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Ryder's blood

Mar 4, 2010
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Given to @captainbag1 by JV.

Nov 14, 2011:
Hb: 16.0
Hct: 44.9
Retic: 1.93

Jan 17, 2012:
Hb: 16.1
Hct: 46.9
Retic: 1.66

Feb 29, 2012
Hb: 14.6
Hct: 42.1
Retic: 1.13

May 3, 2012
Hb: 16.0
Hct: 46.0
Retic: 1.76

May 14, 2012
Hb: 14.1
Hct: 42.3
Retic: 1.56

May 17, 2012 AM
Hb: 14.1
Hct: 43.4
Retic: 1.34

May 17, 2012 PM
Hb: 14.1
Hct: 43.4
Retic 1.71

May 18, 2012
Hb:14.4
Hct: 42.6
Retic: 1.74

http://captaintbag.tumblr.com/post/31367299894/expert-analysis-ryder-hesjedal-2012-giro-blood

I'd like to thank Ryder and JV for being more transparent than 99.9% of the rest of the bunch.
 

the big ring

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Jul 28, 2009
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Still waiting to get a copy of the full ABP paper, but March / April 2012 is 2 months with no tests. Handy.
 
Mar 4, 2010
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may 3rd hgb 16.0

or hgb just before giro start

nearly equals his season high 16.1

not normal

(at this point in the season , yuh’d expect some volume expansion and a lower hgb)

explanations

a. Altitude camp ?

vaughters says no

b. lab error

vaughters says yes


hct at giro start was high across the board

so did the lab screw up ?

ie not good

or was the entire peloton doped ?

hehe

also not good

Wasn't that also the explanation for Brad's Hb peaking in the 3rd week of the 2009 TdF?

during the giro hgb drops from 16 to 14.1

or 11.8% down

remeber 11.5% down is expected based on published lit

again normal

lowest retic is is 1.13 feb 29

or 0.47 below the baseline

retic below 0.7/0.5 threshold or down 0.3/0.5 from baseline

is evidence uv blood transfusion/comming off epo

so 1.13 is unusually low fer ryder

but hgb 14.6

is not elevated

so transfusion or comming off is epo not likely

was he sick ?

vaughters says yes

so low hgb and retic

is consistent with viral suppression

call it normal

Astute observations by the captain on twitter:

@Ben_M_Berry problem is yuh start explainin stuff then you create bigger problems, ex if the16 ain't real then yuh lose the nice hgb decline

@Ben_M_Berry or if yuh toss out the 1.13 retic then yer giro retic is .2 lower than pre giro n yer 16 becomes that much more suspect
 

the big ring

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(Analysis machine error)

Tyler'sTwin said:
Wasn't that also the explanation for Brad's Hb peaking in the 3rd week of the 2009 TdF?

Reality distortion field fits the bill: http://en.wikipedia.org/wiki/Steve_Jobs#Reality_distortion_field

The RDF was said by Andy Hertzfeld to be Steve Jobs's ability to convince himself and others to believe almost anything, using a mix of charm, charisma, bravado, hyperbole, marketing, appeasement, and persistence. Although the subject of criticism, Jobs's so-called reality distortion field was also recognized as creating a sense that the impossible was possible. Once the term became widely known, it was often used in the technology press to describe Jobs's sway over the public, particularly regarding new product announcements.[125][126]

To wit: you can win a GT clean.
 

the big ring

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Ferminal said:
He was racing pretty consistently in those months (just 2 weeks off early March), not a lot of time to **** off to an island and get juiced up.

2 weeks off is still handy. No ABP tests at all for 2 months is even handier. Looking at his Romandie results, he finished 14 minutes down on stage 4 and did not start the TT.

Was he sick?
 
I would expect everybody to have higher hb values right before the giro compared to the latter stages of the race. The reason is that people are well rested and the hb values would increase.

To my understanding, the sensible thing to do would be to train hard, then a week before the Giro take it very easy and gather strength. Hence the HB values increase. I don't see anything fishy here.

But perhaps Ryder does it differently and hence shouldn't have had such an hb increase. Hence JV thinks there is measurement error.

Who knows. Anyway Ryder Hesjedal has Norwegian blood, and Norwegian blood can't be doped.:D
 
Jun 26, 2012
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Yes, but you would expect a linear drop and not like in Ryder's case, where there is sudden drop in first week and then it remains the same throughout the Giro.

Also, results from 17th May should be 27th May (last day of Giro).
 
Don't know why that blog doesn't just write properly or have someone else do it if he's dyslexic or something. Very hard to keep track of.

Anyway, nice to see some values, but this doesn't prove much either way. Giro values drop is expected but sudden.

Maybe JV will come back and have a talk?
 
the big ring said:
2 weeks off is still handy. No ABP tests at all for 2 months is even handier. Looking at his Romandie results, he finished 14 minutes down on stage 4 and did not start the TT.

