9:17 pm - Tue, Aug 26, 2014

videos in support of socks

9:09 pm

an article about saving brains

realy

and

truly

can be about saving babies brains

it’s ok

to just write about a topic

and

stay on topic

8:52 pm
3 notes

You pay more for organic

free range

hormone free

non-gmo

100% post consumer recycled

carbon off-set

would you pay more for

certified dope free

?

ie

companies willing to take an ethical stand

and not ride doper fame for all it’s damn worth

?

would you pay more

to give the ethical

guy/girl

a first chance in cracking through

in the sports industry

?

6:48 pm
@supcat: @chrisplummer that is, until I finally do the MGTHB sock for captain @veloclinic

Flock !

i need each and everyone of you personally

to pressure @supcat into making these

a reality

4:53 pm

Preview and Predictions 2014 Vuelta Climbs

The Vuelta Climbs by the numbers (as usual thanks to @ammattipyoraily and note that some of the numbers may be adjusted prior to the climb as he hunts down the best available climb data):

Across the board the Vuelta climbs are steep, mostly in the 7-10% range (note that for the climbs with a flat finish at the top this portion of the climb has been excluded for the analysis). The outlier climb is Stage 14 La Camperona at 15%.

The climbs are also relatively short mostly in the range of 4-800 vertical meters of climbing. The longest climb on tap is Stage 20 Puerto Ancares with over 1100 meters of climb.

Altitude ranges from the a 500 meter finish on Stage 18 Monte Castrove to just under 2000 meter on Stage 9 Valdelinares.

In general short steep climbs should diminish the effects of drafting and tactics so flat out efforts will be expected on most climbs.

Although the pVAM/DpVAM metrics are probably not entirely suited for the sub 20 minute climbs I used it nonetheless to get the basic gist of times and power outputs that can be expected.

In the blue is the VAM predicted from the 2008-2013 post-biopassport data set and in red is the prediction from the 2002-2007 doped data set. According the model, VAM is positively related to the natural log of gradient and negatively related to altitude and length of the climb. With the extreme range of climbs the model gives some fairly extreme predictions.

From the pVAM prediction its possible to project ascent times for the climbs. As you can see most of the climbs are below 20 minutes so take these predictions with grain of salt.

Lastly, with predicted times in hand the normalized power output expected can be calculated. Note the huge range of predictions here as short low altitude climbs will likely see big numbers well over 6 nW/kg. The longer or higher altitude climbs on Stages 9 and 20 will likely be in the 5.8-5.9 nW/kg range.

12:43 pm - Mon, Aug 25, 2014
1 note

Vuelta a Espana Climb Preview Preview

with 8 climbs to sort out the GC

(only 3 of which will take longer than 20 minutes)

and

a GC field deeper than the Tour

the Vuelta certainly has the potential

for some explosive finishes

what to expect

is

a GC battle

of

a thousand paper cuts

details and graphics to come

11:26 pm - Tue, Aug 19, 2014
Q: Re: MCV. You missed the point here. Dehydration (from alcohol) might cause changes in MCV (hyperosmolarity of plasma when fluid is lost, thus smaller red cells). EPO influence on MCV not discussed in the case.
Anonymous

right but follow along here for a bit

the heart of the case is the probability of doping given the ABP values estimated with Bayesian statistics.

for simplicity and because the actual ABP software is a bit of a black box consider walking through the argument in terms of Bayes theorem.

the probability of doping given the ABP results equals the prior probability of doping times the probability of the ABP results given doping divided by the probability of the ABP results.

