Lactate curves of elite athletes show that EPO/ Blood boosting is pointless.

Good science, bad science wrote:

Indeed. Lydiard also didn't believe in the efficacy of so called 'performance enhancing drugs' either did he?

Now if only the so called 'Lydiardists' could understand this, then they might by true followers. I tried to explain this to Nobby Hashizume last year. He wasn't interested.

Actually, if you look at one of Lydiard's books - the one with Dieter Baumann on the front cover - he does list "drugs" as being one of the factors that can influence a top level performance in addition to other factors such as training/peaking etc...

As far as I know, Prof. Jones did not look at RER or attempt to measure glycogen usage. He measured lactate with an incremental speed treadmill test, and plotted the data versus speed. Running Economy was concluded to be central to Paula's improvement over the 12 year period.

But my problem is, I find all the stuff you call bad science, mythology, and dogma, in these textbooks, often supported by academic research.You said that "ex phys" was derailed by a lack of attention to neuroscience -- wouldn't this be reflected in the modern text books? Don't you have better references that have shaped your thinking? Do you have a list of "bad" references to avoid?The question put to you repeatedly is, can you elaborate? These are your ideas that you claim are supported by good science. If the best answer you can give is "no", and you give up at "Why not?", why even bother?

Good science, bad science wrote:

... Read a physiology textbook just once in your life if you are really interested.

I have sat idly by for some time now and read influential coaches and psuedo-scientists spout unsubstantiated opinions and anecdotal evidence regarding doping on this forum. It has done nothing but confuse many readers and miseducate a great many others. Let there be no doubt; EPO/blood doping improves aerobic performance in endurance athletes. We know this because we have a) countless "superhuman" performances from elite athletes that subsequently tested positive, b) a 20 year culture of EPO and blood doping at the highest levels of sport, and most importantly c) because all available scientific data points to this fact.

So how does it work? Based on the scientific literature, the evidence points to 2 main physiological mechanisms:

1) Increased maximal aerobic power (VO2max) mediated by a rise in blood oxygen content and systemic oxygen delivery (Ashenden et al., 2001; Audran et al., 1999; Conne et al., 2004). VO2max is primarily limited by cardiovascular system and not muscle diffusion capacity (Lundby et al. 2008). In other words, if we can get more O2 pumped to the muscles, the muscle cells will pick it up and use it! This is an important finding, because it means that EPO/blood doping would be as effective in elite athletes as lower level competitors. In fact it may even work better, since elite athletes have greater mitochodrial density, therefore greater capacity to utilize O2 once it has entered the muscle cell.

2) Improved lactate clearance kinetics via increased expression of monocarboxylate transporters, specifically MCT-1 (Conne et al., 2004). By increasing the buffering of lactate, EPO significantly improves performance via an increase velocity at lactate threshold. Keep this point in mind, because the original poster on this forum has been arguing for days that EPO does nothing to the lactate curve. Conne's article categorically refutes this claim.

The article by Conne et al. (2004) is also important as it provides direct evidence that a 4 week regimen of EPO injections not only increased VO2max in highly trained athletes, but also improved the lactate response to exercise. These were well trained cyclists with VO2max's in the mid 60's before they were injected. So despite what Renato might argue, there is scientific evidence of EPO's effects across a wide spectrum of athletes and no available scientific evidence to the contrary. Until he provides scientific evidence that it doesn't work in high level athletes, i will continue read his comments with quite some amusement...

So in conclusion, we have lots of scientific evidence regarding the effects of EPO on aerobic performance vs. the unsupported opinion of Renato Canova and a few other crackpots in here. Who you choose to believe is up to yourself...

REFERENCES:

Ashenden et al. (2001). A comparison of the physiological response to simulated altitude exposure and r-HuEpo administration. J Sports Sci 19: 831–837.

Audran et al. (1999). Effects of erythropoietin administration in training athletes and possible indirect detection in doping control. Med Sci

Sports Exerc 31: 639–645.

Birkeland et al. (2000). Effect of rhEPO administration on serum levels of sTfR and cycling performance. Med Sci Sports Exerc 32: 1238–1243.

Conne et al. (2004). Injections of recombinant human erythropoietin increases lactate influx into erythrocytes. J Appl Physiol 97: 326-332.

http://s1.e-monsite.com/2009/02/28/78114812connes-2004-jap-97-326-pdf.pdf

Ekblom (1996). Blood doping and erythropoietin. The effects of variation in hemoglobin concentration and other related factors on physical performance. Am J Sports Med 24: S40–S42.

