When news of Contador's positive for clenbuterol initially broke, I expressed my surprise and dismay, and also incredulity that the Spaniard would dope with clen during the Tour de France. I accepted that there could be validity to his claim of food contamination, but refrained from suggesting a second possible scenario, the introduction of clenbuterol into his body via a contaminated transfusion. I stick by my initial statement that clenbuterol is a horrible drug and one that you would never use during the Tour - but I want to reiterate that I accept it's absolutely plausible that an athlete would dope with clen while not racing in hopes of slimming down to unnatural levels before a major competition - though in that case clen is only one of several substances that would have to be combined in a veritable weight-loss cocktail (thyroid hormone being one, and perhaps a sleep-aid like Stilnox being another).
I still don't believe that Contador doped with clenbuterol during the Tour de France, and I hope that he can answer the five questions we previously identified here, and explain satisfactorily how the drug entered his body. Unfortunately, that seems less-likely now with this allegation coming from an unnamed source close to the Astana team, as reported by VeloNation:
"Belgian magazine Humo has published claims from an individual with the Astana team, who alleges that Alberto Contador used Clenbuterol after the Criterium du Dauphiné as part of a weight-loss treatment. The person, who spoke on condition of anonymity, claims that the Spaniard had blood extracted between that race and the Tour when, crucially, traces of the banned product were still in his system.
“He had a transfusion performance after the Dauphiné Libéré [Criterium du Dauphiné], and the blood still contained a little bit of clenbuterol from a just-finished slimming treatment,” Humo reported the insider as saying.
“In the Dauphiné Libéré, Contador was still a little overweight. Ordinary people do not see that, but there was still a pound or two to shed. Clenbuterol is used to get rid of the last kilos while, at the same time, to ensure that you do not lose muscle mass - or, in the best case, even gain a little extra muscle mass.”
He described how the technique works, saying that the substance is used in combination with another
“You have to use it in combination with T3 [Triiodothyronine]. This is a thyroid hormone that helps in the digestion of fats. Then you have more rapid effect with a smaller dose of Clen. And the smaller the dose, the smaller the chance that you get caught.”
Contador finished second overall in the Dauphiné, but appeared to be below his usual strength there. He was beaten by an impressive Janez Brajkovic (Team RadioShack), who finished 1’41 ahead at the end of the event. Contador was only sixth behind Brajkovic in the time trial and was unable to drop his rival on the crucial stage to Alpe d’Huez, although he won the sprint to the line..."
And as an aside, in the same report the anonymous source claimed that doping via transfusions continues as before, much like Bernhard Kohl alleged, when he said it was not possible to win the Tour de France if doping was still endemic. VeloNation continues:
"The biological passport is being used as a deterrent to prevent riders from doping. While it has made it more difficult to beat the system, the Astana source told the magazine that some riders continue to manipulate things at a lesser level.
“Of course,” he said, when asked if transfusions continue. “But it’s in small doses of 150cc. Previously, riders during the Tour used two, three big bags of blood, from 400 to 500 cc. Now they cannot afford to, because of the biological passport and the sudden fluctuations in blood levels that occur.”
Sigh. I love this sport, I really do, and I'm sorry for my role in perpetuating the doping problem, but darn, if it's proven that Contador doped (and by proven, I mean there's a CAS ruling that closes the door on any appeals), then maybe that will be the nail in the coffin that will get me out of this trance and help me see the world through lenses other than a cyclist's Oakleys.
Showing posts with label blood. Show all posts
Showing posts with label blood. Show all posts
Friday, October 08, 2010
Sunday, February 21, 2010
We've Got This One in the Bag!
A recent article at SwimNews, Taking The Doping War Into The Shadows, describes what could be a promising new weapon for the war on doping [Ed: Not to be confused with the War on Terror.]. While some individuals in the cycling community are quick to dismiss the idea of a clean future for the sport – stating there will never be a fool-proof method for the detection of autologous blood doping – recent advances in doping control methodologies may compel them to revisit their pessimistic outlook.
