How come "epo time" marathon times were weak?

two oh eight wrote:

EPO doesn't help with marathons, that's why mo can't run them

Lock him up!

Kid running after kipchoge wrote:

You are a very intelligent man. Don't you think there is a reason why the talents skip the track? Bekele talked about it, but I thought since people have more than one brain cell they might look for independently. In your case I was wrong. Well Bekele says that in his track time the Golden League was much more rewarding financially, than today's Diamond League. You dig? Or do I have to tell you as well What are the consequences of a less rewarding track?

Haven't you just answered your own question? There are possibly (according to the 'epo era' hypothesis) two, completely independent factors going on here.

According to the epo era hypothesis:

1. EPO testing in the mid 2000s has resulted in slower times, generally speaking (though there can be exceptions - see #2, below):

2. The huge increase in marathon prize money and - at the same time - reduction in track payouts has resulted in more runners gravitating to the marathon, reducing times in that event.

(I'd add a point 3. Training philosophies have changed significantly; coaches are much less concerned now with a 'develop speed first' mentality, especially w.r.t. the marathon)

One hypothetical we can draw from this is that marathon WRs and the all-time lists could possibly be even faster than they currently are if marathon payouts were as great in e.g. 1995 as they are now (relative to track times).

They're still on EPO, the courses just got faster and they got better at hiding their dope.

Aragon wrote:

if arterial oxygen content is higher

false premise. Why would having more rbc's raise oxygen content in the arteries if the muscles aren't using more oxygen?

Some possible reasons why marathoners are caught on epo

1) they erroneously think it works, just like everyone else

2) it might reduce risk of HVT-induced anemia

Bad Wigins wrote:[/b

Some possible reasons why marathoners are caught on epo

1) they erroneously think it works, just like everyone else

2) it might reduce risk of HVT-induced anemia

0/10 👎

The real speedsters weren't running thons yet. That changed with Tergat and Geb.

Interesting... wrote:

Rocket Fuel Rick wrote:

Sumgong didn't think so. 😉

Sumgong couldn't even break 2:20 with EPO.

Funny, because without EPO Sumgong couldn't break 2:30.

I'm no expert, but here's a theory:

Maybe marathoners can't safely take as much EPO as track athletes. EPO increases red blood cell count, making the blood thicker. This increases the risk of clots developing, which can be fatal.

In the marathon, athletes become much more dehydrated than in the shorter distances. This decreases the water content of the blood, making it thicker. Since marathoners on EPO already have thicker blood to begin with, the increased thickness due to dehydration may be excessively dangerous unless dosages are kept reasonably low.

Take for example Bekele's first fiance, who died during a training run, or some Kenyan marathoner (I don't remember the name) who died during a marathon. Both were likely on EPO, and both were likely dehydrated.

While lower dosages may be safer, they do not enhance performance as much as higher dosages. As a result, marathoners have not seen the same improvements from EPO that runners at shorter distances have.

If someone is an expert, please tell me if I'm wrong on this.

Interesting... wrote:

Sumgong couldn't even break 2:20 with EPO.

C'mon man!...some of you are so obtuse on this issue! Alright then...you want someone using rocket fuel who broke 2:20? Fine...Rita Jeptoo ran *2:19:57* in 2013 and tested postitive for EPO in 2014. Are you satisfied now? She also had quite an improvement from her early times a few years before sub-2:20. Just use some common sense & logic on this issue (which they don't teach anymore in school 😁).

How often do elite Kenyan and Ethiopian marathoners get tested?

Here a possible explanation for the "false premise".

Intraindividual hemoglobin concentration is relatively constant between rest and exercise conditions (it increases slightly during exercise whereas saturation decreases). This is because hemoglobin saturates very easily in lungs, so it follows that cardiac output is the mechanism how body regulates the oxygen flow to the working muscles.

If you want scientific proof, take a look on the rEPO and "blood doping"-literature and look how heart rate reacts to elevated hematocrit during given submaximal workloads. It falls in practically always when it is measured because oxygen demand is met with lower blood flow.