Lundby et al. (2008). Does recombinant human EPO increase exercise capacity by means other than augmenting oxygen transport? J Appl Physiol 105: 583-587

http://acceda.ulpgc.es/xmlui/bitstream/handle/10553/6534/recombinant_human_Epo.pdf?sequence=5

Once again, these comments from Renato are entirely misleading. Here is why....

At an elite level in marathon, the engine's fuel consumption is almost NEVER a deciding factor in the result. They have up to 2800 kcals of glycogen stored for use. If they're burning more energy than that in a marathon, then they had no business being at the front of the race to begin with because their running economy sucks...

All sub 2.10 marathon runners have trained their bodies to such a point that they have the appropriate metabolic efficiency and running economy to survive a marathon without glycogen depleting. They burn an efficient mix of fats:glucose to survive the duration of a marathon without running out of glucose. Couple this with drink strategies during the race, and glycogen depletion should never be a determining factor. For your average 3-4 hr marathon runner glycogen depletion is absolutely a problem but for Bekele, Kipsang and those guys, it is just not a factor that should influence the result.

So if fuel is not an issue, what does determine the result of a marathon? The number one factor is their speed/pace at 2.0 - 3.0 mmol blood lactate. Elite level marathon runners can race a marathon at a speed of 19 - 21 km/hr and maintain a stable blood lactate concentration somewhere between 2 - 3 mmol throughout. Try to run faster, and the lactate accumulates, leading to fatigue. So any intervention which increases the pace at which they can maintain this stable lactate concentration, will undoubtedly improve performance.

Does EPO have the power to do this? As i mentioned above, absolutely it does! By increasing O2 delivery to the mitochondria, we reduce the need to convert pyruvate into lactate at submaximal paces. So you can run faster before your muscles need to start producing lactate. In addition, as Conne et al. (2004) demonstrated, EPO also increases lactate efflux via MCT-1 transporters. So it also has the ability to buffer existing lactate.

So EPO positively influences the most important factor in marathon performance which is the pace you run with stable 2-3 mmol lactate in your system.

Any questions?

Thank you for your two responses. They are the first that actually propose a sensible physiological mechanism for what limits performance.

Thank you for providing such thorough yet concise descriptions of the factors affecting marathon and endurance performance. These are great summaries that should be read by others. You definitely brought some of my knowledge up to date. 10/10

Good science, bad science wrote:

fred wrote:

Explain the neurochemistry in detail if you're not a troll.

Assuming that I even might be trolling suggests to me that you are just an idiot who is not worth the time. Read a physiology textbook just once in your life if you are really interested.

No boy, you can't explain the neurochemistry because you're full of shite

One of these riders just decided to start using EPO and one is already juiced. Guess which is which...

Yeah I have a couple.You seem quite confident that the scientific evidence is already sufficient, and superior to real world experience.1) What do you mean by "countless superhuman performances from elite athletes that subsequently have tested positive"? Keep in mind that cycling long tours is not long distance running -- the demands of the two events are not comparable -- and that cyclists were taking many other things along with EPO. Specifically, with respect to elite long distance running, there doesn't seem to be too many "superhuman" performances, or EPO busts to count. Who are the top few names you have in mind?2) I can see for maximal efforts (especially in "recreational" subjects) how they might respond to an increased red blood cell mass, raising their measured VO2max. But how does increasing VO2max (e.g. from 64 to 68) deliver more oxygen to the muscles at sub-maximal efforts? Assuming a marathon requires only about 84% of VO2max, it is difficult for me to see how VO2 delivery of 54-58 ml/kg/min is limiting in a clean athlete with a VO2max of 64 ml/kg/min.3) Is your wide spectrum wide enough? Your mid-60's well trained athletes compare with 2:30-2:35 marathon runners. What distinguishes a 2:05 runner from a 2:35 runner, and how could this impact any conclusions on athletes outside the data space? Isn't that bad science to represent extrapolation as scientific fact?4) How do you conclude that EPO's impact on MCT-1 expression results in increased velocity at the same lactate level? A quick glance at your paper, and Conne et. al. says "However, we did not measure lactate kinetics, and it is difficult to speculate on the potential effect of increased lactate uptake by erythrocytes on lactate metabolism during the incremental exercise". Did someone else find and conclude an increased velocity for the same lactate due to increased MCT-1 expression?5) Do you have any practical experience with elite level marathoning?6) Do you have any references for your claim that glycogen consumption is NEVER a factor for 2:10 marathoners or better? Seems to me that glycogen management for a 2 hour running event is ALWAYS a major factor. If your 2:10 runner goes out at 2:05 pace, he will disrupt the delicate fat:glycogen balance needed to complete the event without hitting the wall.7) Do you have any reference for your claim that speed/pace at 2.0-3.0 mmol is the number one factor? Maybe it's self-evident, but that seems like a pretty specific (down to the tenth of a mmol) finding, yet over a pretty broad range. Otherwise, what does it even mean? That your marathon pace determines your marathon time? What are some other top factors?

