power of the aerobic engine of the subject, but it is a value not always decisive in competitive results. Derek Clayton, marathon world record holder at the end of the 60’s, had a lower VO2max value than mine, about 69 ml/kg/min, but he could run the marathon in 2h09’, approximately 20 minutes faster than my best performance ever. This simply because he was able to run at an intensity of 90-92% of his VO2max without accumulating relevant concentrations of lactic acid: less than 2.5 mM/L! At the same percentage of my VO2max value, my lactate concentration exceeded 8 mM/l. In cycling the measuring of VO2max has about the same meaning as in running: it is useful and indicative of the potentiality of the athlete, but once again its correlation with competitive results is not so tight. Lance Armstrong for instance was measured a VO2max of 82 ml/kg/min, which is an excellent value, but common to many other professional athletes that obtained far inferior results in their careers. Maybe Lance was not on his top form when taking the test, or maybe he could not give 100% out: surely he also finds the mask or mouthpiece very annoying, but, most importantly, pedaling on a cyclo-ergometer or stationary bike is much different than pedaling on the road. | ||
| Robh Senior Member Username: Robh Post Number: 460 Registered: 12-2007 |
Here's a reply to the Ferrari article from a person who's a power meter users. I am glad you brought these issues up ....I think others have wondered about these things too. Ferrari states his VO2 max is 82. He is well know for protecting HIMSELF and ARMSTRONG by suggesting that Armstrong might not have been in top shape, or that he might not have been going hard, or that the exercise bike will yield different values than riding outside on the road bike. See his squirming bro? He has to protect Armstrong because if he doesn't the big arrow points more strongly to him and his doping of Armstrong. About the exercise bike thing. They DO NOT test pro's on exercise bikes...they test them on their own road bikes on a trainer. You can usually push a little more wattage out of doors due to the less inertial drag, but the VO2 max will read the same. This is how all roadies are tested anyway so it's all "relative". About Ferrari's runners analogy. He conveniently forgot to mention one HUGE thing(or he doesn't know about it)....RUNNING ECONOMY. In running economy, is huge. In cycling there is almost NO cycling economy. In running a very efficient runner with a lower VO2 max can beat a less efficient runner with a lower running economy but higher VO2 max. Same can be said about swimming. Ferrari .....Derek Clayton beat you because he had a higher FTP power(pace in running) and far better running economy too. Lactate at FTP varies between cyclists. What counts is FTP power per kilo and VO2 max. If one guy can can crank out 400 watts at FTP at 70 kilo's with only 4m/mol of lactate and another guy at the same weight can crank out 400 watts at FTP but his lactate is 8 that doesn't mean that the first guy is in better shape or will win the race. They both have the same FTP per kilo....the same 60 minute all out power per kilo. The lactate argument is total BS and a way that guys that are trying to protect THEMSELVES(Ferrrai), and to protect Armstrong, like to spout off about. What about the guy that can crank out 400 watts at 70 kilo's at FTP with 4 m/mol's of lactate and another guy that can crank out 420 watts at FTP at 70 kilo's but with 8 m/mol's of lacate....who is stronger?...who has a higher aerobic capacity? The second man of course. It is NOT lactate or even lactate buffering that counts for a damn thing...it's FTP power per kilo. That is why lactate testing means nothing and is "old hat". Ferrari is a doping doctor and not an exercise physiologist or coach with this type of knowledge. VO2 max sets the ceiling for aerobic capacity and the ceiling for FTP...it's that simple. It is BY FAR the greatest indicator of potential in a rider(but not the only one). The higher your VO2 max the higher your VO2 max power and the higher you can push FTP power with proper training. An 82(undoped) is NOT great Ferrari...stop trying to protect "Lance". It's great compared to the average recreational racer but it is NOT great in the pro ranks. An Undoped 86 is getting great.....88-90 is great and 90 or better it freaky. | ||
| Juerg Senior Member Username: Juerg Post Number: 1706 Registered: 04-2006 |
Hallo Rob, Thanks , as Rob brings us as usual really great articles , who show the real situation we are in this days in testing ideas and " religious" believes. Both articles are making good points. The Vo2 or max VO2 is as so often discussed very much a value, which helps to a certain extend ( Perhaps most of all for a potential genetic profiling ) I like to compare Max VO2 with body size. Just because you are 6 ft 7 or 205 cm tall you are not for sure a good basketball player, but at least you would have the body height. I hope you see what I mean. The second article ( taking the abusing sound out ) makes as well very valid points. I strongly believe , that FTP or in our FaCT testing the performance line, Which is as well a physical information ( speed , wattage ) are the most objective tools to assess performance and or changes in performance. I think people like A. Coggan and as well A. Hunter have an incredible good system from a performance assessment point as well as from a coaching business point. I think the best would be a combination. We use performance ( performance line ) wattage to see as well in an objective way the performance change in a client. The weakness on our performance assessment ( performance line ) is the same weakness we have with the FTP. Yes we see the FTP or performance line is improving . What we don't see or know is, what caused the actually shift in performance. Which system was prior to the improvement the weak link and what system is now as we are on another performance level possibly the weak link ? This is the fundamental difference between any test for the moment existing in performance testing versus FaCT CLR. Just to make it clear again : FaCT CLR is NOT ( NOT ) a performance test. FaCT CLR is a physiological assessment to decide where and how we should design the next little while the stimulation to try to work on the weakest link. In