Was he sick?

I'm not sure, but it's not abnormal to be average at Romandie and win the Giro (Menchov, Basso). Get a bit of racing in your legs but don't overdo it, then have a week off to finalise preparation.

The real work in preparing for the Giro is probably December - March. If you know you're getting ABP'ed no more than once a month... Two months November - January, then 5 weeks after the TDU before the February test.
 
luckyboy said:
Don't know why that blog doesn't just write properly or have someone else do it if he's dyslexic or something. Very hard to keep track of.

Anyway, nice to see some values, but this doesn't prove much either way. Giro values drop is expected but sudden.

Maybe JV will come back and have a talk?
That's his shtick. Pirate speech meets stream of consciousness. He actually toned it down a fair bit for this piece.

I agree we can't reach any conclusions from his file alone, but maybe if more riders released their data we would have more to base our judgment on.
 
Oct 16, 2010
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luckyboy said:
Wasn't there another set of values that JV mentioned there was a lab error recently?

If it was a lab error then that's disturbing. If it wasn't then its disturbing for a different reason.
+1

originally posted by Cathwoorg:
That one point at the start of the Giro looks very much like a lab error.
If I were analysing that data set, I'd be throwing that point out.
could you explain why? (nb: I'm an absolute layman, so I'll accept anything for an answer)
 
Its a sudden change in one value, without a change in Ret%, that immediately reverts with the next data point.

Obviously JV commented that other riders were high (I haven't seen that data so I'll happily accept his word on this), so there is a pattern supporting the supposition.



In my lab, if some brought a similar plot looking at a parameter over time (say the course of a product run) with that sort of spike, I'd ask for a recheck. If that came back so high, I'd except a standard to be run as a verification. If that came back normal I'd probably get the suspect sample run again (a 3rd time, now including a known result showing normal in the middle).

Only then would I really be comfortable releasing the data with a point so high.


Now of course this is with the benefit of hindsight and looking at a longitudinal profile of measurements read over the course of several months.


Taken in isolation the reading is within the expected results for athletes as a population, and as the testing is done blind, the lab cannot know what result is typical for the individual so they cannot really do the above procedure.

The best way to handle it is to discount the data point in discussion.

Compare and contrast to the 2009-10 Lance data that was on here a few weeks ago. Odd Hb results also showed a change in ret%, the pattern was consistent with blood withdrawal and reintroduction, and there were multiple deviations from the baseline (above and below) because of that.
 
Here is a decent primer on some of the variations in Hb by different labs and deceives (and variations due to sample site, and other patient variables as well).

Now I would expect a WADA accredited lab to be better than the labs in that paper (and I'm not up on the protocol, but would also assume they have some sort of verification standard that should be run before the samples), but people should be a little more educated generally about stats and variability of testing, when discussing something like a BP profile.
 
Conclusions? It's not obvious he doped. Further than that, like every good conclusion, we are left with "more research is needed."

More traimning in analysis would be useful. I know what should be expected, as far as ups and downs, but how values should get there is beyond me
 
Oct 29, 2009
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May 14, 2012
Hb: 14.1
Hct: 42.3
Retic: 1.56

May 18, 2012
Hb:14.4
Hct: 42.6
Retic: 1.74

May 27, 2012 AM
Hb: 14.1
Hct: 43.4
Retic: 1.34

May 27, 2012 PM
Hb: 14.1
Hct: 43.4
Retic 1.71


as nogav1ca already mentioned

how is it possible that his hemoglobin and hematocrit levels didn't drop in the last 2 weeks of the Giro :rolleyes:
 

the big ring

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MajorTom said:
May 14, 2012
Hb: 14.1
Hct: 42.3
Retic: 1.56

May 18, 2012
Hb:14.4
Hct: 42.6
Retic: 1.74

May 27, 2012 AM
Hb: 14.1
Hct: 43.4
Retic: 1.34

May 27, 2012 PM
Hb: 14.1
Hct: 43.4
Retic 1.71


as nogav1ca already mentioned

how is it possible that his hemoglobin and hematocrit levels didn't drop in the last 2 weeks of the Giro :rolleyes:

Reticulytes (baby blood cells nawwwwww) are yo-yoing too. We probably need to map the values against rest days?
 
Oct 29, 2009
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Benotti69 said:
microdoping ;)
yeah, this seems to be the only logical answer


AS: Once the Biological Passport program started, this type of masking was no longer sufficient. Let’s get into reticulocytes and their role in the Bio Passport.

MA: Well, here I’d like to once again acknowledge Floyd Landis for enhancing my understanding of what and how pro riders dope. It was Floyd who told me how they had access to a transportable blood analyser that followed them around and allowed the riders to constantly monitor their reticulocyte levels. Whereas I’d anticipated some degree of self-monitoring, it had actually entered the peloton many years before I had ever imagined! So by the time the Passport came around in 2007-8, there was a lot of accrued knowledge about how to manipulate reticulocyte levels.