This was confirmed already during WW2 when a group of naval volunteers reveiced 1000ml of RBCs and their mean hematocrit was elevated from 46 % to 58 % and correspondinly the submaximal heart rate fell from 110 to 100 during 4 MPH treadmill test.

kikKomen Soi sauce wrote:

I'm no expert, but here's a theory:

Maybe marathoners can't safely take as much EPO as track athletes. EPO increases red blood cell count, making the blood thicker. This increases the risk of clots developing, which can be fatal.

In the marathon, athletes become much more dehydrated than in the shorter distances. This decreases the water content of the blood, making it thicker. Since marathoners on EPO already have thicker blood to begin with, the increased thickness due to dehydration may be excessively dangerous unless dosages are kept reasonably low.

⤴but it does help them to run 3, 5, 10 and 21.1k faster.

Take for example Bekele's first fiance, who died during a training run, or some Kenyan marathoner (I don't remember the name) who died during a marathon. Both were likely on EPO, and both were likely dehydrated.

⤴Some athletes were caught out when CERA came on the market, idiots didn’t realize that it was designed to be used less frequently than past versions of EPO. I know a TdF cyclist that mysteriously was rushed home with a "ripped apart heart" later investigations exposed his team for doing cocktails including CERA apparently as a younger guy in the team he tried impressing his superiors by taking copious amounts of everything, it nearly killed him. A few years later he recovered and won an Olympic medal. He never failed a standard drug test.

➡Apparently, Waldemar Cierpinski used blood doping to win two Olympic Marathons and he almost had as little running talent as me. 😉

Don't you think a marathon time of 2:03-2:04 is more or less equivalent to the fast track times of late 90's early 2000's

Bad Wigins wrote:

epo doesn't help marathon. Why would it? It's a relative jog and nowhere near stressful aerobically.

True dat. I'm just average runner and went 3:10 on a pack of Newports and a Martini per day, So VO2 Max is not an issue. Oh yeah - 12 minutes for the last 2 miles.

Subway Surfers Addiction wrote:

Interesting... wrote:

Sumgong couldn't even break 2:20 with EPO.

Funny, because without EPO Sumgong couldn't break 2:30.

The Rio course was some 5 minutes slower than Berlin, Sumgong's 2:24.04 was really closer to 2:19. Where's Calculo when you actually need him? ☺

Subway Surfers Addiction wrote:

Subway Surfers Addiction wrote:

Funny, because without EPO Sumgong couldn't break 2:30.

The Rio course was some 5 minutes slower than Berlin, Sumgong's 2:24.04 was really closer to 2:19. Where's Calculo when you actually need him? ☺

Exactly. Jared Ward was in 2:06 shape on a faster course. Without the rain he might even have gone 2:04 on that day.

Subway Surfers Addiction wrote:

Where's Calculo when you actually need him? ☺

He's on that Mo thread explaining through his totalitarian science how Mo should be running a 3:25 1500 WR. 😅

If never, then when? wrote:

How often do elite Kenyan and Ethiopian marathoners get tested?

That's like asking how often do NBA players get tested for Marijuana....😅

Aragon wrote:

Here a possible explanation for the "false premise".

Intraindividual hemoglobin concentration is relatively constant between rest and exercise conditions (it increases slightly during exercise whereas saturation decreases). This is because hemoglobin saturates very easily in lungs, so it follows that cardiac output is the mechanism how body regulates the oxygen flow to the working muscles.

If you want scientific proof, take a look on the rEPO and "blood doping"-literature and look how heart rate reacts to elevated hematocrit during given submaximal workloads. It falls in practically always when it is measured because oxygen demand is met with lower blood flow.

This was confirmed already during WW2 when a group of naval volunteers reveiced 1000ml of RBCs and their mean hematocrit was elevated from 46 % to 58 % and correspondinly the submaximal heart rate fell from 110 to 100 during 4 MPH treadmill test.

So an increase in RBCs of 26% yielded an decrease in heart rate of just 5%?

I think Bad Wigins is making good point. One that phsyiologists seem afraid to confront.

Don't forget, their funding relies on agreeing that EPO increases oxygen delivery, and if they disagree, bye bye funding, credibility and career.

It's a bit like the statins prevent cardivascuar disease issue, Doctors are obliged to go along with it. Fortunately a lot of Doctors in the last few years are saying no to this diktat.