Currently, the standard testing procedure for detecting autologous blood doping is the UCI's biological passport – an electronic record for each rider tracking the results of all doping tests over a period of time, and collating them. The passport (click for a brochure) creates a hematological profile for the rider consisting of the combined results of all previous haematological parameters analyzed in a series. Limitations to this system are clearly evident in the indirect method of testing threshold values, but testing for blood doping may become more direct in the near future, the reason being – plasticizers.
What are plasticizers?
When athlete stores their blood for future use, they refrigerate it in plastic bags – just like the ones we saw in Dr. Fuentes' clinic. However, these plastic storage bags, just like any other plastic product, contain tiny trace elements – additives to increase the flexibility and low temperature properties of the product. These additives are plasticizers, and they are found in any of the plastic intravenous products used for blood transfusions. But how reliable could a test for plasticizers be?
When athlete stores their blood for future use, they refrigerate it in plastic bags – just like the ones we saw in Dr. Fuentes' clinic. However, these plastic storage bags, just like any other plastic product, contain tiny trace elements – additives to increase the flexibility and low temperature properties of the product. These additives are plasticizers, and they are found in any of the plastic intravenous products used for blood transfusions. But how reliable could a test for plasticizers be?
A previous study by Maxwell et al. investigated the cause of remarkably high levels (200mg/100ml) of plasticizers found in blood for overdose cases. In determining whether test results were real or artefactual, the scientists tested 25 healthy individuals by methods involving only glass and metal. In no case did any of the samples taken show traces of plasticizers, suggesting that the presence of plasticizers in normal healthy individuals should be cautioned. Another study by Gayathri et al. reports that DEHP, or di (2-ethyl hexyl) phthalate, the plasticizer commonly used in PVC blood storage bags, leaks out to approximately 10mg/100ml after 21 days of storage – a significant amount suggesting the feasibility of reliable testing measures. Moreover, reading from a study by Ljunggren reports that DEHP makes up 40% of the weight of plasticized PVC used for manufacturing blood bags and transfusion tubing.
How's that for detectable?
How's that for detectable?
While this method of testing is still in the early stages of development, its effects may be premature to WADA officially adding it to their official list of doping detection methods. While there is currently no approved and legally binding test in place, the threat of a future test applied retrospectively may be enough to deter some athletes from venturing down the dark road of blood doping.
[Editor's Note: The article above was authored by Pappillon contributor, PhDuane.]
Sunday, September 20, 2009
Lance Armstrong Meets BioPassport: Tour Hgb not Explainable

UPDATED (Sept. 20): Part 4 Now Available!
Personally, I think Lance Armstrong Doped. But here is an excerpt from part 4:
"...What becomes evident from the composite prediction is that a rise in Retic between the end of the Giro and 6/16 may have been missed. The low Retic at 6/16 may be consistent with the fall after an initial peak. Similarly, the low point at 1 week after altitude exposure may be consistent with the low point after altitude exposure. Overal, assuming that the Retic did in fact trend up before falling you end up with a somewhat akward but plausible fit.
The explanation becomes less convincing when the Retic stays flat after reaching its low. The Retic does show a recovery, but it comes a week later than expected and is followed by another drop. In the end, altitude could be used to account for the initial drop in Retic, but it is not a solid explanation for a persistent low normal Retic.
Taking into account training status, the effect of a Grand Tour, and altitude exposure the analysis fails to fully explain the persistently low normal retic from 6/16 through the Tour. While other factors may be at play they probably have less of an impact. There is also the possibility of a synergistic effect, but it would be difficult to find data that supports this argument while excluding the possibility of manipulation at the same time..."
UPDATED (Sept. 15): Part 3 Now Available!
According to Local Cyclist:
"Yes the Tour Hgb is explainable. In fact, the Hgb may have behaved in a completely consistent manner... the the expected volume expansion did in fact take place. It simply started before the second grand tour and reached a physiologic limit before the end of the race. The clue to this possibility is listening to the Retic..."
Watch this space for a link to the full, upcoming article.
UPDATED (Sept. 15): Part 3 Now Available!
A Tale of Two Cyclists: Part 2; Part 1
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Sunday, September 06, 2009
New Blood Values - Updated
UPDATED (Sept.6): this is the level at or about which we were encouraged to race in 2006:


58 - 50 - 38 (Hct) - Possible Lotto #?

