Powercranks

[Andy Coggan]

"Frank Day" <[email protected]> wrote in message
news:[email protected]...
> "Andy Coggan" <[email protected]> wrote in message
news:<[email protected]>...
> > "Frank Day" <[email protected]> wrote in message
> > news:[email protected]...
> > > "Andy Coggan" <[email protected]> wrote in message
> > news:<[email protected]>...
> > > > "Frank Day" <[email protected]> wrote in message
> > > > news:[email protected]...
> > > >
> > > > > the abilty to exercise is not limited by the heart or lungs but, rather, by the ability of
> > > > > the muscles
being
> > > > > exercised to extract oxygen from the blood. It is the muscles in
the
> > > > > legs and arms that go anaerobic (ischemia) and not the heart,
> > > >
> > > > And the reason, ultimately*, that the muscles fail is because the
heart
> > > > can't provide them with enough O2-carrying blood. This is proven by
the
> > fact
> > > > that per mass of active tissue, both blood flow and O2 uptake are
much
> > > > higher during small muscle mass (e.g., one leg kicking) vs. large
muscle
> > > > mass exercise.
> > >
> > > It is true that the heart can't provide the tissues with enough O2 carrying blood, but this
> > > isn't because the heart can't deliver more blood, but because there isn't enough capillary
> > > density to deliver the blood flow required by the tissue.
> >
> > ******** - as I told you, per unit of active tissue muscle blood flow is
as
> > much as three-fold higher during small muscle mass exercise (e.g., 1 leg kicking) vs. large
> > muscle mass exercise (e.g., cycling). This clearly demonstrates that there must be active
> > vasocontriction even in
exercising
> > muscle, a point proven by studies using vasodilating drugs. The reason
for
> > this vasoconstriction is apparently to maintain blood pressure: since cardiac output cannot
> > increase beyond that observed at/near VO2max, the
body
> > can't "allow" a large amount of muscle to fully vasodilate because then perfusion pressure
> > would fall.
>
> I would love to see that study that showed that a leg was able to do three times more work being
> used alone than when being used in concert with the other. That would mean we should all be
> pedaling with just one leg because 3 times 1 is more than 1 times 2. Or, was it just shown that
> blood flow was increase but oxygen utilization wasn't. Or what. Blood flow is not power. Your
> study proves nothing as regards this argument.

I said flow, not power, and the data directly refute your claim that VO2max is limited by the
capacity of muscle to accept blood flow.

> > As Loring Rowell put it: the heart's job during exercise is to maintain
the
> > highest possible blood pressure against the smallest possible peripheral resistance.
> >
> > >The heart can only deliver as much as the capillaries in the tissue will allow. If you train
> > >harder you can develop more capillaries and more blood flow can ensue and performance will
> > >increase. The heart adapts to this increased load. This is called training effect.
> >
> > While capillarization does increase with training, this is but one
factor
> > contributing to the improvements in VO2max/performance. More
importantly,
> > changes in capillarization are not required to achieve increases in
VO2max.
> > This is shown, e.g., by the fact that acutely increasing convective O2 deliverly via EPO
> > administration, transfusion, hyperoxia, or even
expansion
> > of plasma volume (in an untrained person) increases VO2max w/o,
obviously,
> > any change in capillary density.
>
> All you say doesn't change the fact that the ability to utilize oxygen is limited by the local
> tissue conditions, which includes hemoglobin concentration, oxygen saturation, capillary density,
> mitochondrial density, contractile element density, etc. etc. The healthy heart does not change,
> affect or limit any of these things because it changes in concert with the same stimulation
> (training). It always has a little in reserve.

Stating it over and over and over again doesn't make it so, Frank. Go read the scientific literature
on the subject and you'll see that I'm right and you're wrong.

Andy Coggan

 

[Andy Coggan]

"Frank Day" <[email protected]> wrote in message
news:[email protected]...
> "Andy Coggan" <[email protected]> wrote in message
news:<[email protected]>...
> > "Terry Morse" <[email protected]> wrote in message news:tmorse-
> > [email protected]...
> > > Andy Coggan wrote:
> > >
> > > > Sorry, but maximal heart rate goes down, not up, with training.
Hence,
> > all
> > > > of the increase in maximal cardiac output - and typically at least
50%
> > of
> > > > the increase in VO2max - is due to the increase in stroke volume.
> > >
> > > Interesting. What changes in the body account for the other 50% of VO2max increase?
> >
> > Increased extraction of O2 from arterial blood. However, since there's
only
> > a limited amount of O2 left in venous blood in the untrained state, you
can
> > only increase VO2max by about 10% by relying on this mechanism - any increase greater than that
> > therefore generally must be due to an
increase in
> > stroke volume and hence cardiac output.
>
> VO2 delivery is cardiac output times the amount of oxygen in the blood, which depends mostly on
> hemoglobin concentration and altitude, and the amount extracted from the blood as it passes
> through the tissues. VO2 max is the maximum amount you as an individual can extract per minute.
>
> The easiest way to increase VO2 max is to increase hemoglobin by living at altitude or by doping.
> The hardest way is through training to increaase cardiac output. Cardiac output is determined by
> stroke vlume time heart rate. So, to answer your question, most of the other 50% increase is
> determined by HR. Increased extraction is a small amount of the total.
>
> I am sure i have made an error above and AC will set you straight as my understanding of this
> stuff (as I have been told) is minimal.

Well at least you got the last part right.

Tim's question pertained to the changes due to training, not what happens acutely during a single
exercise bout. As I pointed out before, maximal heart rate tends to come down with training - ergo,
all of the increase in maximal cardiac output, and typically at least 50% of the increase in VO2max,
is due to an increase in stroke volume.

BTW, if you accept that increased hemoglobin concentration results in an increase in VO2max, how can
you argue that the ability of muscle to accept blood flow and utilize O2 is the limited factor??

Andy Coggan

 

[Andy Coggan]

"Frank Day" <[email protected]> wrote in message
news:[email protected]...
> "Andy Coggan" <[email protected]> wrote in message news:<
> > > > It sets the upper limit to aerobic energy production, yes (and
> > obviously).
> > > > However, it isn't the only determinant of endurance exercise
> > performance, as
> > > > I have explained previously.
> > >
> > > It only sets the upper limit at that point in time. It doesn't mean VO2 max cannot be
> > > increased. It is a number. What is the basis of that number? is it cardiac? pulmonary? or
> > > skeletal muscular limits that set VO2 max? Maybe we should be debating that question. Which do
> > > you believe to be the limiter that determines VO2 max?
> >
> > Personally, I'm more of a subscriber to what's sometimes referred to as metabolic control
> > theory, or distributed control - this helps you get
away
> > from thinking that one thing, and only one thing, limits any particular process. However, if you
> > look at the overall chain of events involved in
O2
> > transport during maximal exercise, there's absolutely no question
whatsoever
> > that convective O2 delivery - which is determined by cardiac output and arterial O2 content - is
> > the primary determinant of VO2max. By
comparison,
> > the ability of muscle to accept blood flow and to take up and utilize O2
is
> > far, far greater, whereas the lungs, although lacking the same degree of safety margin (if you
> > will), are also somewhat "overbuilt" for exercise
(in
> > most cases).
>
> The amount of convective O2 delivery at maximum exercise IS VO2 max.

No, it is not, as there is still some O2 left in mixed venous blood, even during maximal exercise
(although not very much, even in a trained person).