a FTP test we work as good as all the systems are able to work together. The best FTP test would be a 1 hour TT and the winner has possibly the highest ratio of body weight and wattage . ( not automatically the best VO2 / body weight ratio. Again a high VO2 does not mean always a better performance. In fact in an intra individual assessment we like to see a drop in VO2 at a given intensity. The other value we like to see is the comparison of the overall VO2 with the MVO2 ( Cardiac O2 use ) and this is a field we are working on for the moment. As an assumption : If I can reduce the MVO2 by a given performance I may have a marker for a more efficient work of my heart. How can my heart work more efficient. By for example having a bigger EDV and a higher EF %. The bigger EDV will increase my pre load and will create a better extraction fraction in a good trained heart. This without additional O2 use so more efficient. The key is to find now training ideas, where we can control this changes and design this workouts individual. Summary: Both articles really make a summary of the weakness of both sides of the discussion. FTP is the way to go for objective performance assessment. The reason : physiological max information like VO2 , max HR , max respiration rate and max Lactate to name the most common one are exactly that physiological bio markers, which tell us only trends on what is changing due to intensity changes. The key is to combine this two areas. Use for example FTP or any objective intensity measurement tool and than assess during training periods bio markers to understand , what is changing in what direction , and why I make progress or why not. Both above ideas are unfortunately to narrow viewed. By trying to see the advantage from one area and from the other we could make some clear changes in the way we race , but as well we train and recover. Any " extreme " view ends in blind believe and restricts a constructive fair discussion. By using personal abuse hidden in a presentation over the Internet is doing very little to try to have fun and critically but positively move forward in a very interesting field of performance but even more valuable for personal health. I like to make a short example. 2 athletes : FTP the same . FTP ratio the same, so physically the same performance. Problem: The one athlete had a higher plasma volume when they assessed the FTP. This allowed him functionally to have the same EDV as the other guy , who at the same day in his test a low plasma volume due to some unfortunate dehydration in the preparation to his test. Now the bigger ( not normally on that level plasma volume of client A allowed him at that given test to have the same FTP result, compared to the other client , who was on a lower EDV than normal. The next day they race together and both are in their average normal plasma volume situation . Who will win. ? Now this is an example I used to show you , why with certain drugs you see this sudden incredible i performance improvements. Plasma expansion was heavily use in the cross country skiing scandal with the Finnish cross country skiers. Plasma expansion is a typical example of a functional improvement ( a nice example for our UK rowing friend who likes to discuss functional and structural as a word game. In our example there was a functional situation , who created the same FTP , but there is a structural difference ( Bigger EDV - heart ) in the one client) which will allow him to have better results over the long run. This is why FTP could be combined with FaCT CLR . We would see, that over a series of test the client with the dehydration had some bio markers different than normal and could explain the changes and the different result in the race. This just from a group out of the bush, who tries to have fun and some positive inputs in a very nice field of activities. Have a great Sunday . Juerg | ||
| Juerg Senior Member Username: Juerg Post Number: 1707 Registered: 04-2006 |
As we "can't afford" to post based on assumptions we like to go back to some " assumptions" we made and see what the outcome was. 1. Remember the interview: " ""I decided to race it a little differently, to be the pace setter," explained Zandstra. "Geoff and I raced together for the entire Canada Cup in Canmore a few weeks ago, so I knew that I could stay with him." Hmm I was at that time wondering who raced with who or who stayed where. The result of this weekends world cup shows the answer. 10 min back or over 10 % slower would give some information on , how you can race to win or to race smart to have a good workout for a more important race. On the other side we have a top athlete, who missed out over all this years to assess her real physiological ability and the comment : " Premont was gracious in defeat, and philosophical. "The national title was not as big a priority for me this year, and I just have come off a big three week training session as I get ready for Mont Ste Anne. I knew this morning that my legs were heavy, and that it would be very hard to the defend the title." sounds nice, but the "heavy legs seem to stayed even heavier as she lost 2 more minutes and overall 5 minutes to the same girl. This is a very nice example of the problem of the classical ideas of testing just performance. The actual wattage at a step test may be the same or even higher , but as long we have no ideas on how this performance was produced and how much the system contributed to this performance we just simply have a problem, when performance in a race don't match the expectation. With FaCT CLR we still may not win the race, but we know at least in the trainings and in the race, where we have the weakest link . Now we can go back and work on the weakest link and by re-assessing we can see, whether the ideas of training match the result we hope to achieve. I will show this evening a very interesting case study to explain , what it means to have a more physiological approach to assessing , than just based on physical performance. | ||
| Juerg Senior Member Username: Juerg Post Number: 1710 Registered: 04-2006 |