This is the level at which I find myself now, which is about four points below what was normal, healthy, non-EPO baseline for me before the madness:

You can also compare the above to an intermediate blood test done during my "glory" days in 2006 when (almost) fully, fully charged.
58 - 50 - 38 (Hct) - Possible Lotto #?
Friday, September 04, 2009
USADA has broadened its Blood Collection Program

"September 3, 2009 - You may have already received educational information from USADA or your NGB, or even experienced first-hand, the blood collection process…here’s the scoop in case you have any additional questions.
USADA has broadened its Blood Collection Program, to ensure the most effective Testing Program for athletes in the Registered Testing Pool. All athletes in the USADA Registered Testing Pool, as well as others who may be selected for testing by USADA, are subject to blood testing as part of USADA’s Out-of-Competition Anti-Doping Program. In addition, any athlete competing at an event where Doping Control occurs is subject to blood testing if selected.
Blood collection can occur in both In-and Out-of-Competition settings. In both of these settings, the DCO will manage the Blood Collection Session and will work in conjunction with a qualified phlebotomist (also referred to as a Blood Collection Officer or “BCO”), who will perform the actual collection of the blood sample.
At the start of the testing session, a DCO or representative of USADA will notify you that you have been selected for testing and that a blood Sample is required. You may also be required to provide a urine Sample.
The DCO will ensure that the Doping Control Station is suitable for blood collections, which includes maintaining the privacy of the athlete and ensuring that the Station is clean.
You will be asked to be seated for a period of time prior to providing a blood Sample. You will need to remain in a seated position, uninterrupted, prior to the blood collection.
In most cases the amount of blood that will be drawn for Doping Control will be less than a tablespoon. As the human body has approximately 6 liters, or 379 tablespoons of blood, the amount of blood collected for Doping Control is minimal, and your performance should not be affected.
You will be asked a series of questions related to your recent training and the altitude of these locations. These questions are necessary in order to have the full background information needed to evaluate your blood test results.
The DCO or BCO will provide instruction and if you have any questions regarding the process, please ask the DCO or BCO..."
Demystifying the UCI's Biological Passport
For help in understanding the results captured by the UCI's Biological Passport system, or at least in trying to interpret them - may I suggest "A Tale of Two Cyclists" by Local Cyclist, here.
[NOTE: As I am not a hematologist, I take no responsibility for the accuracy of the information contained within the article that I link to or the excerpts presented here. But perhaps if you are of a science/medical background, you'll read the article and leave the appropriate feedback if necessary... You can also download a brochure by UCI on the Passport here.]
Some excerpts from "A Tale of Two Cyclists":
"Any minute now the cycling media is going to unleash a deluge of in depth articles analyzing the recently released bio passport data. Actually, that’s a lie. No instead, you the average cyclist will have to do your own analysis. I know, I know every time bio-passport data gets mentioned it comes with a disclaimer that only super doping experts are capable of looking at it without going blind. Fortunately, that’s not exactly true either.
So lets dive in and look at some Grand Tour data from two cyclists, MJ and BT.
MJ
Hgb 14.8 13.6 13.0
Hgb z 0.39 -1.42 -2.32
Retic 1.3 0.7 0.9
BT
Hgb 14.3 13.7 14.4 14 14.5
Hgb z -0.36 -1.19 -0.2 -0.7 -0.05
Retic 0.5 0.5 0.7 0.5 0.7
So what are we looking at. Hgb stands for Hemoglobin mass. Hemoglobin is the stuff in the red blood cells that carries oxygen. For simplicity, red blood cells = hemoglobin = oxygen = performance.
Rider MJ starts the tour with Hgb 14.8 and drifts down to 13.0. Rider BT starts at 14.3 starts to drift down pops up, drifts down, and pops up again to 14.5 just higher than where he started.
Hgb z stands for Hemoglobin z score. A z score is an indicator of where you are within your normal range, also called standard deviation. Typically, you are considered to be out of your normal range if you are higher than +2 (2 standard deviations above average) or less than -2 (2 standard deviations below your average).
Rider MJ starts the tour with a Hgb z of 0.39, just above average but well within the normal range. By the end of the tour he’s at -2.32, out of his normal range on the low side.