> I guess that in a fashion could be considered to be the "primary" determinant in VO2 max but if
> you were my student

Now that's a laugh!!

> I wouldn't accept that answer as showing an adequate understanding of the physiology, you have
> just regurgitated the definition. What again is the limiter that prevents us from further
> increasing our VO2 max when we are doing these tests?

How many times do I have to say it before you get it through your thick skull? VO2max is (pirmarily)
limited by convective O2 delivery, as proven by the fact that if you increase arterial O2 carrying
capacity (e.g., via EPO administration), you increase VO2max.

> I presume you have excluded the lungs from your answer above

In most cases, yes - but some athletes with relatively high VO2max suffer from arterial O2
desaturation during maximal exercise.

> (I would agree) so now we are down to the heart or the periphery (local tissue blood dynamics).

To paraphrase Bill Clinton (it was Clinton, wasn't it?): it's the heart, stupid.

> Based upon your explanations I am now no longer looking forward to seeing how Erin Mirabella
> performs this season on the track as she has changed the emphasis of her training to include
> PowerCranks.

Helped her a lot this past weekend in Moscow, didn't it? She finished nearly 30th in the points
race, and could only manage 4th in the pursuit against a less-than-stellar field in a relatively
slow time even for her.

> > > > > It makes no sense to me to say VO2 max is limiting and then scale
it
> > > > > to body weight. If it should be scaled to anything it should be
lung
> > > > > capacity
> > > >
> > > > And why, pray tell, is that? Except in special cases, the lungs
aren't
> > > > limiting to VO2max, i.e., most (not all) people have no problem
> > maintaining
> > > > arterial O2 saturation even during maximal exercise.
> > >
> > > And that is why VO2 max is not limiting to aerobic exercise? Thanks for the argument. If
> > > arterial oxygenation is maintained during maximal exercise, why do you presume to claim that
> > > VO2 max is limiting?

You seem to confuse VO2max with the maximal rate of O2 transfer from alveolar air to arterial blood.
That isn't what it represents.

> > > Let us get back to what the limiting organ ireally is. i will accept your argument that VO2
> > > max limits aerobic exercise performance. What limits VO2 max. The heart or the periphery or
> > > something else?
> >
> > Once again, primarily the heart.
>
> Why do you say that? What specifically happens that limits further increases in the hearts ability
> to pump blood? Does the heart become ischemic (for those of you who are still around and now
> familiar with the jargon, that means not enough oxygen) and can't generate any more energy? Why
> doesn't the athlete experience chest pain if the heart can do no more? Give me a physiological
> mechanism for this limitation.

Even in healthy individuals, you can find evidence that brief ischemia/anoxia may occur during
strenuous exercise (esp. w/o an adequate warm-up). However, that isn't common, and isn't what limits
maximal cardiac output. Rather, the heart is simply beating as fast and as powerfully as it can - w/
inadequate filling it can beat faster, but cardiac output will be reduced due to a decline in stroke
volume, whereas increasing filling pressures in an attempt to further increase stroke volume is
ineffective because the heart is already stretched to its limits (remove the pericardium, however,
and all bets are off - at least in a greyhound).

> > > > > > > How do you explain incremental improvements in VO2 max with incremental additional
> > > > > > > training?
> > > > > >
> > > > > > By increases in stroke volume and/or a-vO2 difference (primarily
the
> > former,
> > > > > > at least when talking large changes in VO2max....a-vO2
difference
> > can only
> > > > > > increase by ~10%, since during maximal exercise there isn't much
O2
> > > > > > remaining in mixed venous blood even in an untrained person).
> > > > >
> > > > > Actually, it is mostly a combination of increases in stroke volume
and
> > > > > increased heart rate.
> > > >
> > > > Sorry, but maximal heart rate goes down, not up, with training.
Hence,
> > all
> > > > of the increase in maximal cardiac output - and typically at least
50%
> > of
> > > > the increase in VO2max - is due to the increase in stroke volume.
> > >
> > > Possibly, but age goes up with training which is associated with lowered maximum heart rates.
> > > the top aerobic athletes are not 20 years old but more likely 35. That explains the maximum HR
> > > connundrum.

Not at all, since the reduction in maximal heart rate that occurs with training happens within
weeks, if not days, and is readily reversed with just as short a period of detraining.

Andy Coggan

 

[Andrew Bradley]

Frank Day <[email protected]> wrote in message
news:[email protected]...

> Look, from my (as I have recently come to understand) uninformed background it is really quite
> simple. There are several things that come into play (which makes it not quite so simple in
> practice). What is the energy use (what are the demands for oxygen by the mitochondria that are
> making energy molecules necessary for muscle contraction?) that needs to be made up. What is the
> furthest distance that oxygen must diffuse from the end capillary (where oxygen concentration is
> lowest) to one of these active mitochodria. And, how much oxygen is in the blood (hemogglobin
> concentration) which determines how fast it will drop as it passes through the capillaries. As
> demand in the muscles increase, additional capillaries will open up, reducing the distance from
> the active capillaries to to the mitochodria. Once they are all opened and once the concentration
> at the end capillary drops to a point that the diffusion gradiant to the furthest away mitochodria
> is not sufficient to supply the necessary amount of oxygen then anaerobic metabolism ensues in
> that mitochondria (LT) and any additional effort just makes it worse and the end is near.

Do you feel that, with increasing intensity, there comes a point where the upstoke mitochondria are
easier to supply with extra oxygen than the downstoke mitochondria?

Andrew Bradley

 

[Andy Coggan]

"Phil Holman" <[email protected]> wrote in message
news:[email protected]...

>> since it takes but a small fraction of
> total
> > body muscle to be contracting to drive cardiac output to its limits,
> there's
> > no reason to believe that attempting to bring a few small accessory
> muscles
> > into play would be of any benefit there, either. (If there were, then
> you'd
> > expect that arm+leg trained athletes, e.g., X-C skiers to have higher
> VO2max
> > values than e.g., middle distance runners - but in fact, they don't.)
>
> Odd choice for comparison. What about X-C skiers versus cyclists?

Odd? I merely went for the biggest difference in muscle mass to prove the point. But the same would
be true for X-C skiers vs. cyclists: no difference, on average, of the VO2max values of the elites.

> I have power data on an elite track cyclist showing a 25%
> > increase 5 s and 1 min power in just 2 months, simply as a result of changing the emphasis of
> > their training. (I expect to make similar
> gains
> > myself during my specific prep for the 3k pursuit at master nationals
> this
> > year, which, since I've already gone as fast as Phil for 2k during a
> 3k
> > event w/o any specific training, should enable me to blow away the
> time he
> > always likes to brag about...but that's a different story.)
>
> This is nothing new. Power gains of this magnitude are normal for getting in shape for an event.
> My gain was on top of that.

So you say, but how many times had you trained specifically for a 2k pursuit before adopting the
PowerCranks?

> If you want to impress me, improve you best 40K TT by 1 mph.

Different situation: I've been optimizing my training for TTs for years, and so there's little, if
any, room for further improvement. In contrast, you (if I understand things correctly) went from
racing on the road to preparing for a <3 min event, and in the process changed your training around
radically.

> Beating my time, whatever that was, is very subjective i.e a 2-35 at Marymoor was apparently good
> for a 2-25 at Colorado Springs.

I was talking about your time at Manchester, not Marymoor.