Okay here an assumption: If it is warm outside , I may be not able to push the same wattage or FTP or the same watt/kg body weight ratio. So in the physical calculative and statistical exercise physiology I may find a formula and some statistics together with some tail wind and road condition assumptions and can therefor tell how much performance I may loose or not loose. True ? As we have no back up of big names, nor any accepted ( taxpayer sponsored institution we hae to stay out of assumption and just only can go and test and see, what we can test. You can see the advantage research has, if it is back ed up by names and titles. Nevertheless we like to show here some ideas on FaCT CLT assessment possibilities. This are 2 assessments over 20 min run. One run was done in a room temp of 14 - 16 degrees with good hydration during the day. The second run 2 weeks later ( 2 days ago ) was done during our hot weather period. Room temp was 28 - 30 degrees and very little hydration during the day. Hard to quantify the body water content. Here the lonely cardiac hemodynamic reactions in the two run. The speed was 7.5 mph which is Just below LBP speed and is normally a very comfortable run. The top graph is HR and you can see very little difference in HR . The higher line is the dehydrated stage in the warm temp. You can see a slightly cardiac ( HR ) drift The next up is SV = Stroke volume . Youcan see at rest peretty much the same SV. The upper line is in cool temp.. The three verticales are the time in calibration and you can see in rest tehy are even touching . Interesting is the drop in SV at the start of the run in the warm conditions and if you look carefully at the HR you see in the warm condition a incline in HR. So to get the CO ( cardiac output gong ) In cool I increased SV and HR . In warm I increased more HR but less actually dropped SV. Next up is Cardiac out put with the top line in cool conditions. Next is EDV ( end diastolic volume and again Top line is cool conditions. The second graph shows you LVET which was higher in warm conditions. And the LCW index is higher in cool conditions. No conclusion here and or assumptions, just simple plain research and offering data's so people can make assumptions and conclusions.. Just one simple question: Do we believe , that , by using speed or wattage we really would stress this body the same by using % of a FTP or % of any threshold ? Perhaps a combination of power ( watt / speed ) and physiological information could be used here in a smart way ?? Just a question: no conclusion and or assumptions. ( Smile ) have fun in the heat Juerg   | ||
| Duncan Member Username: Duncan Post Number: 15 Registered: 06-2006 |
Very interesting! We have been playing around with the heat as a stressor here in Abu Dhabi. Did you take lactate samples during the run? Just to confirm, the LVET was longer during the run in higher temperatures? Duncan | ||
| Robh Senior Member Username: Robh Post Number: 461 Registered: 12-2007 |
Satre's Tour this year was very different to last year's and Armstrong's Tour after retiring in 2005 could be seen as a success after being out for so long. Here's some comments from the web :- Carlos Sastre (Cervélo TestTeam) - 109th on stage, 17th overall @ 26:21: "I've realised a number of things. Perhaps the first and for me the most important is that I've come to the conclusion that one can't perform at a very high standard for so long. In my case, I haven't stopped since I won the Tour de France [last year]. "I've competed in four grand tours in less than a year: Tour, Vuelta, Giro and Tour, plus the Olympic Games, as well as an incredible number of events and activities, and that hasn't left me any time to rest. I think that's the reason for my tiredness and for the fact that at the moment I feel as if my body has nothing left to give. So the only thing I can think of right now is resting." Chris Carmichael thoughts on Armstrong:- In reality, while the initial plans for the 2010 season are already in the works, it’s going to be a little while before Lance and I sit down and really pore through the data from 2009. I’ve learned over the years that it’s a good idea to get some distance from the event before going back and analyzing it. Right now, it’s too fresh in everyone’s mind, and you end up micro-analyzing every little detail if you start the process too early. So, it will probably be in about two weeks, or the week before the Leadville 100, when we really delve into the details of what went right and wrong with Lance’s training this year and what we can tweak heading into next year. One thing I know for sure is that the races Lance competed in – and the additional ones he will compete in – this year will have a big influence on his performance in 2010. I told him when we started this comeback journey that if he decided to race for two years, he would almost certainly be better in year two. With two Grand Tours in his legs, plus a bevy of shorter races, he will go into the fall and winter with a fitness level far greater than he had in the fall of 2008. Grand Tours have always been a major component of Lance’s Tour de France preparation. Even before his first Tour de France victory in 1999, the 1998 Tour of Spain was crucial for developing the fitness and power needed to raise his performance level headed into the 1999 season. Lance’s performance in the 2009 Tour de France was exceptional. While there are some who see his third-place finish as a failure based on the dominance he once displayed, I believe those people simply fail to grasp the magnitude of his achievement. Third place at the Tour de France this year wasn’t something we talked about as a realistic goal. At the end of the Giro d’Italia, I thought a top-10 finish at the Tour de France would be good. After seeing how well Lance adapted to the stress of the Giro and the bump in fitness that he achieved in the weeks following the race, I upgraded my expectations and thought that a top-5 finish at the Tour was within reach. I didn’t expect to see Lance standing on the podium in Paris, and the fact that he was there today bodes very well for what he may be able to accomplish in 2010. | ||
| Duncan Intermediate Member Username: Duncan Post Number: 16 Registered: 06-2006 |
