The Powermeter Thread

[acoggan]

http://blog.trainingpeaks.com/posts/2013/3/12/whats-your-power-user-category.html

 

[Tapeworm]

http://journals.lww.com/acsm-msse/A...penditure_of_Constant_and_Variable.98426.aspx


Another little use for a PM - tracking energy expenditure.

 

[FrankDay]

http://journals.lww.com/acsm-msse/A...penditure_of_Constant_and_Variable.98426.aspx


Another little use for a PM - tracking energy expenditure.

It is of little surprise that if one knows GE and power that one knows calorie expenditure. Few people know their cycling GE. IMHO, it would have been more useful if they had also looked at the utility of following HR (which usually correlates pretty well to oxygen consumption/calorie expenditure) for aerobic exercise to see if the PM is more useful/accurate for this purpose. If HR also is reasonably accurate for this purpose it could be used not only for cycling but running or any endurance event.

 

[sciguy]

It is of little surprise that if one knows GE and power that one knows calorie expenditure. Few people know their cycling GE. IMHO, it would have been more useful if they had also looked at the utility of following HR (which usually correlates pretty well to oxygen consumption/calorie expenditure) for aerobic exercise to see if the PM is more useful/accurate for this purpose. If HR also is reasonably accurate for this purpose it could be used not only for cycling but running or any endurance event.

Having a hard time picturing the use of heart rate to measure caloric expenditure. Garmin has been trying to do this for years with what most consider virtually no success. As I get fitter during the season my heart rate is considerably lower for a given work load. I don't really think that means I'm burning significantly less calories. Cycling GE is consistent enough to make a pretty decent estimate based on power. Now if an athlete knew their cycle GE they would be able to make a better estimate.


Hugh

 

[FrankDay]

Having a hard time picturing the use of heart rate to measure caloric expenditure. Garmin has been trying to do this for years with what most consider virtually no success. As I get fitter during the season my heart rate is considerably lower for a given work load. I don't really think that means I'm burning significantly less calories. Cycling GE is consistent enough to make a pretty decent estimate based on power. Now if an athlete knew their cycle GE they would be able to make a better estimate.


Hugh

Well, for this to work one needs to correlate HR to energy expenditure, just like they did for the PM (looking at GE). You can't do this blindly as in a one formula fits all fashion, which may be what Garmin is trying to do. But, if one can do that for any given individual I would expect this would be reasonably accurate, as accurate as the 11% error they saw for the PM I would guess.

 

[sciguy]

Well, for this to work one needs to correlate HR to energy expenditure, just like they did for the PM (looking at GE). You can't do this blindly as in a one formula fits all fashion, which may be what Garmin is trying to do. But, if one can do that for any given individual I would expect this would be reasonably accurate, as accurate as the 11% error they saw for the PM I would guess.

Seems like a lot of guessing going on. With a power meter one gets a pretty reasonable estimate especially when you consider how inaccurate the labeled caloric value of complex food is.

http://www.rawstory.com/rs/2013/02/18/scientists-food-calorie-count-labels-are-often-inaccurate/

On top of that, humans seem to consistently have trouble estimating the actual amount of food they eat on a day to day basis.

With those two factors considered, an 11% error may well be trivial.

 

[FrankDay]

Seems like a lot of guessing going on. With a power meter one gets a pretty reasonable estimate especially when you consider how inaccurate the labeled caloric value of complex food is.

http://www.rawstory.com/rs/2013/02/18/scientists-food-calorie-count-labels-are-often-inaccurate/

On top of that, humans seem to consistently have trouble estimating the actual amount of food they eat on a day to day basis.

With those two factors considered, an 11% error may well be trivial.

Sure, except the PM only works for cyclists. The HRM could, possibly, work for all ultra endurance athletes. It may not make much difference anyhow since the ability to take in calories is limited on a per hour basis so as long as the expenditure is over that limit of what usefulness is the information to the racer?

 

[CoachFergie]

Sure, except the PM only works for cyclists.

What was the name of this forum again and what sport do we all do?