Rider BT starts the tour at -0.36 just below average but well within the normal range. Initially, he also trends down, to -1.19, below average but within the normal range. Then he recovers to -0.05 or basically back to average by the end of the Tour.
Retic stands for reticulocytes or immature (new) red blood cells. For simplicity Retic = how fast your body is making red blood cells.
Rider MJ starts out with a Retic of 1.3 at the upper end of normal. His Retic comes to the low side before recovering to 0.9. Overall MJ came in producing a lot of red blood cells and maintained decent production.
Rider BT starts out at 0.5 at the lower limit of normal trending up a little but still low. Overall, BT had a suppressed production of red blood cells.
To summarize, MJ comes in with an above average Hgb and a ramped up red blood cell production, maintains decent red blood cell production but his Hgb still drops low, well outside his normal range. BT on the other hand comes in with with a low Hgb and suppressed red blood cell production, never really ramps up red blood cell production yet finishes with a higher Hgb than when he started.
Before we try to make an interpretation, lets consider the relationship between Hgb and Retic, and the factors that effect blood values.
Hgb level is a balance between red blood cell destruction and production. It goes up when red blood cells are being produced faster than they are destroyed. It goes down when cells are destroyed faster than they are produced.
Accelerated destruction of red blood cells can be caused by, normal wear and tear, significant physical stress, and illness.
Slowing of destruction can be caused by; rest (less normal wear and tear).
Production of red blood cells (high Retic) can be caused by; low Hgb, altitude training, rest after physical stress, and EPO.
Suppression of red blood cell production (low Retic) can be caused by; high Hgb, physical stress, and illness.
Special considerations:
Dehydration: Hgb looks higher than it really is.
Volume expansion: Hgb looks lower than it really is.
Normal Patterns:
Grand Tour: Hgb decreases despite decent Retic count although retic should trend down as well.
Altitude: A modest rise in Retic is followed by modest rise in Hgb, that should not overcome significant physical stress. Returning to lower altitude should cause a tapering off of Retic and Hgb.
Recovery from physical stress: Initially Hgb and Retic are low followed by a moderate rise in Retic and Hgb. The effect should be suppressed by significant physical stress.
Chronic stress: Low Hgb, low Retic, and poor performance.
Dehydration: Hgb is higher than expected, variable Retic, and performance is decreased.
Enhanced patterns
Epo: Look for a large rise in Retic followed by rise in Hgb, persistently elevated Retic despite high Hgb, and the effect is strong enough to overcome significant physical stress.
Sudden stop of EPO: High Hgb combined with a very low Retic. Retic should fall dramatically and precede a significant fall in Hgb.
Blood transfusion: High Hgb very low retic, maintenance of Hgb despite significant physical stress and low Retic.
Blood withdrawal: Low Hgb despite high retic without some other explanation for red cell destruction.
Masking:
Transfusion plus volume expansion: Very low Retic despite what looks like a low to normal Hgb without other cause for suppression.
EPO plus volume expansion: High retic normal HgB, and an effect that can overcome significant physical stress.
Transfussion plus EPO micro dose: High Hgb, low normal Retic, and an effect that can overcome significant physical stress.
Transfusion plus volume expansion with EPO micro dose: Low to normal Hgb, low normal retic, and an effect that can overcome significant physical stress..." - A Tale of Two Cyclists

Some excerpts from "A Tale of Two Cyclists":
"Any minute now the cycling media is going to unleash a deluge of in depth articles analyzing the recently released bio passport data. Actually, that’s a lie. No instead, you the average cyclist will have to do your own analysis. I know, I know every time bio-passport data gets mentioned it comes with a disclaimer that only super doping experts are capable of looking at it without going blind. Fortunately, that’s not exactly true either.
So lets dive in and look at some Grand Tour data from two cyclists, MJ and BT.
MJ
Hgb 14.8 13.6 13.0
Hgb z 0.39 -1.42 -2.32
Retic 1.3 0.7 0.9
BT
Hgb 14.3 13.7 14.4 14 14.5
Hgb z -0.36 -1.19 -0.2 -0.7 -0.05
Retic 0.5 0.5 0.7 0.5 0.7
So what are we looking at. Hgb stands for Hemoglobin mass. Hemoglobin is the stuff in the red blood cells that carries oxygen. For simplicity, red blood cells = hemoglobin = oxygen = performance.