Looking at this a little closer, it appears that this person can sustain the same performance in the warmer conditions despite approximately 25% less CO - from 20 to 15l/min. So in cool conditions he has a lot of excess cardio capacity. It would be interesting to see the same test on a 'record' hot day in Quesnel. It looks like a couple more degrees higher temperature may have put the cardiac situation out of balance, judging by the CCT which moved from 18-19sec to 28-29sec. Even continuing the run with the small cardiac drift observed may have ended up with CCT reaching 30s, then it would have been interesting to see how the heart reacted. Here in Abu Dhabi, since we have an unlimited supply of heat, we are trying to look at using the addition of a heat stressor to a person performing at close to LBP in a manner similar to adding extra loco-muscles to a person at LBP. As you mentioned before, if you have an athlete with a weak cardiac system adding extra ATP demand while he is already at the balance point can show you that his cardiac system is maxed out. In the run example above, I would expect that this person could run and move his arms at the same time while remaining in a balanced situation (in cool conditions). Maybe we can use heat in the same way but this time instead of asking for more cardiac output we are reducing the EDV and observing the trends. (that is ASSUMING that heat will cause a decrease in EDV!) Maybe you can compare the results of adding two different demands on the cardiac system to get a better idea of the specific limits in the heart? I know these are starting to sound like crazy ideas coming out of Abu Dhabi now! Just looking for ways that we can get an idea of the cardiac situation without access to a Physioflow. For example if we have a person with a CO limitation, either EDV is small, EF is low or LVET is not low enough. Without the inside view we don't know. But when we move to higher temperatures we know that the EDV decreases, I think you said in another thread that it can be common for the EDV to be lower than the SV was in the cool conditions, in the run above the the SV in the cool conditions appears similar to the EDV in the warm conditions. So to maintain performance with lower SV, the HR must increase. If the LVET can not decrease the CCT will then increase and we will see the results as the brain protects the heart's O2 supply. But if the LVET could decrease enough that it could keep the CCT below 30 at the new increased HR then we would see a new balance point at that heart rate. Then we would know that the limitation in the heart is not the ability to decrease the LVET. Does this make sense? Have you seen cases where that happened? Interestingly, in the above example the LVET is higher in the warm conditions but perhaps if the run had continued the central gov would try to reduce the ejection time as the CCT approached 30 seconds? Duncan | ||
| Juerg Senior Member Username: Juerg Post Number: 1713 Registered: 04-2006 |
Duncan : Yes in this case study the LVET was longer in teh heat, which unfortunately in this case worked than negative in both direction: 1. longer CCT by the same HR already in lower intensity . 2. Therefor less ability to increase teh HR above, what you could do in cooler temp. Lactate yes. In the 20 min cool temp run there was no real lactate accumulation. 1.8 after 10 min and 1.5 at the end. In the warm temperature after 10 min ( despite the same HR 2.3 and after 20 min with slightly higher HR but much higher CCT 2.9. Subjective feeling . In cool temp stiff start but great feeling at the end. In warm temp . smooth start but fight at the end with poor running economy. | ||
| Juerg Senior Member Username: Juerg Post Number: 1714 Registered: 04-2006 |
Duncan , very nice thinking and I need some more time to go through all this interesting combinations. Here some trends we see. Non conclusive yet : 1. Younger people seem to have shorter LVET compared with older people. ( 20 years and younger compared with 50 years and older ). 2. It seems that after long slow workouts the trend to a higher LVET is very regular the case. 3. It seems that in hot conditions the LVET seems higher than normal . 4. After short high intensity intervals the LVET seems to drop for a 1 day to 2 day's before returning back to average. 5. Dehydration seems to move LVET slightly up. This are just basic observation , but have to be looked at first in much higher numbers. So we need 500 plus samples and see, whether this is the case. This will mean for us that we should know the ideas and trends in 2 - 3 years time and than can build up on this. Interesting is the trend, which would work towards more thoughts on CCT ( cardiac contraction time) and lactate trends. The question we try to work on is: If the heart is the limiting factor do we therefor can use CCT as a marker. If the CCT does not reach 30 sec, but lactate shows up , do we have another system like respiratory system or muscular system as limitation or weak link ? In My case as Duncan pointed out: In cool conditions my CCT is lower and I feel that my limitation at the current moment in running is muscular. But as I was running in warm conditions I felt different "fatigued" Yes as well heavy legs but some how different and CCT was closer to 30. Question : Was it the lack of actual plasma and blood volume, so that a heart , which could pump close to 30 liter now was pumping very inefficient due to the lack of volume. So too big muscle for not enough liquid so that the preload was not very effective as it would be in bigger volume situation. Duncan's point is well taken , that we may be able to play with hydration situation to add or release some stress on the heart. Have to think more through that as well. My goal is for the moment: I normally in cool condition drop my Stroke volume and EDV if I run above LPB speed. Now if I run below I seem to have a great EDV and SV. To improve my stride length and stride frequency I should run faster. Now I try to produce a specific workout so I can maintain my EDV and SV despite running faster, so I can maintain a better O2 supply to the main working muscles. If I run fast with a lower EDV and SV than I "loose" some main-workers like gluteal from the proper running muscle chain and may train a not optimal running motion. So by now being able to maintain EDV and SV I feel much better coordinated. They key was to have the optimal timing , so that the EDV was not reacting and the speed could be changed. I will do some more tests and If true I will show some printouts for you. Duncan , Thanks so much for asking this questions and your thoughts on the Forum , as this is what the Forum should be. Please all other readers thanks for the emails, but your inputs where all great and worth while to discuss on here, even if you think you are off the line . There is no stupid feedback and we all can learn from each other thoughts. I would be nice as well, when the e mails I get from some of the "higher Institutions " could come on here, Use a different name, if you not like to expose your identity or your institution publicly . Thanks so much | ||