nouse4aname wrote:

Any questions?

rekrunner wrote:

As far as I know, Prof. Jones did not look at RER or attempt to measure glycogen usage. He measured lactate with an incremental speed treadmill test, and plotted the data versus speed. Running Economy was concluded to be central to Paula's improvement over the 12 year period.

This makes more sense. However, lactate kinetics and running economy are independent variables and not directly linked to one another. They are indirectly linked but it is possible to improve a lactate curve without improving running economy.

If Jones was comparing Radcliffe's running economy over a 12 year period then it would be measured via a reduction in O2 consumption at a fixed speed. Running economy is measured in kcal/m or mL/kg/m. So an improvement in running economy equates to a reduction in O2 consumption at a fixed pace. If we look at factors which influence running economy, most are biomechanical and/or neuromuscular. Such factors include:

-Reduced vertical displacement

-Improved activation of the gastrocnemius to enhance stretch-shortening cycle

-Enhanced leg stiffness during the stance phase

-Enhanced passive knee flexion during the swing phase of the stride cycle

In comparison, a shift in a lactate curves is primarily physiological. All athletes will show improvements in their lactate profile over a period of years but that may or may not occur alongside an improvement in running economy. This shift to higher speeds for the same lactate concentration occurs independently of running economy and is a result of substantial changes to your body's physiology and biochemistry. Factors which improve your lactate curve include:

- Increase in Type I muscle fiber proportions

- Increase in mitochondrial density within Type I and Type IIa fibers.

- Increase in MCT-4 and MCT-1 expression (this is a big factor)

- Increased O2 delivery capacity via increased ventricular volume, blood volume and muscle capillary density

All these factors should improve in every endurance athlete over the years, resulting in alterations in the lactate curve. In fact i would be shocked if a runner was training for 12 years and didn't see a marked improvement in their lactate curve. That is why lactate concentrations at fixed speeds are such an accurate predictor of long distance running performance. If i see a lactate curve from an incremental test, i can make a VERY educated guess as to their finishing time in a half or full marathon. This guess is usually quite accurate. It takes a lot of training and time to see significant shifts in the lactate curve (or you could just take EPO and see more rapid improvements). In either case, the original poster probably sat through Jones's talk and then completely misinterpreted the information. Running economy and metabolic efficiency are entirely different variables and to argue that EPO cannot influence lactate kinetics is entirely false, for the reasons stated previously.

How many world world class times and gold medals have been erased from the history books because of subsequent positive test results? I'm talking about across the entire span of endurance sport. The phenomena of retroactively disqualifying athletes for blood manipulation is all too common in endurance sport. Is this not evidence of EPO's positive effects in elite athletes.

With regards to your comment that there doesn't seem to be many "superhuman" performances in running, I'm assuming you are referring to positive drug test results? In my opinion, the reason we have had less running busts in the past is simply down to logistics. It is infinitely easier to manipulate blood values for a long distance running event than it is for a 3 week cycling Tour. I mean, INFINITELY easier! You only have to be clean on a single day. If you understand the pharmacology of EPO and how to manipulate your blood to produce a "psuedo-clean" blood profile, then really you're an idiot if you test positive.

I don't need to name names in order to justify this point, but obviously Jeptoo and the Russian athletes are the most recent examples of positive tests. However, you'd be very gullible if you didn't question some of the performances from the turn of the millenium (prior to the introduction of EPO testing) from athletes that never tested positive. Remember that Lance Armstrong never tested positive and as i mentioned, it is far more difficult to manipulate your blood for a 3 week Tour. Yet those guys did it easily...

