What determines efficiency ???

Fday said:

Wrong, Luttrell demonstrated the ability to improve cycling efficiency

But the Luttrell study provides no data re. possible mechanisms. It would therefore be relevant to the discussion at hand (and the Discussion of Coyle's paper) if Armstrong had used PowerCranks.

Quoted post said:

a greater amount than Armstrong improved his in only 6 weeks. Of course, he wasn't dealing with world class athletes. Such an improvement is unlikely from changing fibre type (since it occurred in only 6 weeks)

The half-life of the myosin protein is measured in days, so significant changes in fiber SUB-type that could contribute to an improvement in efficiency can indeed happen in just a few weeks. (Of course, since Luttrell did little or nothing to accomdate the subjects to the laboratory setting, the improvement in efficiency may not even be real.)

Quoted post said:

the mechanism for the improved efficiency was not invesitgated by Luttrell (he was just trying to see if it changed), it did change so there must be another possible mechanism

As you admit, the Luttrell study did not collect any data that would shed light on possible mechanisms, so why should it have been cited? To do so would have been the epitome of speculation!

Quoted post said:

Why doesn't every pro improve their efficiency every year as they keep piling on the miles.

How do you know that they don't? Certainly, the performance of cyclists (and other endurance athletes) tends to continue to improve long after VO2max and LT have plateaued.

Quoted post said:

Even Coyle remarked right before he goes into his change in fibre type hypothesis that the reasons for this changes as well as "the stimuli that provoked this adaption" are unclear. If they are so unclear to Coyle, why are they so clear to you?

I would have written what Coyle wrote: the mechanisms responsible for Armstrong's apparent (I would have tossed that word in since this was an unplanned, uncontrolled case study) are unclear. That said, it certainly is possible to put forth a plausible hypothesis, i.e., that it was the result of a gradual change in myosin expression.

Quoted post said:

An 8-9% in efficiency in a world class athlete? Show me a single example of another world class athlete where such changes have been documented over any period of time. Better yet, show me a single example where such changes have been documented and there is muscle biopsey data to prove that the changes occurred from changing muscle fibre type.

Now you're arguing in circles: the reason that Coyle's data was of sufficient interest to be published is because data on world class athletes (esp. of Armstrong's stature) are lacking. IOW, it's very uniqueness is what made it worthy of publication.

Quoted post said:

I don't disagree that this is a plausible hypothesis

Then what are you whinging on about???

Quoted post said:

and that, at least, some of his improvement might be explained in this way. What bothers me is Coyle himself stated the reasons for this change are unclear then he puts forth this hypothesis

But ypu have no right to be bothered: Coyle was fully within his rights as an author to write his Discussion the way he did.

Quoted post said:

, without any supporting data to suggest it actually has a basis in fact,

The supporting data that makes Coyle's hypothesis plausible are properly cited in the Discussion.

Quoted post said:

(ignoring the fact that other riders who have trained similarly to Lance, at least mileage and intensity wise have failed to improve similarly)

Again, how do you know that other individuals also don't experience gradual improvements in cycling efficiency when prolonged and intense trainng is performed for years on end? I certainly have, despite the fact that 1) I was biased towards the slow-twitch side from the git-go (thus minimizing the potential for further changes, and 2) I never trained as much as someone like Armstrong did. Furthermore, the fact that VO2max and LT tend to reach a plateau after just a few years of trraining, yet performance doesn't peak (for men) until they are in their late 20s or early 30s provides indirect evidence that efficiency continues to improve over time in any endurance athlete who "keeps their nose to the grindstone".

Quoted post said:

and ignored other potential explanations such that the world now thinks that this in fact occurred in Lance.

That's the world's fault, not Coyle's.

Quoted post said:

My problems with the paper stand.

Unfortunately for you and your business, your opinion of Coyle's paper counts for naught to members of the scientific community.

acoggan said:

But the Luttrell study provides no data re. possible mechanisms. It would therefore be relevant to the discussion at hand (and the Discussion of Coyle's paper) if Armstrong had used PowerCranks.

