I am interested in differences between running on tredmil and real running (on the track) and the validity of tredmil tests on track running.
I find these diferences
Different GRF (ground reaction force) due the slowing of the tredmil belt, because it hasn “infinite” inertia like earth, so this change some kinetic properties of running because speed oscilations.
No air resistance. You theoretically spend less energy for running at the same pace on tredmill
No air convection so you spend more energy on cooling your body – you sweat much more
Coordination problem, because the objects dont pass near you, they are still and this can confuse you and you should use different motor control mechanism for running.
So, if I calculate VO2max and OBLA (on running pace – Conconi test) at tredmill how this can be used in real running to program your workouts, what is the error? Is it big, or is it small? Can this kind of testing can be used with fitness entusiast or athletes (distance runners)?
Your opinion please…
I am in the minority on this board, but I feel that a properly constructed treadmill is a great training tool for athletes.
As for your first point, if the treadmill is constructed properly (rigidity, drum weight, etc.) the ground reaction forces will be the same as over ground forces.
You have very aptly stated the disadvantages of treadmill running with your second and fourth points. There is no wind resistance and there is no visual feedback from the environment (I wouldn’t think that this would change your running mechanisms as you stated, though).
Your third problem can be solved by simply placing a fan near the treadmill. We have one placed in the corner near the treadmill that is powerful enough that it gets a pretty good breeze going and gets pretty good airflow throughout the gym.
Mladen,
have a look at these, perhaps you’ve got them, I don’t know:
Jones, M.A. and Doust, H.J. (1996). A 1% treadmill grade most accurately reflects the energetic cost of outdoor running. Journal of Sport Sciences, 14, 321-327.
Heck, H., Mader, A., Hess, G., Mücke, S., Müller, R. and Hollmann, W. (1985). Justification of the 4mmol/l lactate threshold. International Journal of Sports Medicine, 6, 117-130. (–> I hate this one! but it’s got different inclinations for different surfaces; I think I’ve posted the results on a different thread regarding tempo running on a treadmill; have a look…)
Also, DON’T use a fan directly in front of your participants, if you use a turbine for your measurements (e.g., Oxycon, Metamax, Metalyser, etc); you are confusing the system…
Elevation -as stated in the above references- is much preferred vs. a fan.
As the post above says, such tests for endurance runners can be quite accurate. Depending on the purpose of your study and what you are looking for -or the feedback you’d like to give- you can use different stages’ duration.
Let me/us know what you are looking at; perhaps I could help you with references, or otherwise.
Did you ever try to do Concony test on the track? You have to have pulsmeter, bycicle in front of you to create you a right pace and two collegues on each 200m to write down your pulse… qute hard to do this!
The goal of this test is to determine pulsrate (BPM) on the OBLA (lactate tresholg) for programing distance running programs (see Jansen, “Lactate treshold training”, Human Kinetics)! So I was wondering could I do this on tredmil, it would be quite easyer… but there would be certainly some kind of error especialy if the athlete you were testing is higly prepared and can run at high pace (air resistance then cannot be underestimated)! For fitness purposes this in not so important.
So You proposed 1% inclination, I think that vary according to athltes preparedness, dont you think?
Tnx
I know how the Conconi test works, but I haven’t used it, as it was originally employed for the identification of the HR deflection point, something I don’t believe in; I don’t like it, anyway.
Just to be clear on this, how would you define OBLA? Do you want just to define/determine a Bla breakpoint and for what purposes?
Of course, you could do it on a treadmill! I don’t get though why the highest level of a runner would be a problem? Do you mean in terms of his mechanics while running on the treadmill? Perhaps this is an issue depending on running technique/style, but you shouldn’t be far away from reality…
For everything you want to design, as I said before, appropriate selection of protocols is of great importance, even for fitness/recreational purposes; otherwise, why wasting everyone’s time and effort?
I’ve extensively used the 1% inclination and I’ve found it pretty accurate if you want to transfere your results/speeds outdoors no matter what the preparedness level is, as peak velocity will more accurately reflect that [i.e., transferable with reasonable weather conditions, of course, as it would happen in any kind of test]. Others don’t believe in it -inclination, that is- personal preferences… For an accurate feedback though, yeap, you guessed it, appropriate protocol selection will get you there.
I know how the Conconi test works, but I haven’t used it, as it was originally employed for the identification of the HR deflection point, something I don’t believe in; I don’t like it, anyway.
Just to be clear on this, how would you define OBLA? Do you want just to define/determine a Bla breakpoint and for what purposes?
OBLA is the intesity of work when your aerobic sources cannot cope wit anaerobic and you start accumulating LA in blood.