The anaerobic threshold is at submaximal intensity, yet it is the rate limiting factor for a great many aerobic events (up to and including half-marathon). So what happens metabolically at the anaerobic threshold? The mitochondria in your muscle cells have reached their rate limit of oxidation. Either there is not enough oxygen getting to the mitochondria, or the rate of substrate transport into the mitochondria has maxed out. So to go any faster, your muscle's only option is to increase the anaerobic breakdown of glucose and instead of transporting the end-product (pyruvate) into the mitochondria, the muscle cell is forced to convert the pyruvate into lactate.

Lund et al. (2008) amongst other researchers have shown that providing more O2 to the muscle (via EPO) does allow for increased diffusion of O2 into the muscle cell and by proxy, increases oxidation by the mitochondria. So at submaximal intensities, the mitochondria have more available O2 to continue breaking down pyruvate. Therefore less conversion of pyruvate to lactate; therefore lower lactate concentrations at the same speed; therefore faster speed at anaerobic threshold. By providing more O2 to the muscles, your maximal aerobic power goes up but your submaximal efficiency has to improve as a direct consequence.

Agreed. However it is BADDER science to ignore all available data and instead assume the opposite effect. The scientific literature reporting the effects of EPO in humans consistently shows improvements in aerobic performance. When you couple this with the world records that have been retroactively erased due positive tests, then in my opinion we have ample evidence of it's effectiveness in elite athletes. Regardless, the following statements are true in humans:

1) There is a significant correlation between VO2max and aerobic performance.

2) The rate limiting factor for VO2max is delivery of O2 to the muscles.

3) EPO increases the delivery of O2 to the muscles, therefore enhancing VO2max and aerobic performance.

Until this statement is demonstrated to be untrue in a subset of the population, it is logical to assume it holds true for all humans. I have not heard any rational argument as to why that shouldn't be the case in elites. Obviously, it is not possible to test any such hypothesis on world class athletes for ethical reasons. Yet Conconi's work in the late 80's did just that. He conducted a study on "amateur cyclists" in which EPO was systematically administered. It subsequently turned out that the subjects were in fact members of the Cerrara cycling team which included several Grand Tour winners. That evidence was compelling enough that basically every other pro-cycling team subsequently began using EPO...

Renato argues that we have no data on elite athletes, therefore there is no effect or even a negative effect. This is the scientific equivalent of an ostrich burying their head in the sand. Whats worse, the ostrich happens to be the world's most successful distance coach and is encouraging everyone else to bury their heads in the sand too...

Speculation based on the phyisological effects they presented and combining it with other work on lactate kinetics. Its true that their protocol wasn't set up in such a way as to look at lactate curves or kinetics, however having spoken to one of the authors, they speculated the same thing (they just couldn't say it in the article, since it wasn't measured). The data certainly suggests it, and when you combine that data with George Brook's work on lactate shuttling, it is even more compelling. Intramuscular MCT-4 and MCT-1 expression directly influences lactate kinetics. Extra-cellular lactate shuttling does the same thing. Increased lactate influx into erythrocytes is simply another form of extra-cellular lactate shuttling. Hence my conclusion.

Yes, quite a bit of practical experience.

No reference, but it is a simple math problem. If you measure RER at marathon pace, then you can pretty estimate the calorific cost of running a marathon and how much of that calorific expenditure will come from glycogen.

A sub 2.15 runner will burn somewhere in the region of 2,400 - 2,600 kcal during the race. They will do this at an RER of around 0.9, which means that 32% of that energy is coming from fat metabolism. That means that around 1,700kcals is coming from glucose. Normally humans can store up to 2,500 kcal of glycogen in the liver and muscles. As long as their nutrition leading up to the race has been correct so that they have completely full glycogen stores and they take on some additional glucose at feeding stations during the race, glycogen depletion really should not be the difference between winning and losing...

Also, your logic about the 2.10 runner is flawed. If a 2.10 runner goes out at 2.05 pace, then they will accumulate excess lactate and fatigue long before they glycogen deplete. Again, that is why lactate concentrations at submaximal intensity are such an important variable in determining marathon performance.