Approximately 20-25 people have told us that Lance did use PC's in training. Of course, we have no proof. When asked (such as the example I gave earlier) he has never admitted same but he has also never denied it. If he did use them, he didn't get them from us (although we did provide many of his training partners with them in the very early days). That being said, I think it is a smoke screen for this discussion because it is clear to me that it is possible (albeit very hard) to learn to pedal in the PC fashion (or, perhaps, some other more efficient fashion) without training with PC's - it is just a lot harder. So, perhaps Lance improved his efficiency, to an amount that Coyle found remarkable, in some other way other than PC's. Wouldn't you like to know how he did it?

Quoted post said:

The half-life of the myosin protein is measured in days, so significant changes in fiber SUB-type that could contribute to an improvement in efficiency can indeed happen in just a few weeks. (Of course, since Luttrell did little or nothing to accomdate the subjects to the laboratory setting, the improvement in efficiency may not even be real.)

Do you mean we should be able to turn a world class sprinters legs into those of a world class marathoner in "days" if we can find the proper stimulation to change those fibers? Wow!!! Do you have a reference for that? Maybe there is hope for me on the basketball court, maybe I can learn to jump more than 6 inches off the ground.

If failure to "accomodate to the laboratory" was the supposed reason his study resulted in such improvement, why didn't it occur to the control group? So, maybe Luttrell's noted improvement in efficiency is not real, but until his experiment is repeated and proven to be flawed, the data exists and has been published. Scientists found a need to reproduce the "cold fusion" experiment when that result was published because it was published for two reasons. 1. it might be true and if it were it would require basic changes to all sorts of theories and, 2. if it isn't true it should be debunked asap.

Quoted post said:

As you admit, the Luttrell study did not collect any data that would shed light on possible mechanisms, so why should it have been cited? To do so would have been the epitome of speculation!

It did not need to be cited. However, it is part of the milleau of knowledge that suggests that other mechanisms might exist to explain efficiency gains such that, if this was known about, one has to wonder why Coyle chose this one mechanism (changing fibre type) as the only one to wax on about when he already stated he didn't know how the improvement occurred.

Quoted post said:

How do you know that they don't? Certainly, the performance of cyclists (and other endurance athletes) tends to continue to improve long after VO2max and LT have plateaued.

Show me the data. I am sure Lance is not the only cyclist who has been followed for many years. I mean, if such improvements are commonplace, why on earth did Coyle comment on Lance's improvement and state he didn't know what the stimulus was to cause it to occur?

Quoted post said:

I would have written what Coyle wrote: the mechanisms responsible for Armstrong's apparent (I would have tossed that word in since this was an unplanned, uncontrolled case study) are unclear. That said, it certainly is possible to put forth a plausible hypothesis, i.e., that it was the result of a gradual change in myosin expression.

I don't have any objection to such a statement. I would have an objection to that being the only hypothesized possible mechanism. And, Why would you hypothesize it was a gradual expression? Above you stated such changes can occur in days.

Quoted post said:

Now you're arguing in circles: the reason that Coyle's data was of sufficient interest to be published is because data on world class athletes (esp. of Armstrong's stature) are lacking. IOW, it's very uniqueness is what made it worthy of publication.

I concur. What bothered me about the paper was the discussion. The data itself is very valuable. As I said, I think it gives evidence that can explain Lance's domination for all those years with resorting to drugs. Lance was able to improve his efficiency when others were not able to. It should lead researchers to try to figure out how he did so. No one seems the least bit interested. I guess they think they already know.

Quoted post said:

Then what are you whinging on about???

Becuase the discussion was incomplete and has led unsophisticated (most) readers to conclude this "is" the only plausible explanation. It is not.

Quoted post said:

But ypu have no right to be bothered: Coyle was fully within his rights as an author to write his Discussion the way he did.

Of course he was, just as I have a complete right to criticize (be bothered by) what he did not say.

Quoted post said:

The supporting data that makes Coyle's hypothesis plausible are properly cited in the Discussion.