| Andrew Senior Member Username: Andrew Post Number: 254 Registered: 04-2006 |
Just more proof that wattage might not always be the same stimulus. These laps were done over a 24 hour period, as part of a team event. Lap #2 was fastest, but with a lower average HR (presumably due to the absence of an all out run to start the lap off as was done on lap #1). The night lap was slow for safety reasons, to take into account the technical downhills in the dark. More interesting is the fact that the final 2 laps were almost identical, with the same average HR, which happens to be just below measured LBP. These results are from an athlete new to LBP testing, and he posted the 4th fastest lap of the day on lap #2...we will be talking with him about how he "felt" at different times at the different HRs, and collecting more information before we can give an advice on how he might pace differently for a similar event in the future, but I thought even the simple data was interesting to look at. Lap 1: 58:10 aveHR 173 with a 3min Lemond start. Lap 2: 54:30 aveHR 166 Lap 3: 1:00:50 aveHR 154 (night) Lap 4: 57:10 aveHR 153 Lap 5: 57:20 aveHR 153 | ||
| Juerg Senior Member Username: Juerg Post Number: 1716 Registered: 04-2006 |
Thanks for a very positive critic and encouragement. In short: " Your discussion on RPM and possible limitation of some physiological systems sounds very interesting . Problem : Too much info, too complex and to confusing. Can you take it apart step by step for us ?" Thanks and Yes , at least I can try . I will split it of in 6 different threads to show in more and hopefully easier to understand details what I meant. Let's start with the easiest info. 1' What influence does a change in RPM may have on the cardiac ( reaction ) first let's just look at HR. I like to take a study from " Institute fuer Sportwissenschaft ( University Graz. Prof Dr. Peter Hofmann. Here first the graphic , which is very easy to read :  hat it simply shows is, that with a higher RPM we may see a higher heart rate. Now some "assumption " A higher heart rate means , that we push in a higher frequency per minute blood towards the working muscles, and other working systems, with exception of the heart, which is not getting blood during the systolic phase ( when we push blood out = heart muscle contraction. Now what does that mean for contraction time: Let's assume the contraction time stays the same. 200 ms contraction time ( LVET ). Now you can go back to the graph and see, how much longer the heart is contracted in the higher RPM versus the slower once. If you make an easy example. LVET 200 ms and HR 150 = CCT 30 sec. or LVET 200 HR 140 = CCT 28 sec. Next If the HR is going up and we maintain the same Stroke volume ) the amount of blood we can throw out , than the cardiac output / min will increase. Example SV 100 ml HR 140 = CO 14 L/min SV 100 ml HR 150 = CO 15 L/min Now if that situation occurs by pushing the same wattage ( performance, Than the additional CO of 1 L is only used to upkeep the higher O2 demand for the cardiac muscles. To proof this we can see the reaction of the left cardiac workindex. If this number stayes the same teh heart does not really work harder. In cases , where the SV is the same , but HR is going up we see an increase of the index , which would give us the information of more work for the heart with the same physical performance and we use more O2 for the same performance ( More money for the same service ). If ( assumption ) we have a cardiac limitation and this increase in HR moves us above the "comfort zone " of the heart, we may trigger the CG and we may actually shift from O2 dependent to somewhat O2 independent. How could we proof this. As the CG will reduce recruitment of working muscle fibers to secure O2 supply to the cardiac muscles , but we keep pushing the same wattage we have to find a more efficient way to upkeep the higher ATP demand from less working muscles with ATP production. As now the ATP is faster used , so the demand is faster we have to search for a faster ATP delivery . This would be O2 independent5 glycolysis. This will create a H+ situation and with it ( always still in discussion ) an accumulation of lactate , which we than can test in the blood. The lactate per se will not be of a problem. The problem is the limited efficient energy source to create ATP O2 independent and it will come to some problem of ATP delivery and production over time. You are simply now above LBP. So tomorrow we ill end this section Higher RPM higher HR and possible consequences to the cardiac hemodynamic. | ||
| Juerg Senior Member Username: Juerg Post Number: 1719 Registered: 04-2006 |
Now here is the rest of the story with RPM and HR and you see, that there are some very interesting combination possible. Remember. Higher RPM may in many cases mean higher HR. Higher HR could mean ( but not always is ) higher CO = cardiac output. CO = HR x Stroke volume. Now you have the different versions, ( in the literature often not discussed ) Stroke volume can depend on different factors. a) EDV = End diastolic volume: You only can pump out as much or close to , what you can get in during the filling time ( Diastolic ) So the EDV is the amount of blood you fill in the heart . As bigger the EDV as more likely you will have a bigger SV. But again not always. The EF % = ejection fraction % is the amount the heart pumps out after the end of the filling time. Example 100 ml EDV and 75 ml SV = 75 % EF. The ejection fraction may have a lot to do with simply spoken the elasticity of the heart muscles. Kind of a bad comparison , but something like the elasticity of a elastic band you load and it shortens back to it's original length very fast and smooth. A worn out elastic may as well move back slower. So we can have a situation , where the EDV may stay the same: 100 ml , but the EF % may increase from 75 % to 85 % . So the SV will increase to 85 ml but not due to a bigger EDV but a more "elastic " contraction. So the SV can go up , without increase of EDV. So CO goes up as well. Now EDV can be limited simply by the heart size ,If EDV does not go up anymore, we may have reached the structural limitation of teh heart size . This combination is another example for our friend in UK, who uses structural and functional as a word game only. We can have a fixed ( structural) EDV but a different SV ( functional changes ). Now different workouts for muscles can actually change muscle size and strength. There is something like intramuscular coordination. High power ( weights ) and small reps properly used in strength workouts can develop more strength ( intramuscular ) but no real structural change. Lower weight ( Body building ) with more reps properly used can lead to more muscle mass ( structural ) but not automatically more strength. ( Versonjansky in the early 1960 ) in Trainingslehre by D. Harre) So the same is true for the cardiac system. Longer slow training units will develop if properly done a different muscular cardiac development than interval workouts. EF % could be a bio marker on the efficiency of some of teh workouts. Case studies over the last year show some trends. LSD seems to drop EF % . high intensity seems short term increase EF %. Specific designed "interval " not always high intensity, seem to be able to change EF % during a workout. Now last but not least EDV can increase or decrease during a race and or workout due to different situation. 2 most likely situation where we see this is : 1. Dehydration/ Heat ( which goes with dehydration.) 2. Post workout reaction as plasma expander. ( Specific long workouts in a specific intensity show the following day a supercompensation in EDV , if the EDV was not limited by the heart size. Specific interval session seem to change the EDV the following day due to supercompensation of the plasma volume. ( Again only if the EDV in the pre test was not limited by the heart size. This specific reactions can be used as potential test to look for a base line of an clients EDV ( Indirect heart size ) Here the full combination , how the different values actually may connect with each other. See first just the left ( yellow side of the PP.  | ||
| Juerg Senior Member Username: Juerg Post Number: 1721 Registered: 04-2006 |
Okay step 2. After we where looking at HR and RPM reactions now let's look at Lactate trends and RPM reactions. Here first the graphic from the same study as above.  Now the graphic is pretty much self explanatory. There are some interesting points there. Watch careful the lactate trends. This are "classical" lactate assessments. See, that it just simply does not work by using the "classical" system, as there is no clear answer something called " lactate threshold or OBLA same person only change was RPM and we have different 2 and 4 mmol levels of inclines. This is another example of the problem with "classical" lactate ideas. Now you actually can see indirectly the LBP in this 3 tests. look on the Graphic HR and Watt the HR level at about 160 HR. Now go and see the watts pushed at the three RPM tests and see the wattage. Green line 160 HR - about 175 Watt Blue 160/ 210 Red 160 / 220 Now go to lactate and RPM graphic. Check green lactate by 175 watt just below 4 Check Blue 210 just below 4 and check red 220 just below 4 It is not the 4 which gives you the info, as the wattage by 4 mmol would be very different in each test by the same person. But : The HR seems to be pretty stable at 160 HR. LBP will be in this case possibly close to 160. Now if the cardiac system is the limitation , than the LBP would be used as a marker for the change in the cardiac system. As you can see in this case. The limitation starts somewhere by a HR of 160, What we don't know based on this , what could be the limitation , and this study group as well had no clue what was limiting the ability to go on a higher RPM. In any case. this example shows , that lactate the way people use it still is of limited value for intensity zoning , and if we find something called "threshold " we have no clue what causes this. In FaCT CLR we would know what caused the increase in the Bio marker lactate.. Now if in the case of our discussion in the Tour the limitation in L. A was the cardiac system and he pushes a higher RPM than Contador than he will reach earlier the limitation caused by the heart , as the higher RPM will use more O2 in the heart and therefor will start to limit his legs. Remember his words. I just did not had the legs. Well I think he just did not had the cardiac or respiratory system or some nutritional limitation or some blood transportation limitation. Now the last is ruled out, as our friend from the UK decided , that all of them may be on drugs. So next up will be a closer look at the reaction of the respiratory pulmonary system. So stay tuned as we go along | ||
| Juerg Senior Member Username: Juerg Post Number: 1726 Registered: 04-2006 |
Next up breathing frequency observation with different RPM. Some source as all the time.  Now if we try to make it very basic and simple. The respiratory sysytem may work from the reactions similar to the heart ( very simple but not true ) Here what I mean: HR = respiratory frequency VC = EDV TV = SV Difference between VC and TV ( VC- TV ) = EF % The big difference is, that in the respiratory sysytem we very easy can manipulate some of this values , at least in workout intensities below LBP and in and around LBP. Now stating that I can tell you , that I am slowly be able to "manipulate" some of the cardiac values as well. ( Demonstrated it in Seattle but nobody would believe it ) which is always fun. Now the graphic again explains nicely the trend in breathing frequency in an untrained ( respiratory untrained ) client. Problem here is very similar as with the cardiac hemodynamic. Depending on the elasticity of the rip cage ( and mobility ( costo vertebral joints ) as well as body position in the test ( on the bike ) and in running , as well as on the endurance ability of the diaphragm and the co-ordination between inspiration and expiration, the change in respiration rate can benefit the overall performance ( more efficient ) but as well can add some additional O2 cost to the performance at teh same intensity. Here some ideas of the above points. Faster respiration rate could mean more overall air volume flow. Example . 