The way I look at this is to split masking into two separate activities, one for haemoglobin and one for reticulocytes. Just to clarify those two terms for your readers, nowadays in the antidoping realm, haematocrit has been replaced by haemoglobin because it can be measured more reliably. Haemoglobin itself is the protein bound up inside the red cell which carries the oxygen molecules, so just like haematocrit the haemoglobin value reflects the amount of red cells in circulation. And in order to explain reticulocytes, its necessary to appreciate that when red blood cells are first released from the bone marrow they are not fully mature, and so for the first 24 hours or so they are termed reticulocytes but then transition into mature red cells.

Those differences are quite subtle, but they are very important to antidoping because the number of reticulocytes provides a very good insight into how active the bone marrow has been during the previous 24 hour period. To put it simply, when you stimulate the bone marrow you find more reticulocytes, and when the bone marrow is less active you find fewer reticulocytes in the bloodstream.

Injecting EPO will stimulate the bone marrow, and thus a tell-tale signature of EPO use are higher than normal reticulocyte levels. Conversely, when you stop EPO injections the body will recognise that there are too many red cells in circulation, and responds to this excess by suppressing bone marrow activity and thus you find fewer reticulocytes. If you can grasp that concept, its pretty easy to extend that out to what you would expect to find associated with blood transfusions. Initially, when the blood is withdrawn for storage, the body recognises that the red cells have been depleted and thus stimulates the bone marrow to produce more and to replenish what has been taken out, and so as a consequence reticulocyte levels go up. When the blood is eventually reinfused, the body recognises the excess of red cells and suppresses bone marrow activity, thus causing a decrease in reticulocyte levels.

Because the Passport looks at haemoglobin levels and reticulocytes, it becomes necessary to mask both. You need different strategies to mask them. So for example, whereas flooding the circulation with plasma will hide an excess of red cells, this has no effect whatsoever on reticulocytes because they are measured as a percentage which is therefore immune to changes in concentration. Instead, their levels are dictated by bone marrow activity, which is driven by erythropoietin levels in the bloodstream. When you withdraw blood, the body responds by increasing erythropoietin which causes the reticulocyte levels to spike up. When you reinfuse blood, the erythropoietin levels decrease and after some days lag the reticulocyte levels drop.

So the mobile lab which Floyd described was only one part of the puzzle. Its not enough to know that your reticulocytes have dropped suspiciously, you must be able to do something about it or else risk being flagged by the Passport. And whereas the intervention for red cells is plasma, the intervention for reticulocytes is microdoses of EPO. Those injections are carefully timed and titrated to ensure that the reticulocyte levels are neither too high nor too low.

Whereas this might sound a bit daunting to a novice, in fact it is relatively simple for someone with access to a blood analyser and the freedom to experiment with different microdosages to acquire the knowledge to sustain a masking protocol. But the tricky bit comes when you try and replicate the rider’s ‘natural’ level. Its one thing to avoid high peaks and low troughs, but something entirely different to tweak it just right that you replicate your natural level.

That’s an Achilles Heel that us experts have utilised when reviewing blood passports. There are tell-tale signatures that we’ve come to suspect are caused by microdose regimens. Please don’t expect me to reveal what they are, because I’d like to think that one day that information can be used strategically. However in the meantime it’s frustrating because we see a suspicious signature, but its not easy to persuade authorities to prosecute an athlete when there are no peaks and troughs!


http://nyvelocity.com/content/interviews/2012/behind-scenes-contador-cas-hearing-michael-ashenden


however, I would like to hear JV or anyone else if there is any other logical explanation. Thank you :)
 
Mar 4, 2010
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Catwhoorg said:
That one point at the start of the Giro looks very much like a lab error.

If I were analysing that data set, I'd be throwing that point out.

It's well-known that retics can be manipulated and Hb falls during a GT due to plasma expansion, doping before a GT would not change that. When you see GT-profiles like LA's, Floyd's and The Chicken's, it's because they received refills during the race. The expected fall in Hb due to plasma expansion was offset by an increase in Hb mass.

MajorTom said:
May 14, 2012
Hb: 14.1
Hct: 42.3
Retic: 1.56

May 18, 2012
Hb:14.4
Hct: 42.6
Retic: 1.74

May 27, 2012 AM
Hb: 14.1
Hct: 43.4
Retic: 1.34

May 27, 2012 PM
Hb: 14.1
Hct: 43.4
Retic 1.71


as nogav1ca already mentioned

how is it possible that his hemoglobin and hematocrit levels didn't drop in the last 2 weeks of the Giro :rolleyes:

Because he maxed out on plasma expansion after 11 days (may 3rd - 14th) at the Giro? The drop is certainly large enough.