Yes. Except, like I said above, if this mechanism were in play such changes should be commonplace in almost all professional cyclists. I am not aware of any data to suggest it is. Are you?

Quoted post said:

Again, how do you know that other individuals also don't experience gradual improvements in cycling efficiency when prolonged and intense trainng is performed for years on end? I certainly have, despite the fact that 1) I was biased towards the slow-twitch side from the git-go (thus minimizing the potential for further changes, and 2) I never trained as much as someone like Armstrong did. Furthermore, the fact that VO2max and LT tend to reach a plateau after just a few years of trraining, yet performance doesn't peak (for men) until they are in their late 20s or early 30s provides indirect evidence that efficiency continues to improve over time in any endurance athlete who "keeps their nose to the grindstone".

Hey, show me the data? The book "Bicycling Science" by Whitt and Wilson, which has examined much of the data regarding cycling efficiency certainly does not remark on this. If they did, I missed it.

Quoted post said:

That's the world's fault, not Coyle's.

Coyle contributed to it. If he had only written, "one possible explanation, albeit there might be others, is . . ." I would have had no problem with his discussion. He did not. I found his discussion, for someone of his stature, and for such an important finding, woefully lacking.

Quoted post said:

Unfortunately for you and your business, your opinion of Coyle's paper counts for naught to members of the scientific community.

If you say so.

john979 said:

Please provide peer-reviewed evidence.

The "peer reviewed" evidence can be found in books throughout the world. This third style was demonstrated and studied (peer reviewed) for about 15 years during the fifties and sixties and the general consensus was that it was the most stylish and most powerful of all time trial pedalling styles, the like of which had never been seen before and has not been seen since. Like the Fosbury flop, when you have the perfect style the results supply the evidence, no scientific evidence is required. But unlike Armstrong's ? , the explanation for Anquetil's power is easily explained, max power through 12 o'c and the ability to combine upper and lower body muscles and all of this from a simple change in the pattern of power application to the pedals.

n crowley said:

The "peer reviewed" evidence can be found in books throughout the world. This third style was demonstrated and studied (peer reviewed) for about 15 years during the fifties and sixties and the general consensus was that it was the most stylish and most powerful of all time trial pedalling styles, the like of which had never been seen before and has not been seen since. Like the Fosbury flop, when you have the perfect style the results supply the evidence, no scientific evidence is required. But unlike Armstrong's ? , the explanation for Anquetil's power is easily explained, max power through 12 o'c and the ability to combine upper and lower body muscles and all of this from a simple change in the pattern of power application to the pedals.

Please provide the exact references that I can examine. Title, year, author, publisher, ...

john979 said:

Please provide the exact references that I can examine. Title, year, author, publisher, ...

Don't holdyour breath. I have been trying to understand what he his talking about for years without success. He may be on to something but he sure cannot communicate what it is all about in terms I understand.

Fday said:

Don't holdyour breath. I have been trying to understand what he his talking about for years without success. He may be on to something but he sure cannot communicate what it is all about in terms I understand.

That does not surprise me, first you have got to understand and explain where the advantages of your own expensive equipment lie, maybe then you will get a better understanding of the technique which I refer to. In both cases the advantages can be got from the same source, mental concentration instead of stomping blindly on the pedals but in your case PC's force a rider to do what could be done naturally if he knew what his objective was.

Speaking of efficiency, I just read a newspaper article reporting that according to an article published in Nature Genetics all ancient humans possesed a "sprint" gene responsible for promoting fast twitch muscle development by producing alpha-actin-3 protein in fast twitch muscle fibres. Apparently all sucessful sprint runners have this gene, but a small percentage of the population, approximately one in five have an inactive gene which ends up biasing the person towards slow twich fibre production. Apparently the inactive gene spread amongst asians and europeans during the last ice age 15-30,000 years ago as it was an advantage to have more efficient muscles in a period of restricted food supply.

The scientists in the stude created mice without the inactive gene and found they could run 1/3 as long as normal mice and had a more efficient metabolism.

