Beware of PowerCranks

In article .com,
wrote:

On Jun 7, 11:57 am, Andy Coggan wrote:

In fact, mild-to-moderate arterial desaturation tends to occur
during maximal exercise in a significant portion of the population
(at least discounting young, healthy, untrained men!), indicating
that, at least to some extent, aerobic capacity (i.e., VO2max) is
limited, in part, by pulmonary function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting

Left to right shunting from where to where through what? This term is
usually used to indicate left to right shunting through an atrial septal
defect or cases of tricuspid atresia. There should be little or no left
to right shunting through a patent foramen ovale and should be no
shunting at all in a normal heart. So I am not clear to what you refer.
Thanks.

On Jul 30, 2:53 pm, Tim McNamara wrote:
In article .com,

wrote:
On Jun 7, 11:57 am, Andy Coggan wrote:

In fact, mild-to-moderate arterial desaturation tends to occur
during maximal exercise in a significant portion of the population
(at least discounting young, healthy, untrained men!), indicating
that, at least to some extent, aerobic capacity (i.e., VO2max) is
limited, in part, by pulmonary function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting

Left to right shunting from where to where through what? This term is
usually used to indicate left to right shunting through an atrial septal
defect or cases of tricuspid atresia. There should be little or no left
to right shunting through a patent foramen ovale and should be no
shunting at all in a normal heart. So I am not clear to what you refer.
Thanks.

My bad, I should have said increased right to left shunting although
this is not so much as a physiological shunt but as a ventilation
perfusion defect behaving as a shunt.

In article . com,
wrote:

On Jul 30, 2:53 pm, Tim McNamara wrote:
In article .com,

wrote:
On Jun 7, 11:57 am, Andy Coggan wrote:

In fact, mild-to-moderate arterial desaturation tends to occur
during maximal exercise in a significant portion of the
population (at least discounting young, healthy, untrained
men!), indicating that, at least to some extent, aerobic
capacity (i.e., VO2max) is limited, in part, by pulmonary
function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting

Left to right shunting from where to where through what? This term
is usually used to indicate left to right shunting through an
atrial septal defect or cases of tricuspid atresia. There should
be little or no left to right shunting through a patent foramen
ovale and should be no shunting at all in a normal heart. So I am
not clear to what you refer. Thanks.

My bad, I should have said increased right to left shunting although
this is not so much as a physiological shunt but as a ventilation
perfusion defect behaving as a shunt.

That didn't really clarify. Ventilation defects are generally caused by
obstructions somewhere in the airway; perfusion defects are generally
caused by emboli in the pulmonary vasculature. What is the cause of the
"ventilation perfusion defect" you are pointing towards? Does this
occur in non-pathological individuals?

I trimmed the rest of your previous post in an over-zealous fit of good
netiquette, unfortunately. It would appear that Nielsen (2003) found
that arterial desaturation during exercise is multifactoral and that
large lung capacity does offer some protection from this. Perhaps this
link offers some light on the subject:

http://www.ncbi.nlm.nih.gov/sites/en...bMed&list_uids
=14617055&dopt=AbstractPlus

On Jul 30, 9:56 pm, Tim McNamara wrote:
In article . com,



wrote:
On Jul 30, 2:53 pm, Tim McNamara wrote:
In article .com,

wrote:
On Jun 7, 11:57 am, Andy Coggan wrote:

In fact, mild-to-moderate arterial desaturation tends to occur
during maximal exercise in a significant portion of the
population (at least discounting young, healthy, untrained
men!), indicating that, at least to some extent, aerobic
capacity (i.e., VO2max) is limited, in part, by pulmonary
function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting

Left to right shunting from where to where through what? This term
is usually used to indicate left to right shunting through an
atrial septal defect or cases of tricuspid atresia. There should
be little or no left to right shunting through a patent foramen
ovale and should be no shunting at all in a normal heart. So I am
not clear to what you refer. Thanks.

My bad, I should have said increased right to left shunting although
this is not so much as a physiological shunt but as a ventilation
perfusion defect behaving as a shunt.

That didn't really clarify. Ventilation defects are generally caused by
obstructions somewhere in the airway; perfusion defects are generally
caused by emboli in the pulmonary vasculature. What is the cause of the
"ventilation perfusion defect" you are pointing towards? Does this
occur in non-pathological individuals?