Rider MJ starts the tour with Hgb 14.8 and drifts down to 13.0. Rider BT starts at 14.3 starts to drift down pops up, drifts down, and pops up again to 14.5 just higher than where he started.
Hgb z stands for Hemoglobin z score. A z score is an indicator of where you are within your normal range, also called standard deviation. Typically, you are considered to be out of your normal range if you are higher than +2 (2 standard deviations above average) or less than -2 (2 standard deviations below your average).
Rider MJ starts the tour with a Hgb z of 0.39, just above average but well within the normal range. By the end of the tour he’s at -2.32, out of his normal range on the low side.
Rider BT starts the tour at -0.36 just below average but well within the normal range. Initially, he also trends down, to -1.19, below average but within the normal range. Then he recovers to -0.05 or basically back to average by the end of the Tour.
Retic stands for reticulocytes or immature (new) red blood cells. For simplicity Retic = how fast your body is making red blood cells.
Rider MJ starts out with a Retic of 1.3 at the upper end of normal. His Retic comes to the low side before recovering to 0.9. Overall MJ came in producing a lot of red blood cells and maintained decent production.
Rider BT starts out at 0.5 at the lower limit of normal trending up a little but still low. Overall, BT had a suppressed production of red blood cells.
To summarize, MJ comes in with an above average Hgb and a ramped up red blood cell production, maintains decent red blood cell production but his Hgb still drops low, well outside his normal range. BT on the other hand comes in with with a low Hgb and suppressed red blood cell production, never really ramps up red blood cell production yet finishes with a higher Hgb than when he started.
Before we try to make an interpretation, lets consider the relationship between Hgb and Retic, and the factors that effect blood values.
Hgb level is a balance between red blood cell destruction and production. It goes up when red blood cells are being produced faster than they are destroyed. It goes down when cells are destroyed faster than they are produced.
Accelerated destruction of red blood cells can be caused by, normal wear and tear, significant physical stress, and illness.
Slowing of destruction can be caused by; rest (less normal wear and tear).
Production of red blood cells (high Retic) can be caused by; low Hgb, altitude training, rest after physical stress, and EPO.
Suppression of red blood cell production (low Retic) can be caused by; high Hgb, physical stress, and illness.
Special considerations:
Dehydration: Hgb looks higher than it really is.
Volume expansion: Hgb looks lower than it really is.
Normal Patterns:
Grand Tour: Hgb decreases despite decent Retic count although retic should trend down as well.
Altitude: A modest rise in Retic is followed by modest rise in Hgb, that should not overcome significant physical stress. Returning to lower altitude should cause a tapering off of Retic and Hgb.
Recovery from physical stress: Initially Hgb and Retic are low followed by a moderate rise in Retic and Hgb. The effect should be suppressed by significant physical stress.
Chronic stress: Low Hgb, low Retic, and poor performance.
Dehydration: Hgb is higher than expected, variable Retic, and performance is decreased.
Enhanced patterns
Epo: Look for a large rise in Retic followed by rise in Hgb, persistently elevated Retic despite high Hgb, and the effect is strong enough to overcome significant physical stress.
Sudden stop of EPO: High Hgb combined with a very low Retic. Retic should fall dramatically and precede a significant fall in Hgb.
Blood transfusion: High Hgb very low retic, maintenance of Hgb despite significant physical stress and low Retic.
Blood withdrawal: Low Hgb despite high retic without some other explanation for red cell destruction.
Masking:
Transfusion plus volume expansion: Very low Retic despite what looks like a low to normal Hgb without other cause for suppression.
EPO plus volume expansion: High retic normal HgB, and an effect that can overcome significant physical stress.
Transfussion plus EPO micro dose: High Hgb, low normal Retic, and an effect that can overcome significant physical stress.
Transfusion plus volume expansion with EPO micro dose: Low to normal Hgb, low normal retic, and an effect that can overcome significant physical stress..." - A Tale of Two Cyclists
Full Article HERE. Again, hopefully those of you who are credentialed with provide LC with your feedback.
Labels:
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Monday, February 23, 2009
Thursday, January 29, 2009
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