Here it is in full

Endurance, not speed, key to spread of human race

Sydney Morning Herald, Date: September 11 2007

Deborah Smith Science Editor

MANKIND's switch from sprinter to endurance runner began in earnest in Europe and Asia during the last Ice Age, Sydney scientists have discovered.

And the explanation could be that having more efficient muscles helped people survive the cold, harsh climate when they moved to areas outside Africa.

Kathryn North, of the Children's Hospital at Westmead, said a common genetic variation influenced whether people were "sprinters or stayers".

All Olympic sprinters tested so far have an active form of a gene, which produces a protein called alpha-actinin-3 in the fast-twitch muscle fibres responsible for explosive bursts of power.

About 99 per cent of African people still have this original sprinters' gene, she said. "It's the normal ancestral state."

More than a billion people worldwide, however, have an inactive version of the gene and do not produce the muscle protein, Professor North has estimated.

This includes one in five Australians,she said.

This inactive version of the gene is more common among endurance athletes such as marathon runners and rowers, her team has shown.

For their latest study the researchers wanted to find out when the endurance version of the gene became so common, and what was the evolutionary advantage of losing the sprint gene.

They created mice without the gene and discovered they could run for about a third as long as normal mice with the sprint gene before becoming exhausted. They also found their muscle metabolism was more efficient.

To put a date on the spread of the inactive endurance version of the gene the team analysed DNA samples from 96 people from around the world.

The results, published in the journal Nature Genetics, showed the inactive form of the gene began to rapidly increase in frequency in Europeans and Asians about 15,000-33,000 years ago, during the last Ice Age.

Professor North said that having the endurance gene and more efficient muscles could have been an advantage in a cold climate where food was scarce. "It may have allowed them to adapt to the more hostile environments of Eurasia."

She said that having the inactive form of the gene might not be a benefit now. In a world where food is plentiful and fewer people exercise, slower muscle metabolism could possibly contribute to obesity.

Here's an oldie, but goodie.

Dr. Coggan is right about mysosin expresion. It could happen in just a matter of weeks. I endorse pretty much what Dr. Coggan said.

I have only look at Luttrel´s abstract and see that the study has several drwabacks:
1. The n (number) is very low.
2. There are no statistical significant differences
3. There is no biochemical/histological data.

As Coggan said, it is feasible to improve efficiency even long after your VO2max and LT have reached a plateau. I see that ALL the time with professional cyclists. As he said, an additive accumulation in kilometers year after year after year will lead to dramatical changes. I have seen more than 10% increases in efficiencies in pros I have followed throught years. Actually that is quite common...Anyone working with pros could tell you.

I also would like to say that very few cyclist train so well and so smart as Armstrong did. I have worked with 5 Pro Tour teams (well, 2 Pro Tour teams since Pro Tour birth and 3 former Cat 1 Pro Teams) and I have seen and tested hundreds of cyclists and as a guess, and it is a bit of a shame, about 75% of pro cyclists, in my opinion, don´t train well, or at least near as well as Armstrong did. On top of that we have to considered that Armstrong was already a genetically gifted cyclist before cancer. I have argued many times over this issue with many pro cyclists who where linking Armtrong´s amazing improvement in performance to drugs. I always argued to them that at the age of 21 y.o. Lance was already world champion in one of the toughest WC in the last years with Riis and Indurain behind him. I always asked cyclists to name me how many cyclists nowadays can be a WC at the age of 21??. I can´t think of any name, neither they do....then most pros just won´t continue arguing...
Also Armstrong lost about 7Kg of upper muscle mass wich it is just huge and probably only possible due to an extreme catabolism caused by cancer (isn´t that ironic?).

On the other hand I believe that there has been a lack of talented cyclists, both physiological and psychologically speaking, during Armstrong´s era which have made him his way to win the tour just easier. I have tested 3 TdF podium riders accompaining Armstrong at the podium during his 7 tour wins and although they may get mad at me, and they have very good physiological potential, I was not that impressed by their intelligence and the way they trained... (defenetely and by far near as smart and good as Lance) and I am sure that he would have won 2007´s TdF if he wanted as well since, in my opinion has probably been the TdF with the lowest level in the last decade. Lance was not only the best gifted cyclist, but the smartest at knowing his physiology as well. He pretty much did not need a coach because he knew more about coaching than most coaches.