I trimmed the rest of your previous post in an over-zealous fit of good
netiquette, unfortunately. It would appear that Nielsen (2003) found
that arterial desaturation during exercise is multifactoral and that
large lung capacity does offer some protection from this. Perhaps this
link offers some light on the subject:

http://www.ncbi.nlm.nih.gov/sites/en...b=PubMed&list_...
=14617055&dopt=AbstractPlus

You are right that ventilation perfusion "abnormalities" can be multi-
factorial. However, some differences are normal. Gravity has a huge
effect on blood flow distribution through the lungs and very little
effect on ventilation distribution. Luckily for us God designed us to
accomodate for this gravitational effect and we were designed to
maximize oxygen transfer in the upright position. Turns out that more
of our inspired air goes into the part of the lung near the diaphragm
and less near the apex (the top near the neck). Luckily, that is the
bottom of the lung where gravity makes it natural for more blood to
go, especially at lower flow rates. At rest and when upright this
distribution is very well balanced. However, as one exercises, more
blood flow "forces" a higher percentage of the blood volume to go
towards the apex where ventilation is less (this "forcing" occurs
because once the lower alveolar capillaries are "maxed out" any
additional flow must move further up the chain where there is room to
accomodaate it). This would change the ventilation perfusion
relationship tending to naturally lower arterial oxygen saturation at
higher efforts. Further, in cycling, one isn't necessarily in the
"optimum" upright position, which can change this relationship further.

On Jul 30, 9:56 pm, Tim McNamara wrote:
In article . com,



wrote:
On Jul 30, 2:53 pm, Tim McNamara wrote:
In article .com,

wrote:
On Jun 7, 11:57 am, Andy Coggan wrote:

In fact, mild-to-moderate arterial desaturation tends to occur
during maximal exercise in a significant portion of the
population (at least discounting young, healthy, untrained
men!), indicating that, at least to some extent, aerobic
capacity (i.e., VO2max) is limited, in part, by pulmonary
function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting

Left to right shunting from where to where through what? This term
is usually used to indicate left to right shunting through an
atrial septal defect or cases of tricuspid atresia. There should
be little or no left to right shunting through a patent foramen
ovale and should be no shunting at all in a normal heart. So I am
not clear to what you refer. Thanks.

My bad, I should have said increased right to left shunting although
this is not so much as a physiological shunt but as a ventilation
perfusion defect behaving as a shunt.

That didn't really clarify. Ventilation defects are generally caused by
obstructions somewhere in the airway; perfusion defects are generally
caused by emboli in the pulmonary vasculature. What is the cause of the
"ventilation perfusion defect" you are pointing towards? Does this
occur in non-pathological individuals?

I trimmed the rest of your previous post in an over-zealous fit of good
netiquette, unfortunately. It would appear that Nielsen (2003) found
that arterial desaturation during exercise is multifactoral and that
large lung capacity does offer some protection from this. Perhaps this
link offers some light on the subject:

http://www.ncbi.nlm.nih.gov/sites/en...b=PubMed&list_...
=14617055&dopt=AbstractPlus

By the way, I found the Nielsen article (the link didn't work for me)
that I think you referred to. It supports what I said ("A widening of
the PAO2-PaO2 difference does indicate that a diffusion limitation, a
ventilation-perfusion mismatch and/or a shunt influence the transport
of O2 from alveoli to the pulmonary capillaries."), although I am not
sure the author fully understands all the variables contributing to
these possibilities. Further, I found this sentence very interesting:
"During maximal exercise, an extreme lactate spill-over to blood
allows pH decrease to below 7.1 and according to the O2 dissociation
curve this is critical for SaO2." This finding supports the view that
"exercise is limited by the periphery" over the "exercise is centrally
limited" argument. something I have always maintained to the constant
derision of some of the so-called "experts" here and elsewhere, like
Dr.Coggan. I will add it to my quiver. Thanks for the link

In article
.com
,
wrote:

On Jun 7, 11:57 am, Andy Coggan wrote:
On Jun 5, 11:04 pm, "Phil Holman" piholmanc@yourservice wrote:

wrote in message
In recent times, steam RR locomotives, although not rated in Horse
Power (but rather "tractive effort", the pull at which the wheels
would spin) had a conversion chart to HP based on grate area in the
fire box which governs how much heat can be transferred to steam in
the boiler. Grate area is closely similar to lung displacement for
physically fit racers. That is what limits climbing or TT ability,
not ankling, pedaling style or other external means.