Andy Coggan

 

[Andy Coggan]

"Phil Holman" <[email protected]> wrote in message
news:[email protected]...
>
> "Andy Coggan" <[email protected]> wrote in message
> news:[email protected]...
> > "Phil Holman" <[email protected]> wrote in message
> > news:[email protected]...
> > >
> > > "Andy Coggan" <[email protected]> wrote in message
> > > 1) which motor units/muscles
> > > > (i.e., extensors vs. flexors) are more easily recruited/controlled
> by
> > > the
> > > > motor system, and 2) which motor units/muscles are most capable of
> > > meeting
> > > > the demands placed upon them. Because the motor pattern (i.e.,
> timing
> > > and
> > > > sequence of muscle activation) during cycling is nearly identical
> to
> > > to that
> > > > of walking/running, the answer is the hip/knee extensors, because
> they
> > > have
> > > > been "designed" by millions of years of evolution for this
> purpose.
> > >
> > > As a former runner this doesn't sound intuitively obvious i.e. hamstrings and hip flexors seem
> > > to be used more in running plus the range of motion is greater.
> >
> > Apparently your intuition isn't as good as this former runner's,
> because I
> > think it is obvious: during upright bipedal locomotion, you support
> your
> > body weight and then drive yourself forward using your large, powerful
> hip,
> > knee, and (esp.) ankle extensors (plantar flexors), then bring the leg
> back
> > into position against no external resistance using the hip, knee, and
> ankle
> > flexors. Pedaling a bicycle is just a variation of this basic scheme, corresponding most closely
> > to jogging up a steep hill.
> >
>
> Against no external resistance except the weight of the leg being raised from an almost stationary
> postion which will be (intuitively) greater than in cycling. The foot is raised and accelerated
> from zero to twice running speed with every stride as compared to a fairly large conservation of
> momentum and a constant speed on the upstroke in cycling.

The kinetic energy isn't conserved when pedaling, it is transferred to the pedals. Moreover, the leg
muscle be accelerated from essentially zero upward velocity at/near BDC to some maximum partway
through the upstroke, then slows again near the top. IOW, don't confuse nearly constant crank
angular velocity as meaning that the velocity of the limb segments are constant, as they are not.

Andy Coggan

 

[Andy Coggan]

"Frank Day" <[email protected]> wrote in message
news:[email protected]...
> "Andy Coggan" <[email protected]> wrote in message
news:<[email protected]>...
> > "Frank Day" <[email protected]> wrote in message
> > news:[email protected]...
> > > "Andy Coggan" <[email protected]> wrote in message news:
> > > > > Engaging a motor unit is not a guarantee of purfusion.
> > > >
> > > > It is if cardiac output is still below its maximum.
> > >
> > > No it is not, not if all the precapillary sphincters (that control blood flow to the local
> > > tissue) are open. Once that occurs the only way to increase blood flow to the muscle is to
> > > increase blood pressure.
> > > >
> > > > > If what you said was true then Olympic Kayakers would have the same VO2 max as Olympic
> > > > > Oarsman as Olympic cyclists, etc. It
just
> > > > > isn't true. VO2 max is limited by the exercised muscle mass and
not
> > > > > the cardiovascular system.
> > > >
> > > > Apparently you don't know the differences between VO2max and
VO2peak. I
> > > > suggest that you go read Loring Rowell's now-classic review article
to
> > learn
> > > > the difference.
> > >
> > > Guess I don't. Sorry I don't have it available. I did a google search and was only able to
> > > find books written on the subject.
> >
> > Ever heard of a library, Frank? Surely there's one somewhere near you
that
> > carries medical journals.
> >
> > > I will try to get a copy and read it but it ain't going to happen during this thread. Perhaps
> > > you could enlighten me (and the rest of the list) as to this difference.
> >
> > It's simple:
> >
> > 1) VO2max = the highest attainable rate of O2 uptake, limited by maximal cardiac
> > output/convective O2 delivery.
> >
> > 2) VO2peak = anything less than true VO2max, even if it is the highest
that
> > that person can achieve given the exercise modality. Limited by the inability to recruit
> > (actually, sufficiently vasodilate) enough muscle
to
> > drive cardiac output all the way to maximum.
> >
> > Since trained cyclists can achieve a true VO2max while cycling, all of
your
> > claims with regards to muscle mass are moot, at least when talking about sustainable power
> > output (the energy for which must be derived
aerobically).
>
> I believe you misinterpret what VO2 max means.

Yes, I need an anesthiologist-turned-inventor to explain it to me.

> It is not the highest possible VO2 uptake that could ever be attained by this individual. It is
> the highest attainable VO2 by that individual in his/her current state of training.

I thought that was implied in what I wrote.

> By virtue of your definition of VO2 Peak, it seems to me that you are accepting that VO2 uptake
> (and, hence, VO2 max) depends greatly on the amount of muscle mass that is recruited.

That's why it is called a VO2peak and not VO2max: VO2peak *is* muscle mass dependent, e.g., I can't
reach VO2max by twiddling my thumbs, so the highest rate of VO2 that I can achieve during that form
of exercise would rightfully be called a VO2peak.

> Further, how on earth does one know one has actually tested "true" VO2 max as you define it.

So many studies have been done looking at this issue that people simply accept that the highest VO2
a person can achieve during uphill running is really VO2max, and not a VO2peak.

> These tests are always effort dependant and never truly objective.

That's simply not true. The majority of individuals* show a plateau in VO2 during high intensity
exercise, meaning that even if they summon up the extra motivation to keep going, it doesn't alter
the measurement of VO2max.

*Depending on how the test is designed, of course.

> To say that cyclists can attain "true" VO2 max goes against the facts as I understand them as I
> understand that triathletes frequently will have higher measured VO2 max running than when
> cycling. Of course, in your mind triathletes are not "trained cyclists" which would explain this
> discrepancy. That is not a sufficient explanation to me.

What more explanation do you want? It takes a certain amount of specific training to be able to
achieve a true VO2max while cycling, and most triathletes apparently don't reach this level. OTOH,
there are a few swimmers who can achieve a true VO2max while swimming, despite relying almost
exclusively on their upper body muscles.

Andy Coggan

 

[Andy Coggan]