Increasin intenisty of work (runing for example) linearly increase O2 uptake till deflection point (OBLA) where futher increase in intensity lead to slower rise in 02 uptake. Active muscles reached their aerobic limit and starts using more powerfull anaerobic sources to sustain intesity. Futher (slower) increase in O2 is because LA entered into blood cause higher freq of breathing (and breathing uses 02 too) and enters non-active muscles where is converetd into CHO again (Corry cyclus wich is slow but uses O2 too). This is my theory ®
Jansen proposed intesity system according to OBLA heart rate, wich is quite interesting, and in another book “Marathon training” from Enrico Arcelli and Renato Canova I find out that running at different rates of OBLA cause different adaptations in different systems (central and peripheral facto of aerobic capacity)
Anyway thanks a lot about you tredmil opinion. Onether thing I would say is that you should repeat OBLA testin (Concony) every time weather changes because pulse is higly dependent on outside temp and cond. or you will get bad inf (about pulse at OBLA)
Another thing about testing on trediml is that you should simulate outside conditions. Opinion please
I recently read an article from an Australian publication (Modern Coach & Athlete) that said the mechanics are different and cautioned against using a treadmill for fear of altering running mechanics. I guess that assumes that one’s running mechanics are already perfect. If they were less than perfect, then maybe running of the treadmill might fix the flaw. I’ll try to dig up the article tonight.
You sit in front of your pc in a rested state, but lactic acid (or lactate in your blood, if you want) is in there. It’s always there! In a balanced state, i.e., between production and elimination of it.
As I said before, VO2 (and HR) will increase linearly all the way, there is no deflection point of these corresponding to the lactate threshold. There might be a plateau towards the end for VO2, but it doesn’t happen to everyone; also, a deflection point might appear in HR, but this 90% is >LT, as you define it and for me doesn’t mean anything (original Conconi test).
Perhaps what you are trying to describe here is the mechanism of the ventilatory threshold; in this case the terms you want to use and explain the “isocapnic buffering” are VCO2, which departs from linearity and loses its parallel relationship with VO2 and indicates the ventilatory threshold; or the dissociation between VE/VO2 and VE/VCO2 (ventilatory equivalents) depending on how you want to define it.
Active muscles are impossible, I repeat impossible to reach an O2 limit! The most brilliant example of all, I am sure you’ll agree, is the heart muscle! I don’t think it becomes depleted of O2 at any stage of your whole creative life! In this context, I would try and avoid terms such as “anaerobic” -meaning without O2- as it’s difficult to imagine my system working without O2 up to the VO2peak level! Percentages and contributions of systems change, of course.
The “non-active” muscles you are referring to start contributing to the overall lactate shuttle mechanism, which again involves O2, of course. Also, your association between a breathing, or Ventilatory threshold with a lactate one doesn’t hold truth. It might happen in certain individuals, but it’s not a cause and effect relationship.
In this regard, your theory ® has some flaws.
I would strongly encourage you to read everything writen by George Brooks; most of his brilliant papers are from the 80’s and 90’s, but they are coming more like from the future.
Also, see the whole “lactate threshold” as a dynamic balance between lactate production and elimination -when this balance is achieved you’ve got your threshold point- and not like two different steps -suddenly and from nowhere lactate appears.
Lastly, try and separate in your mind the theoretical and practical aspects of lactate threshold and its uses.
Lactate threshold tests should be done much sooner than weather season changes ( ) and this is the great problem with them, i.e., how often can you keep testing an athlete? Variations exist daily!
The whole point about posting the inclination papers was to give you an idea of how you can simulate outdoor conditions…
You sit in front of your pc in a rested state, but lactic acid (or lactate in your blood, if you want) is in there. It’s always there! In a balanced state, i.e., between production and elimination of it.
This resting LA in blood is due anaerobic metabolism of red blood cells (teaching at my Faculty)
As I said before, VO2 (and HR) will increase linearly all the way, there is no deflection point of these corresponding to the lactate threshold. There might be a plateau towards the end for VO2, but it doesn’t happen to everyone; also, a deflection point might appear in HR, but this 90% is >LT, as you define it and for me doesn’t mean anything (original Conconi test).
This is totaly diferent than the thinks I was reading last couple of years… Please give me supportive source for this “all the time linearity”! (What about supertraining)
Active muscles are impossible, I repeat impossible to reach an O2 limit! The most brilliant example of all, I am sure you’ll agree, is the heart muscle! I don’t think it becomes depleted of O2 at any stage of your whole creative life! In this context, I would try and avoid terms such as “anaerobic” -meaning without O2- as it’s difficult to imagine my system working without O2 up to the VO2peak level! Percentages and contributions of systems change, of course.