No reference. Again this claim is based off work I have done with several top marathoners in the lab i work at. Your speed at 2.0 - 2.5 mmol during an incremental test is very accurate at predicting marathon performance. We base our predictions on these concentrations, but adjust based on other factors such as the shape of the curve and the athlete's lactate tolerance above threshold. But i've seen this method predict the fastest debut marathon time in the world, down to an accuracy of 13 seconds. That is pretty accurate considering the athlete had never even attempted the distance before and we tested her a month out from the competition. Obviously every athlete is individual so there is no set concentration (ie- exactly 2.0 for everyone). The more work you do with the athlete, the more accurate you become. Also, it is obvious that during a race there will be fluctuations in your lactate concentrations. Hence why i gave a rough range of 2.0-3.0 mmol which is what i've observed during race simulations.

But this remains the most accurate performance indicator we have for marathon performance. Therefore, improving this variable becomes the most important training goal and any intervention (legal or otherwise) which achieves this becomes highly valuable to the athlete.

Renato claimed that EPO won't help a marathoner because the most important factor is fuel utilization during the race. I disagree. But if he can accurately predict his runners' marathon times by examining their rate's of glycogen utilization, then he's a better man than I...

rekrunner wrote:

Do you have any reference for your claim that speed/pace at 2.0-3.0 mmol is the number one factor? Maybe it's self-evident, but that seems like a pretty specific (down to the tenth of a mmol) finding, yet over a pretty broad range. Otherwise, what does it even mean? That your marathon pace determines your marathon time? What are some other top factors?

Forgot to include this recent article in my last reply. A very good study which demonstrated the accuracy of blood lactate concentrations in predicting middle and long distance performance. They showed that speed at 4.0 mmol was significantly correlated with 3,000m time (r=0.849) for middle distance runners and 10,000m time (r=0.919) for long distance runners, and that 4.0mmol was more accurate than Dmax as a predictor. We are preparing a similar article for half and full marathon performance, and will compare 2.0mmol, 4.0mmol and Dmax as the dependent variables. I would expect to see similar if not even more significant correlations. In my experience, the longer the duration of the event, the more accurate lactate is at predicting the performance. But we shall see...

Anyways, the article is definitely worth a read!

REFERENCE:

Santos-Concejero et al. (2014) OBLA is a better predictor of performance than Dmax in long and middle-distance well-trained runners. J Sports Med Phys Fit, 54 (5); 553-558.

nouse4aname, you are a perfect example of the kind of bad scientist I am talking about. I do not need a lecture on RER from you. And I certainly don't need a lecture about lactate metabolism from someone who has so little understading of the subject.

So much of what you have written above is dogma. If I had more time I would reply in detail. That will come later.

Your first list is a good one. Your second is based on wrong assumptions about training improvements, pure dogma. These physiological factors don't take years to gain, weeks at most, for an untrained runner.

Mixing good and bad science like this is exactly what frustrates me so much about common misconceptions about running. You might impress a few posters who are easily blinded by science, but that is not going to impress me. You have to do a lot better than that.

rekrunner, thanks for taking the time. You have lots of good questions which I hope to answer when I get time.

So far you haven't impressed anyone either.

You'd better get on that "when you have time".

Trolling is such a go go go lifestyle....

Good science, bad science wrote:

nouse4aname, you are a perfect example of the kind of bad scientist I am talking about. I do not need a lecture on RER from you. And I certainly don't need a lecture about lactate metabolism from someone who has so little understanding of the subject.

So much of what you have written above is dogma. If I had more time I would reply in detail. That will come later.

Thank you for that critical evaluation. Coming from someone who doesn't understand a simple definition like efficiency and stated that "less glycogen means less oxygen" i will not lose any sleep over it.

Seriously, if you're not going to provide a shred of evidence for your crackpot ideas on lactate and EPO then please, for the love of God stop typing!!! You responded to another poster on here that asked for evidence, saying they should "go read an Exercise Physiology textbook". I'm begging you to please listen to your own advice. You're so far off the mark that it wouldn't surprise me if the comments were being typed from a padded room...

Either way, i'm not responding to you anymore if you will not at least engage in a rational scientific discussion. Provide some evidence for your ideas and i'll be happy to read them. Otherwise i'm not responding. I'm happy to have an enjoyable debate with someone like rekrunner, who clearly has an understanding of the subject, is willing evaluate scientific evidence and can put forward some rational arguments. You're doing none of those things, so i can only conclude that you're a troll.

Good science, bad science wrote:

Your first list is a good one. Your second is based on wrong assumptions about training improvements, pure dogma. These physiological factors don't take years to gain, weeks at most, for an untrained runner.

Please provide a citation for this.