"Frank Day" <[email protected]> wrote in message
news:[email protected]...
> "Andy Coggan" <[email protected]> wrote in message
news:<[email protected]>...
> > "Terry Morse" <[email protected]> wrote in message news:tmorse-
> > [email protected]...
> > > Andy Coggan wrote:
> > >
> > > > Terry Morse wrote:
> > > > > What changes in the body account for the other 50% of VO2max increase?
> > > >
> > > > Increased extraction of O2 from arterial blood.
> > >
> > > Okay, that extraction as I understand it shows up as a higher arterial-venous O2 difference
> > > (the "a-vO2 diff" in the literature). But what's the physiological cause for that increase, an
> > > increase in capillary density, or something else?
> >
> > An increase in perfused capillary bed volume may contribute to an
increase
> > in O2 extraction by increasing capillary mean transit time, thus
allowing
> > for more complete "unloading" of hemoglobin. However, as it turns out
the
> > percentage increase in capillary density tends to parallel quite closely
the
> > percentage increase in VO2max/maximal cardiac output - this suggests
that
> > capillary mean transit time is only maintained, not increased, as a
result
> > of training. This in turn implies that other factors must be operative
as
> > well, in particular a reduction in the mean intramuscular pO2 that helps "pull" more O2 from the
> > blood. A lower intramuscular pO2 during maximal exercise after as compared to before training
> > would be an expected consequence of having many more mitochondria* acting as O2 "sinks".
> >
> > *In reality, a more extensive mitochondrial reticulum...and since O2 is
much
> > more soluble in lipid membranes than in aqueous solutions, this detail
may
> > be a factor as well.
>
> Look, from my (as I have recently come to understand) uninformed background it is really quite
> simple. There are several things that come into play (which makes it not quite so simple in
> practice). What is the energy use (what are the demands for oxygen by the mitochondria that are
> making energy molecules necessary for muscle contraction?) that needs to be made up. What is the
> furthest distance that oxygen must diffuse from the end capillary (where oxygen concentration is
> lowest) to one of these active mitochodria. And, how much oxygen is in the blood (hemogglobin
> concentration) which determines how fast it will drop as it passes through the capillaries. As
> demand in the muscles increase, additional capillaries will open up, reducing the distance from
> the active capillaries to to the mitochodria. Once they are all opened and once the concentration
> at the end capillary drops to a point that the diffusion gradiant to the furthest away mitochodria
> is not sufficient to supply the necessary amount of oxygen then anaerobic metabolism ensues in
> that mitochondria (LT) and any additional effort just makes it worse and the end is near.

Uninformed is right: the occurrence of lactate threshold has nothing to do with lack of O2 at the
muscle level, as mitochondrial respiration is limited by O2 availability only at power outputs
greater than VO2max.

Andy Coggan

 

[Andy Coggan]

"Frank Day" <[email protected]> wrote in message
news:[email protected]...
> "Andy Coggan" <[email protected]> wrote in message
news:<[email protected]>...
> > "Frank Day" <[email protected]> wrote in message
> > news:[email protected]...
> >
> > > take the drive train away. The losses are there whether there is a chain attached or not. Put
> > > your bike on a stand and take the chain off and pedal at a cadence of 130 (or the highest
> > > cadence you can sustain) and see if your HR increases. See how long you can do it. If it
> > > doesn't take any energy why does your HR change (or mayby yours won't). Try it and report
> > > back.
> >
> > This experiment is a red herring, since it fails to differentiate
between
> > energy losses due to the properties of biomaterials vs. those that might have a physical basis
> > on a larger scale. As Andrew Bradley has explained
to
> > you (and explained to you, and explained to you, and explained to you),
NO -
> > none, zero, nada, zip - energy is lost simply due to the legs going
'round
> > and 'round. Rather, ALL - every little bit - of the energy loss occurs BEFORE the energy is
> > transferred to the limb segments in the first place (this loss being due to the viscoelastic
> > elements in muscle). Efficiency
is
> > therefore a complex function of cadence, and can't be predicted using
your
> > simplistic calculations that ignore energy transfer to the pedals (and
in
> > the process, violate Newtonian physics).
>
> I'll "accept" your erudite explanation of where the losses are if you will accept that there are
> losses and they vary with the cadence

Of course. But the point is that you don't even understand basic physics enough to realize that you
can't calculate them using your simple model that ignores reality, i.e., the fact that the energy
must go somewhere (into the pedals).

> raised anywhere from the 3rd to the 4th power.

Since the inefficiencies are a complex function of biochemistry, biomechanics, etc., there's no
reason to expect that they will conform to any fixed function.

> Just one question though, since we have two sets of data indicating these loses are not small and
> not directly related to cadence (Phils's numbers and the other study he gave the data from) please
> explain to me how viscoelastic losses vary with the cube or 4th power of the cadence?

See above.

>I missed that in physics class.

It isn't really a physics problem, at least not entirely (or unless you want to think of it as
biophysics). You could *try* to model pedaling using limb segments of appropriate masses, power
transfer to the pedals, and springs and dampers to reflect the viscoelastic properties of muscle,
but I don't know how well you could do so (a simple mass-on-a-spring model works pretty well for
upright locomotion, though).

Andy Coggan

 

[Andy Coggan]

"Phil Holman" <[email protected]> wrote in message
news:[email protected]...
>
> "Andy Coggan" <[email protected]> wrote in message news:b89Xb.2642
>
> > As Andrew Bradley has explained to you (and explained to you, and explained to you, and
> > explained to
> you), NO -
> > none, zero, nada, zip - energy is lost simply due to the legs going
> 'round
> > and 'round. Rather, ALL - every little bit - of the energy loss occurs BEFORE the energy is
> > transferred to the limb segments in the first
> place
> > (this loss being due to the viscoelastic elements in muscle).
>
> The weights used on the legs resulted in significant energy increases and is an indication that
> the losses due to just the legs going around are not nada.
>
> http://tinyurl.com/24qxc

No it does not, as adding additional mass to the legs could also increase energy loss to
viscoelastic elements. The only way to determine where the energy loss occurs is to perform what is
called an inverse dynamic analysis - this requires not only knowledge of the rates and directions of
limb movements and their masses (what Frank has attempted to model based on assumed values), but
also knowledge of power flow to the pedals. It is the latter that he did not include in his
calculations (because he lacks the data, having never used a force pedal in his life), which is why
his conclusions are incorrect (and, in fact, impossible, since they violate the laws of
thermodynamics). If, however, you account for energy transfer to the pedals, you find that there is
complete conservation of the kinetic and potential energy invested in the limbs as a result of
muscle contraction (as you would expect based on simple physics). Ergo, any and all energy loss MUST
occur BEFORE the limbs begin to move in the first place - which is exactly as you would expect,
given the nature of biological materials (i.e., the molecular "motors" of muscle and the properties
of connective tissue, tendons, and ligaments).

Andy Coggan

 

[Andy Coggan]

"Phil Holman" <[email protected]> wrote in message
news:[email protected]...
>
> Andy Coggan states "Since trained cyclists can achieve a true VO2max while cycling, all of your
> (Frank Day's) claims with regards to muscle mass are moot, at least when talking about sustainable
> power output (the energy for which must be derived aerobically)".
>
> 1/VersaClimbing elicits higher VO2max than does treadmill running or rowing ergometry.
>
> Brahler CJ, Blank SE
>
> Department of Kinesiology and Leisure Studies, Washington State University, Pullman 99164-
> 1410, USA.
>
> Collegiate varsity oarswomen and coxswain (N = 11) completed maximal aerobic exercise tests on a
> treadmill, a rowing ergometer, and a simulated climbing machine. Successful completion of each
> test was evidenced by a plateau in oxygen consumption in response to increasing work rates. VO2max
> (l.min-1), and minute ventilation (VE, l.min-1) at VO2max were significantly greater (P < 0.05)
> during simulated climbing compared to treadmill running and rowing ergometry. Maximal heart rate
> (beats.min-1) was significantly greater (P < 0.05) during climbing and running than during rowing.
> Findings indicate that progressive, incremental, whole-body climbing exercise elicits
> significantly greater VO2max values for collegiate oarswomen and coxswain than does graded
> treadmill running or progressive rowing ergometry.end

> The way this can apply to trained cyclists is by illustrating how greater VO2max values can be
> attained outside of one's own discipline (one that uses more muscle mass than cycling) by using
> even more muscle mass thus contradicting your statement that muscle mass is moot.

