I am sorry, what is the evidence for your mechanism. Do you deny that pH plays a role in cardiac function? Do you deny that the peripheral muscles are producing lactic acid well before the cardiac function levels off? What causes the falling off in ability seen in the graph? Surely if it was just the heart once it reached its maximum ability it would continue to stay there. However, I guess that is an explanation, even though there is no eviddence to support it. A better explanation from the cardiac theorist point of view would be that at very high HR or stroke volume, the valves start to leak, interfering with further forward flow. But, there is no evidence for that theory either, that I know of, even though it gives a real etiology instead of "it just can't do anymore". However, I think my peripheral explanation for making the heart fail makes a lot more sense and there is plenty of evidence to surmise that result.

I don't get what part you don't get. Seems like pretty elementary physiology to me. Everybody sees one graph showing the heart failing to increase CO at high exercise intensities and goes right to "the heart is the limiter" without asking why the heart is failing to increase. Why don't you get out one of those physiology textbooks and see how muscle function varies with pH or CO2. If there is no change (or improvement with significant acidosis) I will eat my words.

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Frank,
An original Ironman and the Inventor of PowerCranks

He already explained the mechanism. Once heart rate increases to a certain point, further increases lead to incomplete filling and decreased cardiac output. So it will level off and then start to decline.

This is M1 stuff.

And the mechanism for that incomplete filling (and evidence for) is?

And, what is that "certain point"? And why is that "certain point" different in Lance Armstrong and you?

M1, indeed.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

Oh, I realize right and left sided outputs basically match...but not necessarily from beat to beat, just from minute to minute...if not, you get either pulmonary edema, various areas of systemic edema, or you're leaking blood somewhere!

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

Engineering is a good tool here. What I would say about the pump's potential and it's fields of possible flow is this: The body has an amazing ability to shut down fields of blood flow in order to meet demands in other areas. Unless the mixed venous oxygen content is lower than the venous oxygen content leaving any particular muscle, the body hasn't used up all of it's available pumping resource to provide a particular muscle with increased blood flow. It's a switching/adjusting the valves at the various fields thing that determines how much blood goes where.

The venous oxygen content in the coronary sinus is about as low as anywhere else in the body...maybe it is the lowest? Does anyone know if the venous content exiting a working muscle group is ever lower than the lowest oxygen content seen in the coronary sinus?

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

Mr. Curious,

As an engineer, what you don't seem to understand that the pump we are talking about is a biological pump, so the efficiency of that pump can vary depending upon the conditions it encounters. Human biological systems have evolved to operate mnost efficiently at a pH of 7.4 with certain optimum concentrations of necessary chemicals (and these optimum concentrations are different both inside and outside the cell). In general, muscle contraction is reduced if any of these optimum parameters is outside of the optimum range. It is why peopole drink water and take electrolytes and glucose and everything else they do to improve performance while competing. Unfortunately, close to VO2 max, the changes are so profound that there is nothing that can be done, at least in my view.

What the cardiac limitation people are saying is the heart is immune to this millieu effect. It doesn't matter to them if the periphery is pumping out acid changing both the pH and the concentration of potassium and all sorts of other things from this optimum range, that as long as the pumping effect of the heart is noticeably less, the heart must be the limiting factor. It is an undergraduate understanding of the system. They spout it because they believe it not because they have evidence to support it, but because that is what they were taught. I am simply trying to get them to give me a good medical (biochemical/physiological) basis to explain the the findings. It is what I was taught (or, AC says it) so it must be right is not sufficient to me. It is very uncomfortable to have ones feet held to the fire.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

yaqui,

I believe you are right, under normal circumstances, the coronary sinus has the lowest paO2 normally. However, the heart never goes anaerobic, except during coronary ischemia or heart attack. The body will always shunt blood, if possible, to protect, first the brain, then the heart.

However, peripheral muscle when it is being exercised anaerobically is extracting the maximum amount of O2 possible from the available blood (the resulting acidosis even helps push more off the hemoglobin). Under these circumstances I would expect the blood exiting these muscles to have less oxygen than the coronary sinus.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

That makes sense, since the coronary muscle doesn't operate anaerobically (I dislike the term "anaerobic"...but at least most people have an idea about what it is supposed to mean), and skeleltal muscle does operate anaerobically: venous blood exiting such an anaerobically operating skeletal muscle could exhibit a lower venous saturation.

