Armstrongs pedalling

consider this statement by a scientist regarding Lance Armstrongs muscle type a pedalling cadence:

"One way is to train for higher maximum capacity—in other words, to increase the upper limit of performance (as a sprinter might). Another way is to train for greater submaximal capacity—to expend less energy for sustained performance (as a marathoner might).

Armstrong did both.

“We don’t know exactly what accounted for Armstrong’s muscular-efficiency change,” Coyle said. But he suspects that Armstrong was able to convert fast-twitch muscle fibers to slow-twitch muscle fibers.

While fast-twitch fibers are good for sprinting, for example, slow-twitch muscle fibers are twice as efficient and are good for endurance sports.

With more slow-twitch muscle fibers, and increased muscle power, Armstrong is able to move his legs faster. As a result, his pedaling rate has gone up from 85 revolutions per minute to 105."

how would Armstrong be able to move his legs faster with more slow twitch fibres? would his legs move slower, but for longer with slow twitch? or is pedalling not really comparable to sprinting in using ur muscle type?

or am i missing the point completely?

Fast twitch has very little to do with how fast the muscle can move (in the sense you are talking about)! It is to do with the fatigue characteristic and the amount of force the muscle fibre can output. Anyone can pedle at 105rpm (just as anyone can move thier legs at 5 cycles a second while lying on thier back) but being able to do it over a long period of time against resistances requires slow twitch muscle fibres. Fast twitch fibres can also do this but they will fatigue faster of after a few minutes the rpm would drop off.

If you wanted to maintain say 160rpm (i don’t know if this is possible its just an example) for 30s up a hill (against resistance) then you would want fast twitch fibres because more force is needed and hence a shorter duration is possible.

This is a very simplified answer, do a search on the internet for more info on FT vs ST fibres or pick up a copy of Supertraining or pretty much any physiology text book.


I would focus on the above,quite dense statement to start with -although I am not sure about the fast/slow fibres definition here, and in reality it is more complex than this anyway-but I think this is an extremely interesting perspective:well worth discussing.

Armstrong changed his technique to pedal at a higher RPM as his physical trainer decided that would suit his physical makeup better - Armstrongs strength is his cardiovascular capacity, so the thinking behind his coaches idea was that pedalling at a higher RPM with a lower resistance ( larger rear cog) would stress his cardiovascular system more than his muscular system - he thinks that pedalling with a lower RPM with a higher resistance (smaller rear cog) is more “muscular work”,

I agree. Lower RPM, requiring more power, is likely to use white fibre more.

His trainer, Michele Ferrari studied with Conconi, the guy who discovered the anaerobic threshold. Armstrongs training is based on trying to achieve as high power output as possible, at anaerobic threshold, at a lower body weight as possible.

His magic number is 7.0 watts/kg. If a cyclist can achieve this Ferrari believes there are in shape to win the Tour.

I am also convinced that high power outputs at low heart rates/lactate levels is the key for success in power endurance events,and where I was hoping this discussion was heading to,since most of the people usually concentrate on only one side of the equation (either training pure power or pure cardiovascular/metabolic factors as the limits of performance),failing to consider and indagate the whole,more complex scenario…

try this one on for size:

“however, the most unique aspect of this individual’s blood lactate profile was the extremely low lactate concentration measure 4 min after exhaustion during measurement of Vo2max. Maximal blood lactate in the trained state was only 6.5-7.5mM in the present subject. By comparison, all the competitive cyclists we have tested, including team mates training with this subject, possessed maximal blood lactate postexercise in the range of 9-14mM. The mechanism for this extremely low maximal blood lactate concentration in this individual is not clear, although it probably reflects reduced lactate production when exercising to exhaustion at intensities above V02max. One possibility is that activity of the muscle enzymes largely responsible for lactate production are greatly attenuated in this individual when he is trained.”

Mr. Armstrong dont like producing lactate at high power.

More infor on this from the BASES conference by Nickoluski and myself at the bottom of this thread:

Just a couple of points on the above posts:
I am not sure about the statement of Conconi discovering the “anaerobic threshold” and moreover, I don’t really like his methods (i.e., HR deflection point).

Secondly, really low maximum blood lactate values are also observed in well-trained endurance runners (as low as 7.3mmol.l-1 for a 2:20 marathon runner, let alone his steady state run of 18.5km.h-1 at 1.99mmol.l-1); but this does not necessarily mean that these guys are not capable of producing much lactate, but rather that their ability to clear such products from their blood is superior to others. I reckon the same is true for Armstrong, too!

True, I should have said a lot of research into the anaerobic threshold

“Historically, differences in blood lactate accumulation have been ascribed to differences in muscle lactate production. However, tracer studies of lactate kinetics have highlighted the importance of lactate removal (28, 45) and the importance of lactate as a metabolic substrate in the active and nonactive muscles (4, 46). It is with respect to lactate oxidation that oxidative enzyme activity may be relevant. Endurance training appears to increase the relative contribution of lactate removal (as opposed to lactate production) to the delaying of lactate accumulation (28). Although it has been shown that the plasma lactate in a group of trained individuals is related to oxidative enzyme activity (42, 43), we have no data relating the lactate removal directly to oxidative enzyme capacity. Thus one can only speculate that, in this study, the higher oxidative capacity may be related to plasma lactate concentration via both a reduction in lactate production and an enhancement of lactate removal. The latter is likely to be related to capillarization or lactate transporter density or both. The relationship between the onset of blood lactate accumulation and muscle capillarity has been shown by Tesch et al. (48), and the relationship between the lactate transporter, monocarboxylate transporter 1, and lactate uptake has been shown by McCullagh et al. (30). Regarding possible differences in lactate production, it is unlikely in this study to be due to differences in fiber type because the African athletes had a higher type II fiber percentage than did the Caucasian runners”.

I have posted the same link in another thread, too, but the above paragraph relates directly to the discussion and possible explanations of Armstrong’s and the likes supremacy…
As you can see from the link, this isn’t the only reason, of course; in fact, the whole issue remains unclear.
Please, feel free to comment and provide any further links/information you may have on the subject!