Nice try, Phil, but if you had read the actual study (which, BTW, was supported by VersaClimbar)
instead of just the abstract you would realize that these results actually support my position.
Specifically, VO2peak during treadmill exercise was measured using the Bruce protocol, the slow
speed and steep grade of which would have prevented these trained athletes from reaching their true
VO2max (just like non-cyclists can't reach their true VO2max while pedaling, due to the short
"strides", relatively slow "stride rate", and relatively high forces compared to running, even
uphill). This interpretation is supported by the results of other studies using the exact same
exercise device, which have found VO2peak measured during simulated climbing is lower than VO2max.

> 2/Peak oxygen consumption and ventilatory thresholds on six modes of exercise.
>
> Smith TD, Thomas TR, Londeree BR, Zhang Q, Ziogas G
>
> Department of Health and Exercise Sciences, University of Missouri, Columbia 65211, USA.
>
> In order to compare responses on six modes of exercise for maximal oxygen consumption (VO2peak)
> and ventilatory thresholds (VT-1, VT-2), 10 male recreational exercisers (23 +/- 3 yrs) completed
> incremental maximal tests on treadmill, stationary skier, shuffle skier, stepper, stationary
> cycle, and rower. After extensive habituation, VO2peak, VT-1, and VT-2 were determined during each
> maximal bout. A MANOVA followed by ANOVAs, Tukey post hoc tests, and noncentral F tests indicated
> that the treadmill elicited a significantly higher peak oxygen consumption than did the other
> modes, and the skier and stepper values were higher than the rower. VO2 at VT-1 was higher on the
> treadmill than cycle. The treadmill also elicited a higher VO2 at VT-2 than the shuffle skier,
> cycle, and rower. However, no differences were observed among modes for VT-1 and VT-2 when
> expressed as a percentage of VO2peak. These results suggest that the treadmill elicits a higher
> aerobic capacity measure than other modes, but the ventilatory threshold responses (% VO2peak) are
> similar among modes.end
>
> This again illustrates how a higher aerobic capacity is elicited by more muscle mass i.e.
> treadmill running.

This study simply supports what I've been saying all along: to reach a true VO2max, untrained
individuals needs to be tested during uphill running, not uphill walking, not cycling, etc.

> 3/Laboratoire des Sciences de l'Activite Physique, Universite Laval, Ste-Foy, Quebec, Canada.
>
> The objective of this study was to evaluate the viability of using a single test in which
> cardiorespiratory variables are measured, to establish training guidelines in running and/or
> cycling training activities. Six triathletes (two females and four males), six runners (two
> females and four males) and six males cyclists, all with 5.5 years of serious training and still
> involved in racing, were tested on a treadmill and cycle ergometer. Cardiorespiratory variables
> [e.g., heart rate (HR), minute ventilation, carbon dioxide output (VCO2)] were calculated relative
> to fixed percentages of maximal oxygen uptake (VO2max; from 50 to 100%). The entire group of
> subjects had significantly (P < 0.05) higher values of VO2max on the treadmill compared with the
> cycle ergometer [mean (SEM) 4.7 (0.8) and 4.4 (0.9)
> l.min-1, respectively], and differences between tests averaged 10.5% for runners, 6.1% for
> triathletes and 2.8% for cyclists.end
>
> Again this contradicts your statement that muscle mass is moot.

No, it does not: the trained cyclists were able to achieve VO2max both while cycling and while
running uphill on a treadmill, despite the greater muscle mass used in the latter exercise.

> While some trained cyclists may be able to achieve a true V02max this obviously isn't the case for
> all athletes and cyclists.

Definitely not true for all athletes, since all athletes don't train on a bike. However, I have
never seen a competitive cyclist who could routinely achieve a higher VO2 while running uphill vs.
cycling, and every study of trained cyclists that I am aware of that has made the same comparison
has come to the same conclusion, at least based on mean values.

> This also illustrates the greater PC potential for triathletes which possibly explains why their
> use is more popular in that sport.

The last thing the average tri-geek needs to do is spend even more money on gadgets like
Frank's cranks.

Andy Coggan

 

[Frank Day]

[email protected] (Andrew Bradley) wrote in message news:
> > Then, just look at the thighs during pedaling. they both pretty much cancel each other out from
> > a potential energy point of view, one going up when the other is going down. But, from a kinetic
> > energy point of view, they are both pretty much as maximum speed (albeit in opposite dierection
> > but that is of no consequence from an energy perspective because the velocity is squared) and
> > both pretty much at minimum speed (zero) at the same time. How on earth does one do things with
> > the other elements of the body to zero these out?
>
> Your analysis is roughly correct, the low in energy occurs roughly at TDC/BDC, and the high at mid
> stroke, so you fit a traditional elliptical to speed the legs up over tops and slow them down mid
> stroke. Energy variation is reduced. What more do you want Frank???

What more do I want? I simply want to to show me how such a speed variation can make the energy
variation go to zero. I don't deny that such a device could reduce the variation. If you can't make
it zero though, then my theory still holds.

snip
> >it can't be done as far as I am concerned so even if all the viscoelastic losses and bearing
> >losses are zero, this is cannot be a perpetual motion machine.
>
> You presumably feel that some form of osmosis to the ether accounts for the energy loss. Chain
> off, your model _is_ a perpetual motion machine (note the word "model").

No, the lost energy is lost as heat as all all inneficiencies in the real world.

>
> Your calculations apply equally well to a system of steel rods and hinges with the hips firmly
> stabilised and ankles locked. Why not build one and think about whether your method accounts for
> the energy losses there. It is not a balanced flywheel as Phil points out, so it may not spin for
> long, but the energy loss is via the hinges and bearings. Having contemplated modelling the losses
> in this model you may not feel up to the task of modelling energy losses in real legs.

Many people have built such a model as you describe and point to that as the evidence that the
pedaling stroke conserves energy as these seem to stop "pedaling" slowly. The problem with such
devices is they are stick figures so the mass of the thigh is about the same as the mass of the
lower leg and foot and wheel. The energy loss is less than in "real" world cycling because the
masses are completely different. In people the thigh is very massive compared to the other elements
of the leg.
>
> >Just account for the thighs please and I will come over to the dark
> side.
>
> The "energy saver" ring slows the thighs down where they move fastest. But don't overlook the
> lower leg Frank, and don't overlook shoes, pedals and cranks.

No, they can be pretty much overlooked. The feet move in, essentially, exact circles so their
accelerations are always equal and opposite, they conserve energy. The lower legs are sort of
inbetween, the ankle part moving in an "exact" circle and the knee part pumping up and down.
However, the leg is not very massive, compared to the thighs and because of this mixing, the losses
are small. This difference also accounts for why it will be impossible for your ellipical chain ring
to make up for the thigh losses.

> Consider this: if the funny ring that gives zero mechanical energy variation turns out to be
> impractical, fit heavier pedals - the chainring can then be rounder. By increasing pedal weight,
> the energy-saver can in theory be as round as you want.

Changing pedal weight does nothing because they move in exact circles and conserve energy.

> Reductio ad absurdum for the energy-saving chainrings and by the same token your calculation
> method, I feel.

You feel wrong, I am afraid.