The HRM could, possibly, work for all ultra endurance athletes. It may not make much difference anyhow since the ability to take in calories is limited on a per hour basis so as long as the expenditure is over that limit of what usefulness is the information to the racer?

Then go and discuss that on Slowtwitch. Oh wait, sorry, you can't.

 

[CoachFergie]

http://blog.trainingpeaks.com/posts/2013/3/12/whats-your-power-user-category.html

Bang on the money. So many people new to using a power meter like to compare their watts on a ride or about a ride. Or want to know what type of power the top guns are using.

 

[CoachFergie]

http://www.cyclingnews.com/news/vayer-calls-for-srm-and-blood-data-from-sky

A few points, Wiggins was more than happy to share his data but Sky said no.

What if the team use Quarq or Pioneer?

Dr Yorck Olaf Schumacher has previously called for tracking of power meter data to be able to red flag riders for further testing or scrutiny if their power meter data is suspicious.

http://www.sportsscientists.com/2009/08/doping-control-interview-with-prof.html

 

[CoachFergie]

And David Brailsford (Team Sky) bites back.

http://www.cyclingnews.com/news/brailsford-hits-back-at-accusations-and-criticism-of-team-sky

Responds to Nibali and Contador that on a couple of days at Tirreno-Adriatico the team used compact cranks so were not solely basing their effort on power numbers.

 

[CoachFergie]

Comment on robotic racing with a PM

Response to the argument that racing with a SRM is making the racing robotic...

http://www.biscuittinmedia.com/team-sky-srm-richie-porte-robo-racer/

 

[CoachFergie]

And a great interview with Tim Kerrison highlighting going beyond the numbers. As I mentioned earlier racing and training with a power meter is a part of the performance process!

http://www.biscuittinmedia.com/tim-kerrison-training-wiggins/

 

[FrankDay]

Originally Posted by acoggan

LOTS of things are going on under such an extreme emergency situation for the body. The fact remains, however, that VO2max is not limited by, e.g., some "central governor" as wrongly believed by Noakes or by peripheral O2 utiliation, but the cardiovascular system's ability to deliver said O2.

I agree that there is no central governor as described by Noakes. Where we disagree is the physiological mechanism behind VO2max. You might want to look at what is going on with cardiac pH as one approaches VO2max and how both the ability of the muscle to contract and relax changes with altered pH.

As I said, your approach is simplistic. But, continue to pretend that no one else could possibly know anything more about anything related to physiology than you.

Dr. Coggan, here is an interesting study finding that goes against your explanation as to what is going on with cardiac output. Again, the question really has to be is there a physiological mechanism that can explain ALL of the data seen.

Conclusion:  The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO2 is reached.

Not only do you need to explain the drop in CO after VO2max but now the leveling in the response of CO to intensity above a certain level. Your simplistic mechanism does neither.

 

[FrankDay]

Originally Posted by acoggan

LOTS of things are going on under such an extreme emergency situation for the body. The fact remains, however, that VO2max is not limited by, e.g., some "central governor" as wrongly believed by Noakes or by peripheral O2 utiliation, but the cardiovascular system's ability to deliver said O2.

I agree that there is no central governor as described by Noakes. Where we disagree is the physiological mechanism behind VO2max. You might want to look at what is going on with cardiac pH as one approaches VO2max and how both the ability of the muscle to contract and relax changes with altered pH.

As I said, your approach is simplistic. But, continue to pretend that no one else could possibly know anything more about anything related to physiology than you.

Dr. Coggan, here is an interesting study finding that goes against your explanation as to what is going on with cardiac output. Again, the question really has to be is there a physiological mechanism that can explain ALL of the data seen.

Conclusion:  The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO2 is reached.

Not only do you need to explain the drop in CO after VO2max but now the leveling in the response of CO to intensity above a certain level. Your simplistic mechanism does neither.

 

[acoggan]

Dr. Coggan, here is an interesting study finding that goes against your explanation as to what is going on with cardiac output. Again, the question really has to be is there a physiological mechanism that can explain ALL of the data seen.
Not only do you need to explain the drop in CO after VO2max but now the leveling in the response of CO to intensity above a certain level. Your simplistic mechanism does neither.