It would also make sense that a higher level of oxygen extraction could be achieved in a skeletal muscle (due to the rightward shift of the oxyhemoglobin curve) due to a lower pH that I assume could be found in a skeletal muscle (again, due to it's anaerobic operation capability), compared to the cardiac muscle.

Thanks...

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

The evidence for incomplete filling are all the studies cited in the phys texts I quoted. I don't have the time or inclination to do any more literature reviews tonight. However, you needn't believe those if you go down to the echocardiography lab in your hospital, where you could probably even see it for yourself. That is how it is done. You can only get x amount of fluid though an area of y so fast at physiologic pressures.

I don't know for sure the precise anatomic location where the flow back into the heart limited, so I won't speculate. I will ask my friendly neighborhood cardiologist when I run into him in the ER later, or will check one of those echo texts if I can keep my eyes open.

Why is it that everyone seems to have an "undergraduate" understanding of physiology but you? You malign Coggan, but he *is* fairly well respected in his field, and has published extensively. And the texts I am quoting have been written by people with *lots* of postgrad training, based on papers written by people with as much training. Astrand is the grandfather of sports physiology. But you still persist in this line of physiologic commentary, and still have not provided any support for such.
Citations, please, or give it up. *You* are the one proposing mechanisms that we cannot find literature to support.

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Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!

I didn't realize that the echocardiography lab was imaging patients at VO2 max. I have seen plenty of flowback from valve incompetency from all sorts of pathological conditions. In addition, I have seen "incomplete filling" whatever that means, I assume, less than optimal, from a whole host of reasons from poor filling pressures to incomplete relaxation from inadequate energy sources (as you know, it takes energy to relax, ask your friendly cardiologist about stone heart). However, we are talking about the etiology of the leveling off of the cardiac output curve as the athlete approaches VO2 max.

I still think the best explanation is the less than favorable conditions for optimum cardiac contractility (and, possibly, relaxation) as the peripheral muscles start pumping out lactic acid and the lungs become overwhelmed from the CO2 load and the millieu of the heart changes with both reduced pH and increased potassium, at a minimum.

So, let's accept your explanation that it is incomplete filling. What is the etiology of the incomplete filling? This debate is like blood clotting. We all agree it occurs. What we don't agree on is what is the necessary biochemical or physical precipitating precursor that starts the cascade? Is it in the heart or in the periphery. If in the heart, what is it and what is the evidence? Oh, and why can it change with training?

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

Nonsense, you are obviously well read and it is nice to have a discussion with someone who seems honestly interested in this stuff.

Philbert

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Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!

I would like to keep this on an intellectual and academic footing. I see it as an important issue, not to the ordinary person reading this thread who is incapable of understanding the nuances, but because it has implications for training in the future. Afterall, there are those who say the limit is the heart so it does no good to train additional muscles and PC's are a waste of time, at least from that perspective. So, what is the evidence to support that opinion? I see it as flakey at best.

If the heart is the main cuprit preventing people from going beyond VO2 max, ask your cardiologist friend this: Why can't someone just mentally tough it out and continue exercising those peripheral muscles, and eventually kill himself as the effort keeps going up and the cardiac function keeps going down? What is to stop him? If the heart is the problem, it should be possible and, in fact, watching the number who collapse at the finish line, should be common. I have never heard it happen in the absence of an arrhythmia. Neither have you.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

Bitey wrote: "This is M1 stuff."

Bitey, I don't know if you are a medical student or not, but if you are, a word of advice from someone who has been around the block once or twice, or more. You and your patients will be much better off in the future if you can develop a sense of humility for how much you don't know over that sense of pompousness for what you think you do. And, don't be afraid to question the basis of anything and don't be upset if someone questions your basis. Sometimes the best you can answer is "that is what I was taught". Anyhow, if you are not afraid to continue to ask a lot of questions, someday you will probably be pretty good.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

Philbert,

Ask your cardiologist friend this: Say he has a patient in shock and, as is typical of shock, cardiac function is compromised. Does he care if the etiology is cardiogenic shock (heart is primary etiology), septic shock, hemorragic shock, anaphylactic shock, or any of many other etiologies when he goes to treat the patient?