I think you are wrong (excuse me if I am wrong). There are two factors limiting aerobic capacity - central and peripheral (see my other posts). So if the active muscle cannot get into his O2 consuprion limit why is VO2max higher in running than in cycling, and what about VO2max corelation with muscle mass use? If the heart is the only limiting factor (this is an old theory, I think dropped) for VO2max, than you could improve your heart performance with swimming and have better result with running, but this is not true! Opinion…
Thanks for Brooks book, I will try to have some money and time to read it!
I am going to sleep…
Lactate due to the exclusive presence of “anaerobic” mechanisms? That’s a first! So, what do you breath at rest?
What’s Supertraining? Do you mean the book by Siff? I don’t know…
4th Edition of Exercise Physiology: Energy, Nutrition and Human Performance, by McArdle, Katch and Katch:
p. 307 about the linearity of VO2 vs. power output (or speed, if we are talking about running) for two different exercise modes; VO2 increases linearly in both cases, of course.
p. 302 about the linearity of HR vs. VO2 (or any measure of intensity for that matter) for different populations. This is a good example, as there is a deflection point towards the end for one out of three cases (read my post above, it doesn’t happen all the time), i.e., well above a corresponding lactate threshold -not shown here.
It’s been some time, since I opened that book, thanks!
Look, I know some things might be new to you, or challenge some of the things that you already know and that’s why I am typing these, but this isn’t necessarily a bad thing! Have a look at the sources and decide for your self!
Nobody’s wrong, it’s a discussion. I am pretty sure we are not going to solve this in a few posts, as greater minds haven’t done so before us and the debate continues!
My point about the heart as a muscle wasn’t to say that O2 consumption by the heart is the limiting factor (Goodness me, I would be extremely worried of my heart first before any other muscle!), but rather quite the opposite; that is, if the heart has always “access” to O2 and this is delivered to the muscles, how is it ever possible to talk about lactate coming exclusively from an anaerobic (no O2) metabolism?
According to the traditional Cardiovascular/Anaerobic Model, high intensity exercise is ultimately limited by the development of anaerobic conditions in the active muscles. This absence of O2 results from the heart’s inability to increase its output above some limiting maximum value. As a result, O2 delivery to the active muscles plateaus, forcing the muscle to rely on anaerobic metabolism for their energy supply. The by-products of this anaerobic metabolism eventually accumulate in the muscle, causing exhaustion. The clear charactiristic of this model is that the heart is the slave of the exercising muscles. Ok so far? That’s the traditional one.
However, there are numerous studies and tests (I have examples, if you wish) that clearly show a lack of O2 plateau upon termination of exercise; although sufficient O2 is reaching the muscles at the time the individual stops exercising, there is a limitation, not in the rate of O2 supply to the system, but in other factors inherent in the system itself, i.e., muscles. The heart has no capacity to contract “anaerobically” and to develop an O2 debt; otherwise, it’s contractility would be immediately impaired (angina pectoris). However, exercise is very-very rarely terminated by such factors; in healthy individuals, in fact, never! So if the heart has always adequate O2 supply and this can be delivered, how come and muscles become anaerobic?
So there must be another mechanism in the system, either in the heart muscle or in the nervous system, that causes a slowing down in circulation as soon as a serious degree of unsaturation occurs, i.e., a governor, which acts before, of course, myocardial damage is developed.
The heart’s pumping capacity, determined, in part, by the maximum coronary blood flow, may indeed limit maximal aerobic exercise performance in events lasting a few minutes. This capacity is determined by the heart’s maximal pumping capacity at the point at which the maximal blood flow to the heart is about to be reached. This must be a regulated process, however, as the actual maximal blood flow to the heart must never be achieved (or else chest pain and heart damage will result). Rather, there must be a governor that terminates exercise before the heart and exercising skeletal muscles are forced to contract anaerobically. It is the heart, not the skeletal muscles, that is at greatest risk of developing anaerobiosis during maximal exercise. So there must be a governor anticipating when the blood and O2 supply to the heart is about to become inadequate. This governor presumably is located in the brain and in response to information from the heart, may reduce the recruitment of the muscles already active. That is, exercise will be terminated before a plateau is demonstrated in whole O2 consumption, or rather, more importantly, in the heart’s blood supply and O2 consumption.
Therefore, neither the heart, nor the muscles would develop anaerobiosis in the first place during maximal exericse and exercise will terminate as a result of a plateau in the recruitment of any additional fibres in the exercising muscles by the brain. Fatigue is always sensed exclusively by the brain. Now under such aerobic conditions, lactate is present and can increase of course, not due to the absense of O2 in the system, but because the balance, as I said in previous post, between production and elimination is disturbed, i.e., production outstrips elimination!