You're kidding, right? As I pointed out before, end-systolic volume begins to decline well before VO2max/maximal heart rate is reached.

 

[FrankDay]

You're kidding, right? As I pointed out before, end-systolic volume begins to decline well before VO2max/maximal heart rate is reached.

But, you don't explain a mechanism to explain why it occurs when it does or anything else. You simply are saying that what you observe is what explains what you observe. So, I am not kidding. Your explanation is totally inadequate from an underlying mechanism point of view.

 

[acoggan]

But, you don't explain a mechanism to explain why it occurs when it does or anything else.

I already have: ever-decreasing diastolic filling time leads to a progressive reduction in end-diastolic volume, which can only be temporarily compensated for by a corresponding decrease in end-systolic volume. At/beyond that point, stroke volume plateaus, and sometimes even falls.

EDIT: Or to quote the very study to which you linked:

"The mechanism responsible for the attenuation in the
CO vs. VO2 relationship and the fall in SV is not
entirely clear but is likely related to an interaction of
factors that alter preload, afterload and left ventricular
function. Direct manipulation of HR by pacing the
heart in both humans and dogs demonstrates that
tachycardia leads to disproportional reductions in
diastolic filling time and left ventricular end-diastolic
volume, which reduce preload and compromise SV and
CO (Templeton et al. 1972, Weisfeldt et al. 1978,
Sheriff et al. 1993). Using a combination of direct heart
catheterization and radionuclide angiography, Higginbotham et al. (1986) elegantly determined that during
high-intensity exercise, tachycardia is accompanied by a
decrease in end-diastolic volume despite a progressive
increase in filling pressure, which results in a reduction
in SV. The increased ventricular filling pressure as
exercise intensity increases appears to be inadequate to
fully compensate for the reduction in ventricular filling
time resulting in the plateau and eventual reduction in
SV. Progressive increases in afterload as evidenced by
the linear increase in systemic arterial pressure may also
contribute to the observed plateau in SV (Calbet et al.
2006)."

 

[FrankDay]

I already have: ever-decreasing diastolic filling time leads to a progressive reduction in end-diastolic volume, which can only be temporarily compensated for by a corresponding decrease in end-systolic volume. At/beyond that point, stroke volume plateaus, and sometimes even falls.

EDIT: Or to quote the very study to which you linked:

"The mechanism responsible for the attenuation in the
CO vs. VO2 relationship and the fall in SV is not
entirely clear but is likely related to an interaction of
factors that alter preload, afterload and left ventricular
function. Direct manipulation of HR by pacing the
heart in both humans and dogs demonstrates that
tachycardia leads to disproportional reductions in
diastolic filling time and left ventricular end-diastolic
volume, which reduce preload and compromise SV and
CO (Templeton et al. 1972, Weisfeldt et al. 1978,
Sheriff et al. 1993). Using a combination of direct heart
catheterization and radionuclide angiography, Higginbotham et al. (1986) elegantly determined that during
high-intensity exercise, tachycardia is accompanied by a
decrease in end-diastolic volume despite a progressive
increase in filling pressure, which results in a reduction
in SV. The increased ventricular filling pressure as
exercise intensity increases appears to be inadequate to
fully compensate for the reduction in ventricular filling
time resulting in the plateau and eventual reduction in
SV. Progressive increases in afterload as evidenced by
the linear increase in systemic arterial pressure may also
contribute to the observed plateau in SV (Calbet et al.
2006)."

LOL. See emphasis above. Further, your explanation doesn't explain why SV typically increases with decreasing filling time at lower intensities. Your explanation is not a mechanism as noted by the authors you quote. Just what are those factors that alter preload, afterload, and LV function to explain these findings? You are simply describing the result.

 

[acoggan]

Just what are those factors that alter preload, afterload, and LV function to explain these findings?