Frank

 

[Frank Day]

"Andy Coggan" <[email protected]> wrote in message news:<[email protected]>...
> "Frank Day" <[email protected]> wrote in message
> news:[email protected]...
> > "Andy Coggan" <[email protected]> wrote in message
> news:<[email protected]>...
> > > "Frank Day" <[email protected]> wrote in message
> > > news:[email protected]...
> > > > "Andy Coggan" <[email protected]> wrote in message
> news:<[email protected]>...
> > > > > "Frank Day" <[email protected]> wrote in message
> > > > > news:[email protected]...
> > > > >
> > > > > > the abilty to exercise is not limited by the heart or lungs but, rather, by the ability
> > > > > > of the muscles
> being
> > > > > > exercised to extract oxygen from the blood. It is the muscles in
> the
> > > > > > legs and arms that go anaerobic (ischemia) and not the heart,
> > > > >
> > > > > And the reason, ultimately*, that the muscles fail is because the
> heart
> > > > > can't provide them with enough O2-carrying blood. This is proven by
> the fact
> > > > > that per mass of active tissue, both blood flow and O2 uptake are
> much
> > > > > higher during small muscle mass (e.g., one leg kicking) vs. large
> muscle
> > > > > mass exercise.
> > > >
> > > > It is true that the heart can't provide the tissues with enough O2 carrying blood, but this
> > > > isn't because the heart can't deliver more blood, but because there isn't enough capillary
> > > > density to deliver the blood flow required by the tissue.
> > >
> > > ******** - as I told you, per unit of active tissue muscle blood flow is
> as
> > > much as three-fold higher during small muscle mass exercise (e.g., 1 leg kicking) vs. large
> > > muscle mass exercise (e.g., cycling). This clearly demonstrates that there must be active
> > > vasocontriction even in
> exercising
> > > muscle, a point proven by studies using vasodilating drugs. The reason
> for
> > > this vasoconstriction is apparently to maintain blood pressure: since cardiac output cannot
> > > increase beyond that observed at/near VO2max, the
> body
> > > can't "allow" a large amount of muscle to fully vasodilate because then perfusion pressure
> > > would fall.
> >
> > I would love to see that study that showed that a leg was able to do three times more work being
> > used alone than when being used in concert with the other. That would mean we should all be
> > pedaling with just one leg because 3 times 1 is more than 1 times 2. Or, was it just shown that
> > blood flow was increase but oxygen utilization wasn't. Or what. Blood flow is not power. Your
> > study proves nothing as regards this argument.
>
> I said flow, not power, and the data directly refute your claim that VO2max is limited by the
> capacity of muscle to accept blood flow.

Phooey! What possible advantage is there to increasing the flow if there is also not a concommitant
increase in power? I have no clue what that study shows. Guess I am going to have to find one of
those dratted medical libraries so see for myself cause I can't trust you to interpret it properly.

>
> > > As Loring Rowell put it: the heart's job during exercise is to maintain
> the
> > > highest possible blood pressure against the smallest possible peripheral resistance.
> > >
> > > >The heart can only deliver as much as the capillaries in the tissue will allow. If you train
> > > >harder you can develop more capillaries and more blood flow can ensue and performance will
> > > >increase. The heart adapts to this increased load. This is called training effect.
> > >
> > > While capillarization does increase with training, this is but one
> factor
> > > contributing to the improvements in VO2max/performance. More
> importantly,
> > > changes in capillarization are not required to achieve increases in
> VO2max.
> > > This is shown, e.g., by the fact that acutely increasing convective O2 deliverly via EPO
> > > administration, transfusion, hyperoxia, or even
> expansion
> > > of plasma volume (in an untrained person) increases VO2max w/o,
> obviously,
> > > any change in capillary density.
> >
> > All you say doesn't change the fact that the ability to utilize oxygen is limited by the local
> > tissue conditions, which includes hemoglobin concentration, oxygen saturation, capillary
> > density, mitochondrial density, contractile element density, etc. etc. The healthy heart does
> > not change, affect or limit any of these things because it changes in concert with the same
> > stimulation (training). It always has a little in reserve.
>
> Stating it over and over and over again doesn't make it so, Frank. Go read the scientific
> literature on the subject and you'll see that I'm right and you're wrong.

I think the same can be said for yourself. You have given no scientific evidence to prove that
exercise performance is limited by cardiac output. There is plenty of evidence to suggest it is
limited by local conditions. Show me a single study that shows the healthy heart entering more
substantial anaerobic conditions than the exercising skeletal muscle during exercise and maybe we
can talk. Until then you are blowing smoke in this insistence.

 

[Tom Sherman]

Andy Coggan wrote:

> ... To paraphrase Bill Clinton (it was Clinton, wasn't it?): it's the heart, stupid....

It was Clinton's 1992 campaign strategist, James Carvill who originated the saying; "It's the
economy, stupid."

Tom Sherman - Quad Cities

 

[Phil Holman]

"Andy Coggan" <[email protected]> wrote in message
news:[email protected]...
> "Phil Holman" <[email protected]> wrote in message

> The kinetic energy isn't conserved when pedaling, it is transferred to the pedals.

The legs end up back where they started and any energy transfer between KE and PE balance out. The
input from the muscles is simply divided between the pedals and the associated losses. Why over-
complicate this unless you specifically want to study the internal stresses.

> Moreover, the leg muscle be accelerated from essentially zero upward
> velocity at/near BDC to some maximum partway through the upstroke,
> then slows again near the top. IOW, don't confuse nearly constant
> crank angular velocity as meaning that the velocity of the limb
segments
> are constant, as they are not.

I didn't, I specifically used the word *foot* in my description.

>>The foot is raised and accelerated from zero to twice running speed with every stride as compared
>>to a fairly large conservation of momentum and a constant speed on the upstroke in cycling.

Phil Holman

 

[Phil Holman]

"Andy Coggan" <[email protected]> wrote in message
news:[email protected]...
> "Phil Holman" <[email protected]> wrote in message
> news:[email protected]...

> > >since I've already gone as fast as Phil for 2k during a 3k event w/o any specific training,
> > >should enable me to blow away the time he always likes to brag about...but that's a different
> > >story.)

> >This is nothing new. Power gains of this magnitude are normal
for getting in shape for an event. My gain was on top of that.
>
> So you say, but how many times had you trained specifically for a 2k pursuit before adopting the
> PowerCranks?

USCF didn't have a 2k for under 50s. I was doing 16 times 1 minute on 1 minute off back in 1991 not
long after I started to race and I've done these ever since (450 - 500 watt range). Except for the
PCs and the standing starts, nothing changed. As a track runner I ran 800s. I was no novice to
middle distance events.

>
> > If you want to impress me, improve you best 40K TT by 1 mph.
>
> Different situation: I've been optimizing my training for TTs for years, and so there's little, if
> any, room for further improvement. In contrast, you (if I understand things correctly) went from
> racing on the road to preparing for a <3 min event, and in the process changed your
training around radically.

You do not understand things correctly. Part of my test was *not* to change the way I was training.
I did lots of intervals as a carryover from my track running days. I still do.

>
> > Beating my time, whatever that was, is very subjective i.e a 2-35 at Marymoor was apparently
> > good for a 2-25 at Colorado Springs.
>
> I was talking about your time at Manchester, not Marymoor.

2-29. Don't make the same mistake as those disappointed when going from 3k to 2k. 2-29 with a 6
second start is 2-23 pace. Factored up to 3k gives 3-34.5 plus the 6 second start gives 3-40.5. This
assumes the same average constant speed minus the start. What can I say. Even though I think you're
a bit of an asshole, I wish you the best of luck in your 3k.

