How vo2 max relates to fitness

Thank you once again for the new information which clarifies many items. I don't think I am the only one whose knowledge is based mostly on articles by Ross Tucker (sportscientist) and on views of Mike Ashenden (mainly JAP-letters + interviews) which leave easily the impression that the DE equations were wrong and that Coyle just didn't want to share his data. In the end it is unfortunate that Ed Coyle ended up almost accidentally into the wrong camp in the Armstrong-saga if he sparked this interest into the cycling efficiency issue and many of his ideas turned out to be true. While I follow the literature very unsystematically, I can even recall Norwegian scientists observing quite recently that there is a relative increase in type IIa fibres vs. type IIb in endurance cyclists after resistance training, when the fibre type "switch" was one "never observed" item when he speculated about it in the Armstrong-paper.

Andrew Coggan wrote:

Obviously Walsh/Lemons/Vie Diemen (who?) didn't understand the meaning of the term "mechanical efficiency". It isn't automatically linked to bio*mechanics* - in fact, Ed's hypothesis (since supported by additional studies by others) was/is that improvements in cycling economy/efficiency with training are due to bio*chemical* adaptations.

Yes, of course LeMond and Walsh are debunking the efficiency issue with an unintentional straw man-argument because they are clearly talking about different thing. The same confusion of seeing efficiency as a "skill" is evident when e.g. people presume that Paula Radcliffe had very inefficient running economy because his style looked quite "ugly" or Lasse Viren had a great one because his form was so smooth (It has been alleged that Soviet scientist even calculated in the 1970s from his body movements that his running his technique was the most economical in the world).

Andrew Coggan wrote:

it's genetic wrote:

It's relevant to Starling's law though isn't it?

Non-sequitur.

No, it's not. Cardiac function is maintained in a healthy heart regardless of fitness. Your hypothesis is flawed.

Andrew Coggan wrote:

Aragon wrote:

Here is the actual quote from Walsh's book From Lance to Landis (pp. 183-184) about LeMond listening to one Ed Coyle lecture in 2001:

Obviously Walsh/Lemons/Vie Diemen (who?) didn't understand the meaning of the term "mechanical efficiency". It isn't automatically linked to bio*mechanics* - in fact, Ed's hypothesis (since supported by additional studies by others) was/is that improvements in cycling economy/efficiency with training are due to bio*chemical* adaptations.

Biochemical adaptions? Such as?

Improved biomechanical efficiency comes from increases in muscle tension of the agonists and relaxation in the antagonists. So more power output is generated for the same bioenergetic output or blood lactate measurement.

But the good new is, I like your table:

https://www.cyclinganalytics.com/blog/2012/06/watts-kg-on-the-power-curve

I see a lot of numbers that are obviously wrongly calibrated with numbers much higher than those.

it's genetic wrote:

Andrew Coggan wrote:

Obviously Walsh/Lemons/Vie Diemen (who?) didn't understand the meaning of the term "mechanical efficiency". It isn't automatically linked to bio*mechanics* - in fact, Ed's hypothesis (since supported by additional studies by others) was/is that improvements in cycling economy/efficiency with training are due to bio*chemical* adaptations.

Biochemical adaptions? Such as?

Improved biomechanical efficiency comes from increases in muscle tension of the agonists and relaxation in the antagonists. So more power output is generated for the same bioenergetic output or blood lactate measurement.

Increased muscle tension requires MORE energy, which is supplied by a heart and circulatory system . which has adapted to the increased demand.

Often aided by EPO.

No, muscle tension is controlled by the nervous system. If you're not interested in the subject, don't post here.

it's genetic wrote:

No, muscle tension is controlled by the nervous system. If you're not interested in the subject, don't post here.

Still need the energy to make it all work. Try to keep up.

it's genetic wrote:

Biochemical adaptions? Such as?

Ed's hypothesis was/is changes in myosin expression.

Others have shown changes in UCP3 as a result of endurance exercise training.

Separately, it has been shown that enhancing nitric oxide availability (via dietary nitrate supplementation) can reduce the O2 cost of exercise, at least in some individuals/populations. Since training enhances NO production, this could be yet another mechanism.

The bottom line is that although cycling efficiency/economy is rather constrained, it isn't completely immutable, as some "hobby jogger" sports scientists have mistakenly claimed.

Aragon wrote:

Thank you once again for the new information which clarifies many items. I don't think I am the only one whose knowledge is based mostly on articles by Ross Tucker (sportscientist) and on views of Mike Ashenden (mainly JAP-letters + interviews) which leave easily the impression that the DE equations were wrong and that Coyle just didn't want to share his data.

That is unfortunate, because they really aren't the people you should be listening to.

Aragon wrote: I can even recall Norwegian scientists observing quite recently that there is a relative increase in type IIa fibres vs. type IIb in endurance cyclists after resistance training, when the fibre type "switch" was one "never observed" item when he speculated about it in the Armstrong-paper.

I think you may have misinterpreted/misunderstood something, or else those Norwegian scientists are literally out in the cold. It has long been known that endurance training results in rapid replacement of type IIb fibers (now called type IIx, since that is the myosin isoform that they express) with type IIa fibers. In fact, back in the 1970s Dave Costill doubted whether type IIb fibers actually existed, because he observed them so rarely in the highly endurance-trained individuals (e.g., Frank Shorter) he was biopsying at the time. (Most endurance athletes - even "hobby joggers" - have

it's genetic wrote:

No, it's not. Cardiac function is maintained in a healthy heart regardless of fitness. Your hypothesis is flawed.