About Coyle´s study about Lance evolution why not doing it on such an amazing cyclist like Armstrong?. I think it is really plausible. If others publish simple papers with college students...why not a paper about the evolution of one of the greatest cyclists of all times?.
As Coggan said, there is not much data published with world class cyclists...in part due to the lack of time to publish that people working with world class athletes have (🙁 ). Believe me, it is frentic out there working with the pros...

About inprovements in efficiency I would like to add changes at the cellular level, not only about fiber type composition. There are important events, regardless of fiber type composition, occuring at the cellular level and independent of oxygen uptake. It brings up to my mind the "controversial" lactate shuttle mechanisms proposed by Brooks, both cell-cell and intracellular lactate shuttles. I believe that many of the adaptations at the cellular level go in that direction as well as in changes in fiber type composition and energy fuel utilisation and economy.

Urkiola2 said:

Dr. Coggan is right about ....<snip>

A really interesting post, thanks for that. Some really good quotes in that lot.

Hope the spam doesn't drive you away!

Urkiola2 said:

As Coggan said, it is feasible to improve efficiency even long after your VO2max and LT have reached a plateau. I see that ALL the time with professional cyclists. As he said, an additive accumulation in kilometers year after year after year will lead to dramatical changes. I have seen more than 10% increases in efficiencies in pros I have followed throught years. Actually that is quite common...Anyone working with pros could tell you.

Which is good news for many of us with consideration of genetics in the discussion as Armstrong being the prime example and most everyone else falling somewhere below that point.

I have experience in training in strength related sports both naturally and with AAS. While using PED'S, I would guess that I have never had more than a 10% gain while on a cycle period of AAS. Yet even a 3% gain in a field of equally genetic gifted athletes can be enough edge to win.

A few years after retiring from competition I wanted to see if I could take my expanded training knowledge and apply it with my genetics and see if it would be possible to reach a strength related goal in a natural state that I had reached on almost every cycle of drug use. Over a slightly longer training period (longer since I could not sustain the training load when compared to the enhanced recovery period while using AAS) I did eventually reach and exceed that goal which surprised me greatly. The difference was my training knowledge at that point had much more depth than in earlier years. The drugs with less training knowledge gave me xx% gain, but the expanded training knowledge along with understanding my genetic limitations also gained me a near equivalent xx% gain. So based on my own personal experiences in a different type of training environment I am a believer that it is possible to continue to progress with the broadened training knowledge applied to a persons genetic limitations for recovery.

I have used this information to try to convince some local athletes (in strength training) not to cross the line of temptation of using drugs when they feel they have hit a plateau. That there may something else that can be tweaked to gain just a bit more without crossing that line.

Urkiola2 said:

Dr. Coggan is right about mysosin expresion. It could happen in just a matter of weeks. I endorse pretty much what Dr. Coggan said.

I have only look at Luttrel´s abstract and see that the study has several drwabacks:
1. The n (number) is very low.
2. There are no statistical significant differences
3. There is no biochemical/histological data.

As Coggan said, it is feasible to improve efficiency even long after your VO2max and LT have reached a plateau. I see that ALL the time with professional cyclists. As he said, an additive accumulation in kilometers year after year after year will lead to dramatical changes. I have seen more than 10% increases in efficiencies in pros I have followed throught years. Actually that is quite common...Anyone working with pros could tell you.

[could you clear something up here? I understand how Vo2max is measured in terms of the rate of oxygen consumption and then scaled to body mass. But for measurement of LT ... isn't it a fixed lactate concentration (or an increase over baseline) with output power as the other variable? very sorry for my poor wording here but if power is part of the determination of the LT point, how do you separate efficiency out of the equation? Or in other words, how do you 'know' what change in power is due to changes in LT and what is due to changes in efficiency?

Hmmm ... or do you measure efficiency at Vo2max oxygen rate and with power measured there and infer what's happening at the LT level???