You continue to repeat this misconception. Lung displacement or lung
capacity is not the limiting factor in climbing or TTing or cycling in
general. If you understood the cause and effect elements you would
understand that extreme "out of breath" is caused by excess CO2 in the
blood stream as a result of lactic buffering.

Great! Now we have one engineer feeding misconceptions about how
physiology functions to another engineer...

No, now we have an exercise physiologist trying to correct someone
with a correct understanding of the limiter. I am truly amazed that
you haven't figured out what is going on here yet.


Fact: CO2 plays only a very limited role in regulating ventilation
during exercise.

Fact: There are two main drivers for ventilation. CO2 and O2. The main
one is CO2. The body adjusts ventilation to maintain the arterial
partial pressure of CO2 at 40torr. CO2 is the prime determiner of
ventilatory function at all times except during extreme hypoxia, which
never occurs during normal exercise.


That is, the limits of
aerobic capacity were reached upstream (cardiac output, blood muscle
interface limitations etc) and no further limitations are imposed by the
lungs. It wouldn't matter if you doubled lung capacity, blood lactate
concentrations wouldn't change and this is the culminating event in
limiting aerobic performance. Heavy breathing is an effect not a cause.

In fact, mild-to-moderate arterial desaturation tends to occur during
maximal exercise in a significant portion of the population (at least
discounting young, healthy, untrained men!), indicating that, at least
to some extent, aerobic capacity (i.e., VO2max) is limited, in part,
by pulmonary function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting and ventilation perfusion mismatch at
the extremes and is probably has no effect on performance because of
the oxyhemoglobin saturation curve. There could be other explanations
also such as a shift in the curve due to changes in pH. Small levels
of desaturation have almost no effect on oxygen carrying capacity to
the tissues.

I am incompetent to assess these matters. I have read
very little, but got the impression that the limiting
factor in aerobic work capacity is the mitochondria
themselves.

--
Michael Press

Michael Press writes:

I am incompetent to assess these matters. I have read
very little, but got the impression that the limiting
factor in aerobic work capacity is the mitochondria
themselves.

That's why I am desiging nanopowercranks;
they allow the mitochondria to train themselves!

--
Joe Riel

On Jul 31, 11:02 am, Michael Press wrote:
In article
.com
,



wrote:
On Jun 7, 11:57 am, Andy Coggan wrote:
On Jun 5, 11:04 pm, "Phil Holman" piholmanc@yourservice wrote:

wrote in message
In recent times, steam RR locomotives, although not rated in Horse
Power (but rather "tractive effort", the pull at which the wheels
would spin) had a conversion chart to HP based on grate area in the
fire box which governs how much heat can be transferred to steam in
the boiler. Grate area is closely similar to lung displacement for
physically fit racers. That is what limits climbing or TT ability,
not ankling, pedaling style or other external means.

You continue to repeat this misconception. Lung displacement or lung
capacity is not the limiting factor in climbing or TTing or cycling in
general. If you understood the cause and effect elements you would
understand that extreme "out of breath" is caused by excess CO2 in the
blood stream as a result of lactic buffering.

Great! Now we have one engineer feeding misconceptions about how
physiology functions to another engineer...

No, now we have an exercise physiologist trying to correct someone
with a correct understanding of the limiter. I am truly amazed that
you haven't figured out what is going on here yet.

Fact: CO2 plays only a very limited role in regulating ventilation
during exercise.

Fact: There are two main drivers for ventilation. CO2 and O2. The main
one is CO2. The body adjusts ventilation to maintain the arterial
partial pressure of CO2 at 40torr. CO2 is the prime determiner of
ventilatory function at all times except during extreme hypoxia, which
never occurs during normal exercise.

That is, the limits of
aerobic capacity were reached upstream (cardiac output, blood muscle
interface limitations etc) and no further limitations are imposed by the
lungs. It wouldn't matter if you doubled lung capacity, blood lactate
concentrations wouldn't change and this is the culminating event in
limiting aerobic performance. Heavy breathing is an effect not a cause.

In fact, mild-to-moderate arterial desaturation tends to occur during
maximal exercise in a significant portion of the population (at least
discounting young, healthy, untrained men!), indicating that, at least
to some extent, aerobic capacity (i.e., VO2max) is limited, in part,
by pulmonary function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting and ventilation perfusion mismatch at
the extremes and is probably has no effect on performance because of
the oxyhemoglobin saturation curve. There could be other explanations
also such as a shift in the curve due to changes in pH. Small levels
of desaturation have almost no effect on oxygen carrying capacity to
the tissues.