20 breath / min and 1 liter TV = VE of 20 liter. 30 breath / min with 1 L TV = 30 liter. But there are additional 10 more muscle contractions , which need more O2 as well. 1 liter TV is actually not 1 liter fresh O2 sat air. You have to take in to account the so called dead space which can vary depending on the size of the athletes and may be around 200 ml =-. Now if we take an athlete with a lungv. VC of 2.5 liter and he moves 1 L TV and we have an athlete who has a 5 L lung ( VC ) and moves 1 liter than we have a very different intrapulmonary distribution of the "fresh " air , as well the O2 pressure on the surface ( exchange area of the lungs. O2 moves due to pressure difference to the blood. Now you may already get the picture what may be in the two different lungs. Does the guy with the bigger lungs and the same TV has an advantage or not. I always have to smile ,when we get this requests for an opinion when athletes mail in and in their summary they tell us all this maximal values. VO2 max of 85 and VC of 7 liter , why is my performance only good enough for a Cat 2 racer. Well read the above ideas and you see, how little maximal values are of a help , if we don't know the % of use of this maximal values. So a faster respiration is not always an advantage either. Here one possible reason ( most common reason ) . If we see increase in respiration rate we often see a stable TV at the beginning but than later a drop in TV. Now the drop in TV often goes together with and increase in FeO2 % ( lower true O2 ). Here now we use a very simple assessment. If we see a clear increase in a FaCT CLR test , than we repeat the same step again ( same wattage for another 3 - 4 minutes ( We take in the first same step even if it is on the way up a lactate sample and check the lactate as we stay on the same performance for 1 min. If the lactate has a trend to go up already, we stay another 3 min there and tell the client to force himself to breath slower ( at least 10 breath slower and deep and than observe live on the Fitmate the FeO2 % trend as well the heart rate and the lactate after that effort , before we go back to the normal step test. I can explain later why we do that and the possible info we may get. In the same time when we "manipulate " the respiration rate we as well see on teh physio Flow , whether there is a cardiac hemodynamic reaction and have immediately a whole lot more of info on the team work in muscle . metabolic reactions pulmonary reaction as well as cardiac respond. This will help us in the recovery part of the FaCT CLR to understand possible reactions of one or teh other system. Now all regular readers will see now , why we simply don't have a "protocol " but we produce a individual protocol in the first assessment. We have a physiologically plan of assessing a client with a basic idea on how we do that , but each client will force us due to the individual reactions to develop some side branches of the FaCT protocol. I had lately a request from a coach to sent a protocol so they can "validate" our FaCT idea. Now he had as it seems major problem to comprehend the situation , when I told him that there is no protocol to validat and even if there would be one , against what test would he validate the FaCT. Against 2 and 4 mmol , against a slope on a "classical" lactate test, against a field test over 5 -6 steps on a track or what . It may be time for many coaches to understand , that the "classical " education gives us a great education base , but simply no ideas on actual physiological testing . In fact it makes most coaches blind to maximal values with very little help on physiological information. So let's come back and summarize the respiration rate and the lactate reactions on the different RPM situations. | ||
| Juerg Senior Member Username: Juerg Post Number: 1727 Registered: 04-2006 |
Summary so far of the above three graphics. 1. RPM increase is increasing in some cases the heart rate. A higher HR may need more O2 as well. If w e have a Max VO2 than the available O2 is limited and if the heart needs more O2 we would have less O2 for the other systems. Now as we not always bike on "max VO2" ( very seldom ) we seem not to care about the higher HR. At least if you read wattage forum , where they claim , that you don't worry if your HR drifts up as you stick to your wattage zone. As we know there are limitations on how your HR can go and higher HR does not always mean higher CO. Now in FaCT CLR we are not interested in the Max values, but rather in all the different " shifts " ( zones" where teh physiological system may shift from FFA to glucose or from O2 dependent slowly to involvement of O2 independent. On each of teh " critical " shifts a change from one or the other system can move you out from one zone to the next zone, which you may like to avoid. You may like to stay longer in the more FFA zone to save glucose storage for later parts of the race. Or you like to stay as long as possible in the O2 dependent zone to safe higher energy phosphate for the end sprint and so on. An increase in HR or respiration rate may just push you over teh limit to the next higher zone and this may happened just a little bit too early so you lose the contact in the mountains or the en sprint or what ever you had planned. Exactly the same may be true by increasing the respiration rate. As you may reduce your TV you increase your FeO2 % and you may have to switch from mainly FFA to now more glucose and O2 and digging in the storage somewhat too early in the race . Now you run empty to early of the more efficient O2 glucose supplier and so on. So an increase in HR and in respiration rate at the same wattage level due to an increase in RPM shows an increase in lactate at the same wattage level which is a biomarker of a more involved O2 independent supply situation , which is a "time Bomb " in a race over a certain duration. In this case the higher RPM is clearly less efficient. The only moment possibly the higher RPM is more efficient is, if teh muscular system is the limiting factor. In every client where the respiratory or teh cardiac system are the limitation a higher RPM may be of some disadvantage and has to be assessed carefully . In case of L. A . ( assumption ) the three years of changed trainings may have shifted his limitation from one system to another. He may have still optimal muscles situation , but heart and or respiration may be not up to the level he was before,. By keeping his co-ordination and his high RPM he may actually worked himself into a problem , as this may be for now not the most efficient way to bike. As long they don't assess physiologically the different systems they just simply try and hope and use a potential genetic ability and teh drive to be the best to move up to the top. With FaCT CLR we don't need to dry , we simple can find the weakest link and work specifically on that to get it up to par. | ||