For the average person on their bike, they don't have access to Vo2 measurements nor accurate lactate measurements so this is more of an academic question. Increased sustainable power on the road is proof enough.]

I also would like to say that very few cyclist train so well and so smart as Armstrong did. I have worked with 5 Pro Tour teams (well, 2 Pro Tour teams since Pro Tour birth and 3 former Cat 1 Pro Teams) and I have seen and tested hundreds of cyclists and as a guess, and it is a bit of a shame, about 75% of pro cyclists, in my opinion, don´t train well, or at least near as well as Armstrong did. On top of that we have to considered that Armstrong was already a genetically gifted cyclist before cancer. I have argued many times over this issue with many pro cyclists who where linking Armtrong´s amazing improvement in performance to drugs. I always argued to them that at the age of 21 y.o. Lance was already world champion in one of the toughest WC in the last years with Riis and Indurain behind him. I always asked cyclists to name me how many cyclists nowadays can be a WC at the age of 21??. I can´t think of any name, neither they do....then most pros just won´t continue arguing...
Also Armstrong lost about 7Kg of upper muscle mass wich it is just huge and probably only possible due to an extreme catabolism caused by cancer (isn´t that ironic?).

On the other hand I believe that there has been a lack of talented cyclists, both physiological and psychologically speaking, during Armstrong´s era which have made him his way to win the tour just easier. I have tested 3 TdF podium riders accompaining Armstrong at the podium during his 7 tour wins and although they may get mad at me, and they have very good physiological potential, I was not that impressed by their intelligence and the way they trained... (defenetely and by far near as smart and good as Lance) and I am sure that he would have won 2007´s TdF if he wanted as well since, in my opinion has probably been the TdF with the lowest level in the last decade. Lance was not only the best gifted cyclist, but the smartest at knowing his physiology as well. He pretty much did not need a coach because he knew more about coaching than most coaches.

About Coyle´s study about Lance evolution why not doing it on such an amazing cyclist like Armstrong?. I think it is really plausible. If others publish simple papers with college students...why not a paper about the evolution of one of the greatest cyclists of all times?.
As Coggan said, there is not much data published with world class cyclists...in part due to the lack of time to publish that people working with world class athletes have (🙁 ). Believe me, it is frentic out there working with the pros...

About inprovements in efficiency I would like to add changes at the cellular level, not only about fiber type composition. There are important events, regardless of fiber type composition, occuring at the cellular level and independent of oxygen uptake. It brings up to my mind the "controversial" lactate shuttle mechanisms proposed by Brooks, both cell-cell and intracellular lactate shuttles. I believe that many of the adaptations at the cellular level go in that direction as well as in changes in fiber type composition and energy fuel utilisation and economy.

....

Three quick points:

1. How are intracelluar adaptions trained- if cells don't live that long, barring genetic therapy how can what happens at the celluar level be modified over the long term, other than than as a result of external changes- ie a change in the environment in which an individual cell operates?

2. If changes in fibre composition can be achieved relatively quickly, why do we see much longer term efficiency increases in elite athletes, such as shown in the study quoted. Is there a short and long term mechanism for the same adaption or two seperate adaptions being responsive to short and long-term stimuli respectively? What is actually going on??

3. If position changes affect efficiency, then this would be a result of biomechanical changes, as in different muscles being recruited at different loads over different ranges of movement. If this is the case then other changes, such as to pedalling style or systems which alter the pattern of force application and muscle recruitment may change efficiency too, although not necessarily for the better. But if there is a correlation, then efficiency improvements may be possible if ones current position and pattern of force recruitment are less than ideal.

This article gives a good treatment of the subject:

pubmedcentral.nih.govarticlerender.fcgiOpen ↗

Still interested in the biomechanical aspect of efficiency variability. Will have to check the references in the article.

11ring said:

This article gives a good treatment of the subject:

pubmedcentral.nih.govarticlerender.fcgiOpen ↗

Still interested in the biomechanical aspect of efficiency variability. Will have to check the references in the article.

bump

Felt_Rider said:

Which is good news for many of us with consideration of genetics in the discussion as Armstrong being the prime example and most everyone else falling somewhere below that point.