The principle to take from this common connundrum is the simple fact that even though we may know that cardiac output and/or cardiac function is compromised does not mean the heart is the main problem. It may be, but we need more data to draw the right conclusion. That is the basic error I believe many are making in interpreting the experimental data in this instance.

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Frank,
An original Ironman and the Inventor of PowerCranks

 
Frank shows a clear lack of understanding in relation to exercise physiology, not just in relation to limiting factors in endurance exercise, but other basic principles. i've corresponded but with Frank on two separate occasions and the first one, which was several years ago showed a complete lack of understanding of exercise physiology, as Frank was unaware that lactate was present at all times, except when people have McArdle Syndrome. Frank wasn't even aware what McArdle Syndrome was.

Within that first correspondence Frank was adamant about the 40% increase in power with Power Cranks. I assume he still sticks with this Frankly (!) ridiculous claim. As i pointed out to him then, and as anyone with inkling of power output knowledge will tell you a 40% increase in power would take me from average to being a World class contender at the TdF... And, that really isn't going to happen! If there was any improvement then people such as Museeuw who are using them would be winning the TdF, and not just 'limited' to the Classics

At the same time Frank mentioned that some triathletes (i can't recall the names or whether that was omitted) were using the Cranks and were going to break the World Hour Record.... (and take the cycling world by storm).

Indeed, if the Cranks gave a 40% improvement in power or even a number of 50% or 25% of this 40% then the performance increments would be obvious and everyone would want them (in a similar manner to how people recognise that rH-Epo gives a huge performance increase).

Franks stand on physiology is interesting, and fits the bill of Quack Watch. You'd have thought that Frank would have written at least one text in relation to cardiac physiology as it's so different from everything else out there. According to Frank everyone else is wrong (on cardiac output and pedalling mechanics). For anyone interested in the physiology, an excellent read is Limiting factors for maximum oxygen uptake and determinants of endurance performance. Bassett and Howley (2000).

Caveat emptor

Ric

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http://www.cyclecoach.com

 
I would like to keep this on an intellectual and academic footing. I see it as an important issue, not to the ordinary person reading this thread who is incapable of understanding the nuances, but because it has implications for training in the future. Afterall, there are those who say the limit is the heart so it does no good to train additional muscles and PC's are a waste of time, at least from that perspective. So, what is the evidence to support that opinion? I see it as flakey at best.

If the heart is the main cuprit preventing people from going beyond VO2 max, ask your cardiologist friend this: Why can't someone just mentally tough it out and continue exercising those peripheral muscles, and eventually kill himself as the effort keeps going up and the cardiac function keeps going down? What is to stop him? If the heart is the problem, it should be possible and, in fact, watching the number who collapse at the finish line, should be common. I have never heard it happen in the absence of an arrhythmia. Neither have you.


=====================================

The limiting factor with the PC idea is not medical, it
is time. Just as with ANKLING, as cadence increases
your extra muscles do not have sufficient time to do
all that is required for effective power contribution and trying to use them can eventually be more of a
hindrance than a help. I cannot see a PC user
producing more power than the perfect ANKLER.

ahhh yes.

dr testa, who needs no introduction as to pamares or experience/results/knowledge after direct work with PC's and the best cyclists in the world on them sez " “It’s something that nothing else forces you to do and it makes you do work that is without a doubt of benefit.”

but r stern, ( whoever the F he is ) and a gaggle of other similar self-impressed yayhoos with no such experience - not even close in any sense of the word - other than perhaps a stunning BS or MS degree in exercise disagree.

whatever.

ahhh, but what about the capillaries ability to diffuse an ion concentration against a deformative gradient. The neuron will not fire across a synaptic gap given the myelin sheath has been deprived of lactate inhibitors. Thus when muscles are contracting, the myosin and actin relationship has therefore been compromised due to anaerobic inhibition obviously brought on by glycogens inability to convert to ATP under mitochondrial stress brought about by hormonal fluctuations in the sphincter muscle. My proctologist told me all of this over lunch.