"The mechanism responsible for the attenuation in the
CO vs. VO2 relationship and the fall in SV is not
entirely clear but is likely related to an interaction of
factors that alter preload, afterload and left ventricular
function. Direct manipulation of HR by pacing the
heart in both humans and dogs demonstrates that
tachycardia leads to disproportional reductions in
diastolic filling time and left ventricular end-diastolic
volume, which reduce preload and compromise SV and
CO (Templeton et al. 1972, Weisfeldt et al. 1978,
Sheriff et al. 1993). Using a combination of direct heart
catheterization and radionuclide angiography, Higginbotham et al. (1986) elegantly determined that during
high-intensity exercise, tachycardia is accompanied by a
decrease in end-diastolic volume despite a progressive
increase in filling pressure, which results in a reduction
in SV. The increased ventricular filling pressure as
exercise intensity increases appears to be inadequate to
fully compensate for the reduction in ventricular filling
time resulting in the plateau and eventual reduction in
SV. Progressive increases in afterload as evidenced by
the linear increase in systemic arterial pressure may also
contribute to the observed plateau in SV (Calbet et al.
2006)."

 

[FrankDay]

"The mechanism responsible for the attenuation in the
CO vs. VO2 relationship and the fall in SV is not
entirely clear but is likely related to an interaction of
factors that alter preload, afterload and left ventricular
function. Direct manipulation of HR by pacing the
heart in both humans and dogs demonstrates that
tachycardia leads to disproportional reductions in
diastolic filling time and left ventricular end-diastolic
volume, which reduce preload and compromise SV and
CO (Templeton et al. 1972, Weisfeldt et al. 1978,
Sheriff et al. 1993). Using a combination of direct heart
catheterization and radionuclide angiography, Higginbotham et al. (1986) elegantly determined that during
high-intensity exercise, tachycardia is accompanied by a
decrease in end-diastolic volume despite a progressive
increase in filling pressure, which results in a reduction
in SV. The increased ventricular filling pressure as
exercise intensity increases appears to be inadequate to
fully compensate for the reduction in ventricular filling
time resulting in the plateau and eventual reduction in
SV. Progressive increases in afterload as evidenced by
the linear increase in systemic arterial pressure may also
contribute to the observed plateau in SV (Calbet et al.
2006)."

My friend, that is not a mechanism. What they are describing is a change in compliance ("despite a progressive
increase in filling pressure"). That is not a simple reduction in stroke volume due to decreased filling time as you propose. Your "mechanism" is inadequate. The authors stated it correctly, at least to them, the mechanism was not clear to them but probably involved many factors.

While many factors may be involved I personally think there is one major one underlying them all. One basic one that primarily affects left ventricular function and compliance that all of you have missed because you don't have the same background I do. But, what would I know?

 

[acoggan]

what would I know?

Not much...but that's already been established.

 

[sciguy]

My friend, that is not a mechanism. What they are describing is a change in compliance ("despite a progressive
increase in filling pressure"). That is not a simple reduction in stroke volume due to decreased filling time as you propose. Your "mechanism" is inadequate. The authors stated it correctly, at least to them, the mechanism was not clear to them but probably involved many factors.

While many factors may be involved I personally think there is one major one underlying them all. One basic one that primarily affects left ventricular function and compliance that all of you have missed because you don't have the same background I do. But, what would I know?

Jeepers how long are you going to keep us on the edges of our seats in anticipation?

 

[FrankDay]

Jeepers how long are you going to keep us on the edges of our seats in anticipation?

Do you folks ever read what I write? I have brought up a mechanism before in a response to Dr. Coggan that he and you, and apparently everyone else, ignored. If you want to understand this issue you have to ask the right questions. Start by asking the question as to how pH affects muscle function, both contractility and relaxation (compliance)? Then, ask if pH might be changing as one passes threshold? Then, ask what might be causing a change in pH at this time, assuming it does change? Now, if you do all this you are getting closer to describing a real mechanism to describe this physiological phenomenon. But, what would I know?

 

[coapman]

And a great interview with Tim Kerrison highlighting going beyond the numbers. As I mentioned earlier racing and training with a power meter is a part of the performance process!

http://www.biscuittinmedia.com/tim-kerrison-training-wiggins/

What powermeters (if any) take accurate measurements of torque at every 15 or 30 degrees of the pedaling circle ?