I have experience in training in strength related sports both naturally and with AAS. While using PED'S, I would guess that I have never had more than a 10% gain while on a cycle period of AAS. Yet even a 3% gain in a field of equally genetic gifted athletes can be enough edge to win.

A few years after retiring from competition I wanted to see if I could take my expanded training knowledge and apply it with my genetics and see if it would be possible to reach a strength related goal in a natural state that I had reached on almost every cycle of drug use. Over a slightly longer training period (longer since I could not sustain the training load when compared to the enhanced recovery period while using AAS) I did eventually reach and exceed that goal which surprised me greatly. The difference was my training knowledge at that point had much more depth than in earlier years. The drugs with less training knowledge gave me xx% gain, but the expanded training knowledge along with understanding my genetic limitations also gained me a near equivalent xx% gain. So based on my own personal experiences in a different type of training environment I am a believer that it is possible to continue to progress with the broadened training knowledge applied to a persons genetic limitations for recovery.

I have used this information to try to convince some local athletes (in strength training) not to cross the line of temptation of using drugs when they feel they have hit a plateau. That there may something else that can be tweaked to gain just a bit more without crossing that line.

Good point!. I totally agree wuth you!.🙂

11ring said:

Three quick points:

1. How are intracelluar adaptions trained- if cells don't live that long, barring genetic therapy how can what happens at the celluar level be modified over the long term, other than than as a result of external changes- ie a change in the environment in which an individual cell operates?

2. If changes in fibre composition can be achieved relatively quickly, why do we see much longer term efficiency increases in elite athletes, such as shown in the study quoted. Is there a short and long term mechanism for the same adaption or two seperate adaptions being responsive to short and long-term stimuli respectively? What is actually going on??

3. If position changes affect efficiency, then this would be a result of biomechanical changes, as in different muscles being recruited at different loads over different ranges of movement. If this is the case then other changes, such as to pedalling style or systems which alter the pattern of force application and muscle recruitment may change efficiency too, although not necessarily for the better. But if there is a correlation, then efficiency improvements may be possible if ones current position and pattern of force recruitment are less than ideal.

Sorry about answering back to the post. I have been pretty busy this week (testing time!..everyone wants to get ready for the season!).
Thanks for the link!. Very interesting!.
The paper is based on cycling efficiency which according to Donovan and Brooks is a measure of the body's effectiveness in converting energy from nutrients into external work. However I believe we can qualify efficiency in more different ways, although the effectiviness in utilizing fuels (CHO and FAT) is extremely important. But efficiency can also be as you point out related to biomechanical effectiviness. There could be important changes in cycling efficiency depending on the bike position, especially during time trials. Also Cycling efficiency could be the ability of oxidize (wash out) lactate and therefore accumulate less lactate in muscle and blood.

I believe you adress very good and challenging questions.
At the cellular level there seem to be more events happening as well as adaptations other than just mitochondrial density increases or fiber type composition. I believe the short-life of myocites (muscle cells) could be changed despite of their short-life due to changes in mRNA expression (change of "factory pattern"😉 in those cells. Other important changes are the increase in MTC´s (Metacarboxylate Transporters) for lactate. MCT1 are typical of Type I muscle fibers and responsible to transport lactate in those fibers. MCT4 are typically linked to more glycolytic fibers (Type IIa and IIb). This has to be with the cell-cell lactate shuttle proposed by Brooks. There is an increase in mRNA expression as well as MCT1-4 production in muscle fibers after a short period of adaptation to exercise, so you will have changes almost from the start.
On the other hand. we can find changes in isoform change of LDH (lactate Dehydrogenase) enzime, which is in charge of oxidizing lactate back to pyruvate as well as reducing pyruvate to lactate. LDH 1-2 are more typical of Type I fibers and tend to oxidize lactate into pyruvate and LDH 4-5 more typical of glucolytic fibers (Type IIa and IIb) and tend to reduce piruvate to lactate. It has been proposed an isoformic change in LDH 4-5 to LDH 1-2 in muscle fibers due to endurance training.