It is not a hypothesis, but an established fact: maximal cardiac output increases with endurance training.

Andrew Coggan wrote:

it's genetic wrote:

No, it's not. Cardiac function is maintained in a healthy heart regardless of fitness. Your hypothesis is flawed.

It is not a hypothesis, but an established fact: maximal cardiac output increases with endurance training.

Absolutely! High-intensity aerobic training signficantly increases maximal cardiac output which improves stroke volume, circulation, metabolism, etc. IIRC, only maximum heart rate is influenced by genetics.

I'm an old cat (59) who can't run as much as I did in my younger days due to OA and other chronic pathologies, but I get my HIIT in a couple of times per week; one at the running track and one on the spin bike. Blood pressure is normal, circulation is excellent and I have a RHR of 48 - all compliments of endurance training.

arguing with real physiologists from a shelf stocker perspective wrote:

it's genetic wrote:

Biochemical adaptions? Such as?

Improved biomechanical efficiency comes from increases in muscle tension of the agonists and relaxation in the antagonists. So more power output is generated for the same bioenergetic output or blood lactate measurement.

Increased muscle tension requires MORE energy, which is supplied by a heart and circulatory system . which has adapted to the increased demand.

Often aided by EPO.

Energy is not supplied by the heart or the circulatory system.

Can we leave rhEPO out of this? It only muddies the water more.

Luv2Run wrote:

arguing with real physiologists from a shelf stocker perspective wrote:

Increased muscle tension requires MORE energy, which is supplied by a heart and circulatory system . which has adapted to the increased demand.

Often aided by EPO.

Energy is not supplied by the heart or the circulatory system.

Can we leave rhEPO out of this? It only muddies the water more.

Sure it is. How do you think food gets into your muscles, teleportation?

pumping gas wrote:

Sure it is. How do you think food gets into your muscles, teleportation?

I assume that luv2run's point is that food (metabolic fuels) aren't energy per se - just a potential source of energy.

When you say endurance training results in rapid replacement of IIx with IIa, how would you define endurance training? Once the IIx have been replaced does it take a significant period of bedrest or time in space for the IIa to be replaced with IIx again?

I’m thinking of how I’ve done a few easy endurance rides in the socal mountains with Jamie Staff and wonder would that sort of ride, lasting about 3 hours, be enough to convert some of his IIx fibers to IIa?

Essentially once a IIx is replaced with IIa is that effectively the last you’ll see of the IIx fiber? It’s as if the IIa fiber is an invasive species the IIx can’t compete with and by the time we are in old age the IIx fibers are all gone. Or maybe they start coming back if we are laid up in a bed unable to move?

Aragon wrote:

The training-induced increase in cardiac output as a key factor in Vo2Max increase has been established since the 1960s, here is a chart from the1968 Dallas bed rest study for instance (Saltin et al):

https://wol-prod-cdn.literatumonline.com/cms/attachment/156e1c1c-16cf-4d65-9d69-ff281cc6c2b2/sms12597-fig-0001-m.jpg

For grins-and-giggles, I thought that I would try to track down the earliest study definitively demonstrating an increase in maximal cardiac output with training. By "definitive", I looked specifically looked for longitudinal, not cross-sectional, data, and for studies in which maximal cardiac output was directly measured (rather than, e.g., inferred from submaximal measurements, or chest X-rays of athletes, which have been around for >100 y). Somewhat to my surprise, I couldn't chase things back any further than 50 y ago, as you did:

Interestingly, in doing this research I came across several longitudinal studies from the 1940s (from the Harvard Fatigue Lab and also by Sid Robinson at Indiana University) clearly demonstrating an increase in exercise economy with training. Thus, I remain baffled as to how the notion that this was immutable arose.

It is unclear whether the sort of endurance training that a sprint track cyclist typically does would be sufficient to result in conversion of all type IIx fibers into type IIa.

On the one hand, even the greater habitual physical activity of Europeans vs. Americans seems to be enough to convert at least some IIx into IIa. I say that because although the typical fiber type distribution of untrained subjects in studies here in the US is ~50% type I, ~25% type IIa, ~25% type IIx, in studies from Europe it is usually more along the lines of ~50% type I, ~33.3% type IIa, ~16.7% type IIx.

On the other hand, this study:

Mackova E, Melichna J, Havlickova L, Placheta Z, Blahova D, Semiginovsky B. Skeletal muscle characteristics of sprint cyclists and nonathletes. Int J Sports Med 1986; 7:295-297.

that the sprint cyclists were 58% type I, 20% type IIa, and 22% type IIx.

In any case, a fiber's "type" is defined by the isoform of myosin that it (primarily) expresses, and the myosin protein has a fairly short half-life. Thus, if you stop training, and hence stop recruiting those type IIa fibers, within a few weeks they will (largely*) revert to type IIx.

*It has been hypothesized - by Ed Coyle, in fact - that many years of strenuous endurance training may lower the recruitment threshold of faster motor units, such that they called upon more often even in daily life, and therefore tend to remain skewed more towards the slow-twitch end of things, at least in terms of, e.g., mitochondrial respiratory capacity. Unlike the increase in maximal cardiac output with training (and decrease with detraining), however, this is only a hypothesis.

Awesome, thanks!

Thanks for the wealth of information, Andrew. And thanks for this . . .

Andrew Coggan wrote:

That is unfortunate, because they [Ashenden and Tucker] really aren't the people you should be listening to.

Johnson brothers, take note!