P(doping/ABP) = P(doping)*P(ABP/doping) / P(ABP)

UKAD basically argued that the probability of doping was astronomically high because the probability of the results were astronomically low

^P(doping/ABP) = P(doping)*P(ABP/doping) / vP(ABP)

JTL’s side argued that dehydration was likely so the probability of the ABP results was actually high and therefore the probability of doping low

vP(doping/ABP) = P(doping)*P(ABP/doping) / ^P(ABP)

UKAD countered and said that since the MCV was normal then the probability of dehydration was so low as to be negligible

^P(doping/ABP) = P(doping)*P(ABP/doping) / vP(ABP)

the issue is that if you argue that MCV is good enough to rule out dehydration (which its not) then you can argue that its certainly good enough to rule out high dose EPO (which again it is not) AND since the results can not be explained by micro dose EPO then EPO can be ruled out all together.

that last part is a MAJOR issue for UKAD had JTL’s side been savvy enough to pick up on it. 

since the entire argument revolves around a Bayesian estimate of probability as soon as UKAD introduced evidence of a normal MCV and also insisted on no dehydration then this evidence must be used to update the Bayesian estimate. (I understand this is not how the legal system works as you seem to get to coast through if your opponent is weak but it is how stats/science/reality works)

so with this evidence (if its good enough for UKAD then its good enough for this blog for the sake of discussion) we can populate the equation with some numbers to see how ruling out EPO changes the probability.

UKAD calculated P(doping/ABP) at 99.9999%

a conservative estimate of the prior probability of doping p(doping) might be 15%

plugging these values in

.999999 = .15*P(ABP/doping) / P(ABP)

6.6666 = P(ABP/doping) / P(ABP)

in terms of oxygen vector doping EPO likely accounts for the majority of doping and we’ll use 65% here as a reasonable example

taking EPO out of the equation means that your prior probability of doping is no longer 15% but now 5.25%

ie

vP(doping/ABP) = vP(doping)*P(ABP/doping) / P(ABP)

or solving for the probability of doping given the values

P(doping/ABP) = .0525 * 6.6666

P(doping/ABP) = .350

probability of JTL doping = 35%

JTL not guilty

the values were more likely a lab or physiological anomaly

now this is a bit of an oversimplification but had JTL’s side picked up on the above then this case would likely not have played out as such a clear slam dunk decision

on the other hand

if UKAD had said fine there could be dehydration they could have then gone on to point out that the MCV must have come down from an elevated value making high dose EPO all the more likely given the extremely low retic and a still high for even a dehydrated state in season Hgb concentration 

for those wondering what MCV has to do with EPO

when EPO stimulates red cell production the new cells tend to be larger in size so that the mean corpuscular volume MCV tends to get elevated. after coming off of EPO the MCV drifts back down as the cells age. MCV has in the past been proposed as an indirect marker for EPO use. MCV can also be affected by blood storage conditions so could potentially have some utility in picking up transfusions as well.

12:40 pm
3 notes

looking for Open Source performance analysis software ?

check it out

10:31 pm - Mon, Aug 18, 2014
1 note

Southern Hemispherers can i get some retweets ?

We are currently recruiting participants for a performance modelling study.

Requirements for participation are that you race and train with a power meter.

Please contact Dr Jonathan Baker; jrb07@aber.ac.uk for more information.

10:04 pm

JTL biopassports experts botch the MCV detail

One of the points that the UKAD side used was that a normal MCV (mean corpuscular volume) was evidence against the presence of severe dehydration.

The issue is that taking enough EPO to get your Hgb to 17.9 should also have increased the MCV (young red blood cells are larger and shrink as they age and to still have a Hgb of 17.9 at a point in time when the MCV has normalized would imply that the peak Hgb would have been high enough to even impress Bjarne Riis). So it would be expected that had the mechanism been EPO use then a potentially normal MCV could be expected in a dehydrated state as the MCV was reduced from a drug elevated level.

Alternatively, to make the conclusion they did regarding dehydration, they would need to take the stance that the method was more likely blood transfusion than high dose EPO and that the amount of transfusion was several units. Remember that part of the reason high dose EPO raises Hgb concentration is due to a diuretic effect that does not occur with transfusion. So to get a 90s era Hgb would take more relative doping with blood transfusion than EPO.

Overall, dehydration seems plausible on top of a recent cycle of high dose EPO.

just thought that was interesting

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