Another player is mLDH (mitochondrial LDH) which also regulates red-ox (reduction-oxidation) status inside the mitochondria and could have an important roll in oxidazing lactate to piruvate. Hashimoto, from Brooks group isolated and located in 2006 this enzime and showed the existance of this controversial mitochondrial enzyme.

On the other hand, there are also other important players like the hormonal adaptations which could cause very profund effects in terms of fuel utilization and muscle fiber mRNA expression. GH (growth Hormone), IGF-1, Cortisol, Epinephrine (Adrenaline), testosterone...can play a very important roll in cycling efficiency, although we could talk for a very long time about this...as well as about the above🙂 .

Anyways, I believe that there are many different adaptations that could lead to cycling eficiency as well as different approaches of what we can andesrtand of cycling efficiency. When biomechanics talk about cycling efficiency they don´t talk about the cellular events occuring. They talk about the many different biomechanical approaches towards reaching a correct position to increse cycling efficiency and I believe they are right. I have seen at the wind tunnel, for example, dramatic improvements in "cycling efficiency" by changing positions.

Cheers.

rmur17 said:

....

Good questions!.
I was talking about the general idea of VO2max and LT. VO2max has been proven to plateau during cyclists or any endurance athlete´s carrere even if they keep improving their prtformance for a long time without changing his VO2max. About LT, it is a general parameters used worldwide. Honestely and modestely, I don´t believe in a "threshold for lactate" or LT (please don´t get mad at me). 1st there are many deffinitions about AT and LT and there is no concordance among scientific community. In my opinion if any accumulation point exists could be a MLSS (Maximal lactate Steady State) over time. That is the lactate rate of production and oxidation, then accumulation that a cycist can handle over time. We can translate these parametrs to watts as most labs do, althogh this is in my opinion not correct.

About what you mentioned about a fixed lactate concentration vs a power...I hope I will tell you in a few months more about this since I am finishin writing a paper on this with some cool results and will hope to be admitted before the spring.

Too bad you don´t have access to a lab for lactate testing...I should move to the US to start my own lab (I am sure it could be a good bussiness and less stress than working with the elite pros here!). Anyways you are right if you don´t have access to a lab an increased sustainable power on the road it is a very good indicator of improvement due to possible cycling efficiency. Same for those who don´t have a power meeting...and increase speed going up ending up 2 mins faster than before.. and even on the flat, it is a sign of increased efficiency. Also for those who use only speed and HR. A decreased in HR and increased in Speed it is defenetely an increased in cycling efficiency whatever it could come from but it sure it is...

For testing yourself on the road you do not need necessarely a power meter. You can test yourself in different ways but with the same approach. You are just using different tools to test what you want which is, e.g. increase in performance and feedback.

Cheers.

Urkiola2 said:

Good questions!.
I was talking about the general idea of VO2max and LT. VO2max has been proven to plateau during cyclists or any endurance athlete´s carrere even if they keep improving their prtformance for a long time without changing his VO2max. About LT, it is a general parameters used worldwide. Honestely and modestely, I don´t believe in a "threshold for lactate" or LT (please don´t get mad at me). 1st there are many deffinitions about AT and LT and there is no concordance among scientific community. In my opinion if any accumulation point exists could be a MLSS (Maximal lactate Steady State) over time. That is the lactate rate of production and oxidation, then accumulation that a cycist can handle over time. We can translate these parametrs to watts as most labs do, althogh this is in my opinion not correct.

About what you mentioned about a fixed lactate concentration vs a power...I hope I will tell you in a few months more about this since I am finishin writing a paper on this with some cool results and will hope to be admitted before the spring.

I am eager to see your results. I also have problems with the "LT" concept and generally avoid its use. Certainly Coyle did not find any strong correlation to lactate levels and hour power, just a slight postive one.

I am thinking that there is more to power production than just efficiency as if so, then those with the most Type I would be the most powerful, but I am not sure this is the case.