I've been avoiding this thread for several days, but this morning I took my punishment and went through it. My summary:



- 301 posts and I would guess Frank and Rip contributed 70% of them (~210 posts)

- ~90 posts by other people weighing in on everything from red shoes to diarrhea.

- Lots of reasons why PCs can’t work, the majority, of course by Rip. Reasons why they do mostly by Frank.

- Absolutely no posts from anyone who has bought PCs and either found them not to work, or were totally disgusted with PCs, or even merely mildly unhappy, let alone comments that they weren’t worth the money. Similar (identical) pattern in other PC threads. For this forum, I think that speaks volumes.

- Not to say that there weren’t comments that PCs don’t work, weren’t worth the money, and weren’t happy with them. However, it appears that every individual who made these comments has never ridden PCs. The possible exception is the rather enigmatic Ken Willet who won’t clearly acknowledge or deny he has rode/bought/fondled PCs and won’t state experience of said riding (or fondling). One feels that there is considerable underlying politics going on, but being relatively new to the forum (March of this year), I haven’t got a clue. Mr. Day does have a tendency, as evident in other threads, of excessive handwaving and shooting from the hip. I could be gracious and chalk it up to the symptoms of a busy individual, not an uncommon trait in this population (i.e. triathlete culture). However, it is a trait that can and readily does annoy some people

- I get the impression there are people who bought the PCs but didn’t stay with them. Nothing really new there. Any idea of the number of people who buy health club memberships and never go after the first three months (as an example, please don’t debate the specifics e.g. 2 months vs 4 months, yada yada yada.)

- Good science and good scientists repeat other people’s work to verify and validate for themselves. Rip seems to have ample opportunity to borrow PCs and evaluate for himself. Not evaluating the cranks considerably weakens his argument for me. I appreciate the time available to invest argument, however, for someone who has spent this much time arguing against PCs in this and other threads, that argument does not hold a microliter of water.



Full disclosure: I do not own PCs, I have not tried PCs. I have not seen the PC website (I believe there is one based on the thread.) I hate one legged spin drills (only started them this past winter and can only go about a minute and a half per leg).



Gotta go do my 6 hr ride so I can think of my most favorite movie line.

Cheers.

Parke

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Behold the turtle! He makes progess only when he sticks his neck out. (James Bryant Conant)
GET OFF THE F*%KING WALL!!!!!!! (Doug Stern)
Brevity is the soul of wit. (William Shakespeare)

Who gave you the right to come in here and make such good, common sense? Don't you realize you may spoil the whole thing with comments like this?

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

Ric,

Sorry my knowledge is incomplete esp as regards McArdle sydrome. Never have claimed to have absolute knowledge of every aspect of physiology and medicine. Whether lactate is present in small quantities at all times is irrelevant to my argument here. If it is in small enough quantities that the body can compensate then the body can compensate. The issue is what is the lactate doing to the body as a whole when at or near VO2 max? Anyhow, your comments that my knowledge of McArdles syndrome is lacking doesn't answer the question at hand, what is the underlying mechanism causing the "heart failure" at VO2 max.

Sorry you think my 40% power increase (in the typical user) is rediculous. Yes, I still claim it. The hour record guy actually posts here once in awhile. Maybe he will read this and explain himself. I only reported what he told me he thought he could do and was going to try to do.

Anyhow, it takes substantial time to see bigimprovements at the Museeuw level and it isdifficult for them to put in the time necessary and still keep the mileage up for racing (which is what they are paid to do). I am just happy that those who try them at this level, generally find them useful.

It is clearly reasonable for someone to say they don't work because they haven't seen the expected records. Yaqui and Goat boy and Phil Holman, who have seen the expected results (or something similar), weren't at an age or level to set those records. But, most of my customers who are shelling out good money aren't at the Museeuw level. In fact, that is the case with most bicycle products. Anyhow, I expect those records to still happen but, it looks like we will all hove to wait. Some of you think we will be waiting forever. We will see.

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Frank,
An original Ironman and the Inventor of PowerCranks

Hey, last week I noticed I responded to 4-5 threads and killed them in the process. I was only hoping....

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Behold the turtle! He makes progess only when he sticks his neck out. (James Bryant Conant)
GET OFF THE F*%KING WALL!!!!!!! (Doug Stern)
Brevity is the soul of wit. (William Shakespeare)