Phil Holman

 

[Frank Day]

"Andy Coggan" <[email protected]> wrote in message news:
> > > > > Sorry, but maximal heart rate goes down, not up, with training.
> Hence, all
> > > > > of the increase in maximal cardiac output - and typically at least
> 50% of
> > > > > the increase in VO2max - is due to the increase in stroke volume.
> > > >
> > > > Interesting. What changes in the body account for the other 50% of VO2max increase?
> > >
> > > Increased extraction of O2 from arterial blood. However, since there's
> only
> > > a limited amount of O2 left in venous blood in the untrained state, you
> can
> > > only increase VO2max by about 10% by relying on this mechanism - any increase greater than
> > > that therefore generally must be due to an
> increase in
> > > stroke volume and hence cardiac output.
> >
> > VO2 delivery is cardiac output times the amount of oxygen in the blood, which depends mostly on
> > hemoglobin concentration and altitude, and the amount extracted from the blood as it passes
> > through the tissues. VO2 max is the maximum amount you as an individual can extract per minute.
> >
> > The easiest way to increase VO2 max is to increase hemoglobin by living at altitude or by
> > doping. The hardest way is through training to increaase cardiac output. Cardiac output is
> > determined by stroke vlume time heart rate. So, to answer your question, most of the other 50%
> > increase is determined by HR. Increased extraction is a small amount of the total.
> >
> > I am sure i have made an error above and AC will set you straight as my understanding of this
> > stuff (as I have been told) is minimal.
>
> Well at least you got the last part right.

There you have it ladies and gentlemen, even AC agrees that I occasionally get something right so it
is no longer possible to discount everything I say.
>
> Tim's question pertained to the changes due to training, not what happens acutely during a single
> exercise bout. As I pointed out before, maximal heart rate tends to come down with training -
> ergo, all of the increase in maximal cardiac output, and typically at least 50% of the increase in
> VO2max, is due to an increase in stroke volume.

Well, under those circumstances I would say over 90% of the increase in VO2 max that comes with
training is due to increase in stroke volume. It takes energy to relax the heart the trained heart
is much more effective at relaxing, hence, the increase in stroke volume. If max HR comes down with
training it probably because it takes more time to contract and refill the larger stroke volume such
that HR cannot further increase and is forced to decrease.
>
> BTW, if you accept that increased hemoglobin concentration results in an increase in VO2max, how
> can you argue that the ability of muscle to accept blood flow and utilize O2 is the limited
> factor??

That is easy, since an increaing hemoglobin increases VO2 max without increasing cardiac output. An
increased hemoglobin means there is a higher oxygen concentration in the blood such that at the same
(or somewhat reduced blood flow through the capillaries as flow tends to reduce with increased
hemoglobin above about 10) the partial pressure is reduced more slowly such that higher energy
expenditures can be tolerated without reaching the critical end capillary pO2 value associated with
anaerobic metabolism. At some point, if hemoglobin is increased to high, sludging reduces flow in
the capillaries to such an extend that potential O2 delivery starts to drop. This can present quite
a risk when one gets dehydrated and one is starting at a very high value. Don't try this at home
folks, it is against the rules and presents substantial dangers to the athlete.

Sorry to keep saying this but it is all pretty straight forward, albeit somewhat advanced,
physiology (you won't find all of this in those basic physiology books AC keeps referring me to).

 

[Frank Day]

"Andy Coggan" <[email protected]> wrote in message news:
> > > >
> > > > As a former runner this doesn't sound intuitively obvious i.e. hamstrings and hip flexors
> > > > seem to be used more in running plus the range of motion is greater.
> > >
> > > Apparently your intuition isn't as good as this former runner's,
> because I
> > > think it is obvious: during upright bipedal locomotion, you support
> your
> > > body weight and then drive yourself forward using your large, powerful
> hip,
> > > knee, and (esp.) ankle extensors (plantar flexors), then bring the leg
> back
> > > into position against no external resistance using the hip, knee, and
> ankle
> > > flexors. Pedaling a bicycle is just a variation of this basic scheme, corresponding most
> > > closely to jogging up a steep hill.
> > >
> >
> > Against no external resistance except the weight of the leg being raised from an almost
> > stationary postion which will be (intuitively) greater than in cycling. The foot is raised and
> > accelerated from zero to twice running speed with every stride as compared to a fairly large
> > conservation of momentum and a constant speed on the upstroke in cycling.
>
> The kinetic energy isn't conserved when pedaling, it is transferred to the pedals. Moreover, the
> leg muscle be accelerated from essentially zero upward velocity at/near BDC to some maximum
> partway through the upstroke, then slows again near the top. IOW, don't confuse nearly constant
> crank angular velocity as meaning that the velocity of the limb segments are constant, as they
> are not.

If kinetic energy isn't conserved when pedaling (AC's words I want everyone to note), then it is not
conserved. It makes no difference whether it is transferred to the pedals or not. AC has only taken
half the equation, the part where the leg slows and assumes this energy is transferred to the
pedals, as it "could" be, although this is hard to visualize when the thigh is slowing in a vertical
direction while the pedal is mostly moving horizontally. Then, where is the energy coming from that
speeds the leg back up again, it cannot come from the pedals except in the case of a fixed gear
bike, so it has to come from the the muscles of the leg. And what do you do in the case of there
being no load on the pedals, when one is just looking at the pedaling motion per se. For energy to
be conserved when pedaling requires a fixed gear bike and substantial variation in pedal speed which
will vary bike speed to keep the energy of the system constant. Doubt that it ever happens in real
life. It can never happen on a bike with a freewheel.

 

[Phil Holman]

"Andy Coggan" <[email protected]> wrote in message
news[email protected]...
> "Phil Holman" <[email protected]> wrote in message
> news:[email protected]...

>
> > 3/Laboratoire des Sciences de l'Activite Physique, Universite Laval, Ste-Foy, Quebec, Canada.
> >
> > The objective of this study was to evaluate the viability of using a single test in which
> > cardiorespiratory variables are measured, to establish training guidelines in running and/or
> > cycling training activities. Six triathletes (two females and four males), six runners (two
> > females and four males) and six males cyclists, all with 5.5 years of serious training and still
> > involved in racing, were tested on a treadmill and cycle ergometer. Cardiorespiratory variables
> >[e.g., heart rate (HR), minute ventilation, carbon dioxide output
> >(VCO2)] were calculated relative to fixed percentages of maximal oxygen uptake (VO2max; from 50
> > to 100%). The entire group of subjects had significantly (P < 0.05) higher values of VO2max
> > on the treadmill compared with the cycle ergometer [mean (SEM)
> >4.7 (0.8) and 4.4 (0.9) l.min-1, respectively], and differences between tests averaged 10.5% for
> > runners, 6.1% for triathletes and 2.8% for cyclists.end Again this contradicts your statement
> > that muscle mass is moot.
>
> No, it does not: the trained cyclists were able to achieve VO2max both while cycling and while
> running uphill on a treadmill, despite the greater muscle mass used in the latter exercise.

In the case of cyclists, they were on average 2.8% lower. Triathletes are 6.1% lower which is even
more significant.

> > The entire group of subjects had significantly (P < 0.05) higher values of VO2max on the
> > treadmill compared with the cycle ergometer.