I am incompetent to assess these matters. I have read
very little, but got the impression that the limiting
factor in aerobic work capacity is the mitochondria
themselves.

--
Michael Press

In my opinion, the limiter is the ability to deliver oxygen to the
mitochondria so the mitochonria compensate by using another mechanism
with lactic acid as an end point. Once there are enough mitochondria
in this situation the amount of lactic acid being produced overwhelms
the bodies ability to compensate for this and the "failure cascade"
starts.

In article
.com
,
wrote:

On Jul 31, 11:02 am, Michael Press wrote:
In article
.com
,



wrote:
On Jun 7, 11:57 am, Andy Coggan wrote:
On Jun 5, 11:04 pm, "Phil Holman" piholmanc@yourservice wrote:

wrote in message
In recent times, steam RR locomotives, although not rated in Horse
Power (but rather "tractive effort", the pull at which the wheels
would spin) had a conversion chart to HP based on grate area in the
fire box which governs how much heat can be transferred to steam in
the boiler. Grate area is closely similar to lung displacement for
physically fit racers. That is what limits climbing or TT ability,
not ankling, pedaling style or other external means.

You continue to repeat this misconception. Lung displacement or lung
capacity is not the limiting factor in climbing or TTing or cycling in
general. If you understood the cause and effect elements you would
understand that extreme "out of breath" is caused by excess CO2 in the
blood stream as a result of lactic buffering.

Great! Now we have one engineer feeding misconceptions about how
physiology functions to another engineer...

No, now we have an exercise physiologist trying to correct someone
with a correct understanding of the limiter. I am truly amazed that
you haven't figured out what is going on here yet.

Fact: CO2 plays only a very limited role in regulating ventilation
during exercise.

Fact: There are two main drivers for ventilation. CO2 and O2. The main
one is CO2. The body adjusts ventilation to maintain the arterial
partial pressure of CO2 at 40torr. CO2 is the prime determiner of
ventilatory function at all times except during extreme hypoxia, which
never occurs during normal exercise.

That is, the limits of
aerobic capacity were reached upstream (cardiac output, blood muscle
interface limitations etc) and no further limitations are imposed by the
lungs. It wouldn't matter if you doubled lung capacity, blood lactate
concentrations wouldn't change and this is the culminating event in
limiting aerobic performance. Heavy breathing is an effect not a cause.

In fact, mild-to-moderate arterial desaturation tends to occur during
maximal exercise in a significant portion of the population (at least
discounting young, healthy, untrained men!), indicating that, at least
to some extent, aerobic capacity (i.e., VO2max) is limited, in part,
by pulmonary function.

Phoeey. A small arterial desaturation is most likely explained by
increased left to right shunting and ventilation perfusion mismatch at
the extremes and is probably has no effect on performance because of
the oxyhemoglobin saturation curve. There could be other explanations
also such as a shift in the curve due to changes in pH. Small levels
of desaturation have almost no effect on oxygen carrying capacity to
the tissues.

I am incompetent to assess these matters. I have read
very little, but got the impression that the limiting
factor in aerobic work capacity is the mitochondria
themselves.

In my opinion, the limiter is the ability to deliver oxygen to the
mitochondria so the mitochonria compensate by using another mechanism
with lactic acid as an end point. Once there are enough mitochondria
in this situation the amount of lactic acid being produced overwhelms
the bodies ability to compensate for this and the "failure cascade"
starts.

Minor biochemistry quibble here.
As I understand the matter, the mitochondria are not
involved directly in the process leading to lactic acid
production. Rather it is ATP hydrolysis outside the
mitochondria that produces H+, which is then buffered
by lactate in the cell, outside the mitochondria. The
necessity for buffering H+ occurs only when the
mitochondria are working at full capacity and cannot
metabolize any more H+. (The mitochondria runs
ADP + n H+ + other stuff - ATP + other stuff)

I would like to know how much O2 concentration varies
in the tissue and how that affects mitochondria
capacity during heavy exercise, and if O2 concentration
is the, or a, limiting factor.

--
Michael Press

In article ,
Joe Riel wrote:

Michael Press writes:

I am incompetent to assess these matters. I have read
very little, but got the impression that the limiting
factor in aerobic work capacity is the mitochondria
themselves.

That's why I am desiging nanopowercranks;
they allow the mitochondria to train themselves!

Ooohhhh! Here you go--$$$$$$$$$
When can I get some nanopowercranks?

--
Michael Press