| Juerg Senior Member Username: Juerg Post Number: 1728 Registered: 04-2006 |
Here the add on of the respiratory reaction due to the RPM changes. We had already the info, that the higher RPM was increasing the respiration rate. Now here the VE (total air they moved at the different RPM.)  As it is easy to see, by a given wattage , you move different amount of air.(VE) This is not surprising after we saw, that the respiration rate was up as well. What looks more interesting is , that when you combine the information from the VE and the respiration rate you can in fact calculate the TV ( tidal volume or amount of air moved / breath) Now if you take, based on the lactate curve the green line and 4 mmol you have app. 170 watt performance. You move that down the the VE and BF graphic and you calculate based on this info the TV at 170 watt you can see that in this study the TV for teh higher RPM is 2.3 L versus 2.6 by the lower RPM. So less pO2 due to lower TV. More O2 needed due to higher respiration rate will similar like in the cardiac assessment work against an economic use of O2. If ( assumption ) the respiration system is the limiting system , than by coming close to LBP ( or if you don't accept LBP ) close to what ever threshold you believe in , the more O2 use by the respiration system will push you exercising muscles early towards O2 independent involvement ( m measured and shown by a higher lactate accumulation at that given limitation. ( Dempsey's metaboreflex ) Now we have either a overload of the cardiac system due to a too high uneconomic RPM or an overload of the respiration system out of the same reason. A high RPM is of some advantage on athletes, who know that their respiratory and cardiac system is not the limitation . Summary : If the cardiac system works more and the respiratory system works more and the muscle system works the same at a given wattage level, than we will see a higher VO2 at a given wattage level. But we may see a lower maximal wattage at the same "Max. VO2 " By actually assessing this in the same way you can find out your current optimal RPM. You can see in all the tests, that 50 and 80 had on teh parameters tested very little difference.. The biggest difference was not tested, which is muscle contraction and with it the pressure on the blood vessels and this could limit the optimal blood flow the the working muscles. We could assess the SVR ( systemic vascular resistance in the different RPM and use that additional for a bio marker to find the optimal RPM at the current moment. Problem : RPM has a lot to do with the CNS and co-ordination. It is very difficult to change that motion pattern. So as we may gain or loose abilities in teh cardiac and or respiratory sysytem we could afford to go a higher or have to reduce to a lower RPM, which is very difficult to do (Brain motion slings ) and it is nearly easier to learn a new movement , than changing an old very established one. Now let's see , what the VO2 results where in this full study .  | ||
| Juerg Senior Member Username: Juerg Post Number: 1729 Registered: 04-2006 |
It is actually interesting to see, how a simple TT at a tour leads us to a very nice discussion on influences on performance. I had a question concerning the respiration and the possible connection to the RPM. The question in simple words was: What drives the respiration to increase.: Here a nice summary from a Doctor , who explains the drive very slick and simple. " Let's start with a discussion of why we breathe. The short answer is that carbon dioxide, oxygen, and muscle stretch receptors in our chest drive respiration. About 85% of our drive to breathe comes from carbon dioxide receptors that “measure” (through a number of mechanisms) carbon dioxide levels in the blood. The receptors are in the brainstem and measures blood acid level (which is related to the carbon dioxide level). After 24 hours of elevated carbon dioxide levels (“chronic ventilatory failure”), the body’s compensation system (using something called bicarbonate) changes the pH (a measure of acid level) at the carbon dioxide receptor and (insert mysterious action at which we can only guess at the wonders of the human body here) either decreases carbon dioxide sensitivity or, like a thermostat, increases the CO2 level necessary to drive respiration. Either way, the CO2 receptors in these chronically hypercarbic patients still appear to have some function in the real world (which is where we take care of our patients). About 10 - 15% of our drive to breathe comes from oxygen receptors located in the carotid arteries and the aortic arch. Normally, your oxygen pressure (a way of measuring oxygen levels) in your arteries (PaO2) is 80-100 mm Hg (millimeters mercury, a common pressure measurement). For most people, when the PaO2 drops to 60 mm Hg or below, there is a drive to breathe. However, there are a number of factors including CO2 levels, acid levels, and insert even more mysterious actions at which we can only guess at the wonders of the human body here, which can change this level. In other words, in people with COPD, this response to breathe may be triggered at higher oxygen levels (PaO2 above 60 mm Hg). At a PaO2 above 170 mmHg, this trigger theoretically turns off since you are no longer hypoxic (however, read the Aubier article for a great study which shows just how smart our bodies really are). Finally, there are a variety of conscious and unconscious triggers that also drive you to breathe. These include stretch receptors in your chest wall, a concern that you’re going to die if you don’t keep breathing, and people telling you to breathe." |