Based on the above, the best athletes will be those with the highest maximum rates of coronary blood flow, perhaps because they have larger coronary blood vessels with a greater capacity to dilate during exercise and the most economical hearts and muscles with the greatest contractility and elasticity and their governor in their brain perhaps allows their hearts to continue contracting to lower O2 concentrations in their hearts.
Basically, it’s a combination of the two, the maximum pumping capacity of the heart and the athlete’s exercising muscles (superior contractility and myosin ATPase activity, or enhanced capaciry to bind calcium, superior efficiency, superior elasticity and superior fatigue resistance).
Brooks has an Exercise Physiology book with another guy, I think, but his many papers would be just fine! Let me know if you need any references, as they’ll change the way you see lactate kinetics.
Nikoluski,
thanks for writting down that huge post. It is quite confusing and totaly new for me. You cut my feet, I feel like flying and have no thing to cath with… but I like this! There are new things that I dont know, but I am opened (and critical mind) student for new ideas… so thanks!
I was a software programmer and I know some thigs about cybernetics and automatization (I am not just some kind of sport student) so I developed some kind of theory (wich is in progress ) of factors limiting aerobic capacity. I dominantly think that the limiting factors are the number and size of mitochondria in active muscle (if the O2 supply is ok). That is why you get bigger VO2max results with cross-country skiing than with running (you use bigger muscle mass, so there is bigger ability to spend oxygen). But maybe in some cases the ability of the heart to pump minute volume of blood is the limiting factor. Pumping volume falls down during maximal heart rate so the neto product (HeartFreq * HeartPumpVolume) is less. So agree with you that factors limiting aerobic capacity is the combination of heart (central factors) and muscles (peripheral factors) but wich of them is dominant I dont know. I could be individually too.
About that anti-heart failure mechanism… very interestin.
So to conclude… we can argue about this for month, but one thing is true… I am lacking of knowledge, and you seems like a nice guy (no I didnt dream of you ) so please be free to tell me what to read and what not to read. OK? Thank for that two references! If you have some (anything considering training) in e-book format or HTML please send me! Thanks a lot!
I will come back in monday… bye friend!
What you are saying about mitochondria is very true, of course! And the key is to develop them around the actual fibres that you’ll need for your event.
According to the above post, the “limiting” factor, or rather the protective mechanism could be the brain itself (Central Governor)!
It’s not a matter of what I can tell you to read; I would read as much as I could and from different sources to make my own decisions and conclusions. Your Faculty and every university can’t teach you things that haven’t been proven scientifically 100% -although there is a lot of support about the above- but more traditional ideas should not limit your interests IMO.
The only thing I could do is to send you the references I’ve gathered and challenge traditional lactate kinetics mechanisms -mainly via Brooks references and perhaps a couple of books. I am not sure if you’ve got access to academic journals; if yes, no problem!
But remember, theory and understanding is one thing and application and practice is another!
What on earth are you guys going on about? Let’s get back to planet earth. If you think in terms of high/low intensity and you classify treadmill as low (most of you wouldn’t have access to a treadmil that could generate medium or high anyway- nor should you want to) then you don’t have to worry about all this.
Then the discussion can move to the various actual sessions you can do on the treadmill as a replacement for tempo on grass or the track if grass is not an option.
Agreed, Charlie! I was just trying to have a discussion with Mladen about the whole “lactate threshold” concept, or the mid-range intensity, as you might want to refer to, as this is highly regarded/accepted at universities, or sports science centres, by the most at least and Mladen is at such an environment.
It just so happened that I didn’t agree with some of the things he was saying -at a theoretical level.
Whether you want to apply any of these to the track is a different issue; I tried to briefly refer to this and that’s why I ended up with the sentence I closed -that such theories (i.e., referring specifically to the “lactate threshold” one) and every day practice can be two different things, when it comes to the track and it might worth separating the two in your mind…
Science is great and all but things that are couched in fancy terminology can sound fine when really they’re not.
Simply put: High/Low - good, Medium - Bad.
So tell me about training tempo on a treadmill rather than grass.
I have been experimenting with this (because I don’t like getting rained on and then having to cycle home) and I like the concept but I’m not so sure about what adjustments I need to make.
I run tempo at 18-20km/h (around 60-70% of my max mean velocity) and use foot contacts to measure distance (e.g. 50 for 100m). However, I find a tempo session on the treadmill is a lot easier on my legs than running on grass though the apparant CV affects seem greater (I just feel more out of breath). I also run far more relaxed on the treadmill because I can monitor my shoulders at all times.
So what does everyone think of Frappier speed training on a treadmill? I absolutely hate it! I live in Fargo, ND and Frappier is huge here. Everyone here think it is the greatest speed training device ever made.
but it’s got different inclinations for different surfaces; I think I’ve posted the results on a different thread regarding tempo running on a treadmill; have a look…)