Phil Holman

 

[Frank Day]

"Andy Coggan" <[email protected]> wrote in message news:<[email protected]>...
> "Frank Day" <[email protected]> wrote in message
> news:[email protected]...
> > "Andy Coggan" <[email protected]> wrote in message news:<
> > > > > It sets the upper limit to aerobic energy production, yes (and
> obviously).
> > > > > However, it isn't the only determinant of endurance exercise
> performance, as
> > > > > I have explained previously.
> > > >
> > > > It only sets the upper limit at that point in time. It doesn't mean VO2 max cannot be
> > > > increased. It is a number. What is the basis of that number? is it cardiac? pulmonary? or
> > > > skeletal muscular limits that set VO2 max? Maybe we should be debating that question. Which
> > > > do you believe to be the limiter that determines VO2 max?
> > >
> > > Personally, I'm more of a subscriber to what's sometimes referred to as metabolic control
> > > theory, or distributed control - this helps you get
> away
> > > from thinking that one thing, and only one thing, limits any particular process. However, if
> > > you look at the overall chain of events involved in
> O2
> > > transport during maximal exercise, there's absolutely no question
> whatsoever
> > > that convective O2 delivery - which is determined by cardiac output and arterial O2 content -
> > > is the primary determinant of VO2max. By
> comparison,
> > > the ability of muscle to accept blood flow and to take up and utilize O2
> is
> > > far, far greater, whereas the lungs, although lacking the same degree of safety margin (if you
> > > will), are also somewhat "overbuilt" for exercise
> (in
> > > most cases).
> >
> > The amount of convective O2 delivery at maximum exercise IS VO2 max.
>
> No, it is not, as there is still some O2 left in mixed venous blood, even during maximal exercise
> (although not very much, even in a trained person).

I guess it depends upon how you define delivery. One could define it as the total oxygen in the
blood "delivered" to the tissues. This is hardly a useful definition as oxygen extraction is never
100% so what does it mean. I chose to define it as the amount of O2 "delivered" to the mitochondria
by the "convective O2 delivery" system. Under that definition, it is.
>
> > I guess that in a fashion could be considered to be the "primary" determinant in VO2 max but if
> > you were my student
>
> Now that's a laugh!!
>
> > I wouldn't accept that answer as showing an adequate understanding of the physiology, you have
> > just regurgitated the definition. What again is the limiter that prevents us from further
> > increasing our VO2 max when we are doing these tests?
>
> How many times do I have to say it before you get it through your thick skull? VO2max is
> (pirmarily) limited by convective O2 delivery, as proven by the fact that if you increase arterial
> O2 carrying capacity (e.g., via EPO administration), you increase VO2max.
>
> > I presume you have excluded the lungs from your answer above
>
> In most cases, yes - but some athletes with relatively high VO2max suffer from arterial O2
> desaturation during maximal exercise.
>
> > (I would agree) so now we are down to the heart or the periphery (local tissue blood dynamics).
>
> To paraphrase Bill Clinton (it was Clinton, wasn't it?): it's the heart, stupid.
>
> > Based upon your explanations I am now no longer looking forward to seeing how Erin Mirabella
> > performs this season on the track as she has changed the emphasis of her training to include
> > PowerCranks.
>
> Helped her a lot this past weekend in Moscow, didn't it? She finished nearly 30th in the points
> race, and could only manage 4th in the pursuit against a less-than-stellar field in a relatively
> slow time even for her.

Surely such results represent the scientific proof of the folly of PowerCranks in the eyes of AC.

>
> > > > > > It makes no sense to me to say VO2 max is limiting and then scale
> it
> > > > > > to body weight. If it should be scaled to anything it should be
> lung
> > > > > > capacity
> > > > >
> > > > > And why, pray tell, is that? Except in special cases, the lungs
> aren't
> > > > > limiting to VO2max, i.e., most (not all) people have no problem
> maintaining
> > > > > arterial O2 saturation even during maximal exercise.
> > > >
> > > > And that is why VO2 max is not limiting to aerobic exercise? Thanks for the argument. If
> > > > arterial oxygenation is maintained during maximal exercise, why do you presume to claim that
> > > > VO2 max is limiting?
>
> You seem to confuse VO2max with the maximal rate of O2 transfer from alveolar air to arterial
> blood. That isn't what it represents.

No, the ability to transfer oxygen across the alveoli is greater than VO2 max. VO2 max happens to be
how much oxygen IS taken up at maximal exercise because that is how much is delivered to the
tissues. It is the definition.
>
> > > > Let us get back to what the limiting organ ireally is. i will accept your argument that VO2
> > > > max limits aerobic exercise performance. What limits VO2 max. The heart or the periphery or
> > > > something else?
> > >
> > > Once again, primarily the heart.
> >
> > Why do you say that? What specifically happens that limits further increases in the hearts
> > ability to pump blood? Does the heart become ischemic (for those of you who are still around and
> > now familiar with the jargon, that means not enough oxygen) and can't generate any more energy?
> > Why doesn't the athlete experience chest pain if the heart can do no more? Give me a
> > physiological mechanism for this limitation.
>
> Even in healthy individuals, you can find evidence that brief ischemia/anoxia may occur during
> strenuous exercise (esp. w/o an adequate warm-up). However, that isn't common, and isn't what
> limits maximal cardiac output. Rather, the heart is simply beating as fast and as powerfully as it
> can - w/ inadequate filling it can beat faster, but cardiac output will be reduced due to a
> decline in stroke volume, whereas increasing filling pressures in an attempt to further increase
> stroke volume is ineffective because the heart is already stretched to its limits (remove the
> pericardium, however, and all bets are off - at least in a greyhound).

I didn't say you couldn't find some evidence of such occuring ever but it is hardly a common
occurance during strenuous exercise and is never the limiter in the healthy individual. The main
change to the heart that occurs with training is an improved ability to relax (which requires energy
to do as I mentioned earlier) which allows increasing stroke volume. If blood flow is restricted to
the heart the one of the main problems that occurs is the inability to relax. In severe ischemia
this can cause what is called a "stone" heart. In the OR, when this happens the heart feels as hard
as a rock and the patient is soon to be dead unless the heart can be induced to relax.
>
> > > > > > > > How do you explain incremental improvements in VO2 max with incremental additional
> > > > > > > > training?
> > > > > > >
> > > > > > > By increases in stroke volume and/or a-vO2 difference (primarily
> the former,
> > > > > > > at least when talking large changes in VO2max....a-vO2
> difference
> > > can only
> > > > > > > increase by ~10%, since during maximal exercise there isn't much
> O2
> > > > > > > remaining in mixed venous blood even in an untrained person).
> > > > > >
> > > > > > Actually, it is mostly a combination of increases in stroke volume
> and
> > > > > > increased heart rate.
> > > > >
> > > > > Sorry, but maximal heart rate goes down, not up, with training.
> Hence, all
> > > > > of the increase in maximal cardiac output - and typically at least
> 50% of
> > > > > the increase in VO2max - is due to the increase in stroke volume.
> > > >
> > > > Possibly, but age goes up with training which is associated with lowered maximum heart
> > > > rates. the top aerobic athletes are not 20 years old but more likely 35. That explains the
> > > > maximum HR connundrum.
>
> Not at all, since the reduction in maximal heart rate that occurs with training happens within
> weeks, if not days, and is readily reversed with just as short a period of detraining.

You are probably right, as I think about it and as i put in another post, this is probably due to
the increased stroke voume that comes with training.