I would be interested to see a copy of this abstract.  What exactly is Mr.
Robergs' point?  Is he asserting that acidosis is not a factor in fatigue;
fatigue is not related to lactate accumulation during exercise; some other
metabolic substrate is involved with pH?  Being somewhat familiar with
physiology, the contention that "lactate" and "lactic acid" are dissimilar
is incorrect.  The "-ate" modifier is common nomenclature in chemical
analysis reserved for the identification of the hydrogen donor in solution.
Therefore, in biological systems, the term "lactate" is often synonomous
with "lactic acid."  To take the literal stance on this word is merely
symantics.  Lactate accumulation, and its accompanying H+ accumulation, is
local and is a derivative of O2 insufficiency.  In biological systems,
lactate production is far removed from the energy chain because the energy
coupling involved with glycolosis in with the citric acid cycle favors ATP
production and complete glycolosis (despite some molecules of glucose
leading to lactate).  Even when energy demands outpace the ATP production
locally and lactate accumulates (accompanied by the increased H+
concentration and thus lower pH) the increase in CO2 (a metabolic byproduct
of glycolosis) will trigger a neural response at the muscle causing a
sympathetic response to increase bloodflow at that location.  The increased
O2 exchange at that point would create an energy environment that would
decrease the lactate concentration.  Therefore, where is this pH being
measured, what substrates are being analyzed, and what type or level of
exertion is being used to create this environment?

Regards
Bob



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[Will here.  There has been a problem with the forum@...
mailbag--a long story in itself--with the result that
<anything>@sportsci.org has come to me.  To get messages to the list, at
the moment I have to redirect them to sportscience@....  This
glitch occurred first with this message of Rob's, but I stupidly redirected
it to forum@..., then didn't notice that it hadn't gone to the
list (because of the way I filter my messages to various mailbags)!  So
here is his complete message to the list, which I quoted briefly from in my
reply to the list.  Naturally Rob is irate!  Hope this fixes things.]

Date: Mon, 23 Jul 2001 16:24:51 -0600
From: "Robert Robergs, Ph.D., FASEP" <rrobergs@...>
Subject: Reply to Source of acid in high-intensity exercise
To: Will Hopkins <will.hopkins@...>

Hi Will;

Here is my reply that I promised earlier today.

  > one molecule of glucose C6H12O6 -> 2 molecules of lactic acid C3H6O3

This is a source of confusion, as this biochemical summary is not correct.
When you summarize glycolysis and lactate production you get the following:

glucose + 2 ADP + 2 Pi + 2 NAD+ ---> 2 pyruvate + 2 NADH + 2 ATP + 2 H+ + 2
H20

2 pyruvate + 2 NADH + 2 H+ ---> 2 lactate + 2 NAD+

These summary equations are straight our of Lehninger, and have been fact
since the 1950's!

It seems that somewhere along the path of time we in exercise physiology, as
well as clinical medicine, pure physiology, and even biochemistry, have not
looked at the facts on the issue of acidosis.  Ironically, there is no
chapter on metabolic acidosis in any biochemistry text, yet as far as
exercise is concerned, it is difficult to find a more important topic!!

The biochemistry of glycolysis tells us that when starting from glucose,
lactate production is not acidifying.  To the contrary, lactate production
consumes protons.  It just so happens that when the muscle cell is
contracting to an ATP demand that exceeds the mitochodrial rate of ATP
regeneration, then additional cytosolic ATP is hydrolyzed that is not
immediately replenished by mitochondrial respiration.  Thus, the following
reaction occurs;

ATP ---> ADP + Pi + H+

When the ATP is not regenerated by the mitochondria, this free proton
contributes to acidosis.  You do not immediately see this result from
assaying concentrations of ATP, as CrP hydrolysis buffers the cellular ATP.
Consequently, this is why there is a temporal association between CrP
hydrolysis and intramuscular acidosis.  Furthermore, the decline in CrP with
increasing exercise intensity also coincides with an increase in lactate
production due to the mass action of glycolysis and enzyme kinetics of LDH
favoring lactate production under these conditions.

Given this last fact, the reason why people claim that lactate production
eventually causes acidosis is an oversimplification of the truth.  Lactate
production and acidosis are not cause and effect, just associated results of
a cell that is being overtaxed.  One could argue, based on the biochemistry,
that it is very advantageous for the cell to produce lactate to help
overcome the accumulating protons, as well of course to regenerate the NAD+.
Why have well viewed lactate production as the culprit?  My explanation is
that it is easy to do, lactate is easy to measure, and also makes the
explanation of acidosis more simplified.  In reality, the explanation of
acidosis is very complex, requires an understanding of more advanced
biochemistry, and the conditions change with changing pH due to the buffer
potential of Pi as pH lowers towards 6.8.  Unfortunately, the recent work on
the monocarbolylat lactate-H+ transporter might further reinforce the
cause-effect association/belief  between lactate production and proton
accumulation.

Finally, remember that you do not need a large increase in the concentration
of free protons to significantly lower pH from a value of 7.0.  For example,
we are talking about mmol increases in metabolites, when we are concerned
with one thousand fold less changes in protons.  Thus, acidosis does not
lend itself to stoichiometric comparisons to changes  in ATP, ADP, Pi, or
CrP.

  > Glucose or glycogen does not ionize and so does not produce hydrogen
  > ions.  Lactic acid ionizes and produces hydrogen ions.  Therefore lactic
  > acid is indeed a source of acid.   So when you go from rest (lactate ~1
mM)
  > to high-intensity exercise (lactate ~5-10 mM), you do indeed get lactic
  > acidosis.  The intermediate steps in this process are irrelevant,
  > surely?  It's a question of conservation of matter, surely?

As I have said, the intermediate steps do matter, as they show that no
protons leave lactic acid to form lactate in the LDH reaction.  The
carboxylic acid function group of 2 phosphoglycerate is not protonated when
it is formed, and remains unprotonated for the remainder of glycolysis.
Stryer provides a nice summary of glycolysis that shows where protons are
released - Hexokinase, PFK, Glyceraldehyde-3P dehydrogenase reactions.
Interestingly, the pyruvate kinase reaction consumes a proton.


  > Now, I know other things are going on.  Are those other things a source or
  > a sink of hydrogen ions?  For example, at an intensity that evokes 5-10 mM
  > lactate, phosphate will be higher, presumably from hydrolysis of creatine
  > phosphate to creatine and phosphate.  (ATP and ADP don't change
  > much.)  When you hydrolyze creatine phosphate, I presume you also get more
  > hydrogen ions, because the phosphate that was bound to creatine has picked
  > up an H (from a molecule of water; the OH goes onto the creatine, or vice
  > versa), so it will tend to ionize and release that H as H+.

No.  When you hydrolyze CrP you transfer a phosphate from ADP to ATP.  The
biochemistry of the equation is as follows;

CrP + ADP + H+ ---> ATP + Cr

The phosphate transfer of this reaction does not need water to provide an
oxygen and proton, leaving a free proton.  These events occur for ATP
hydrolysis, as a proton is required to remain on the terminal phosphate
group of ADP, thus necessitating the use of an OH- from water to use to bind
to the phosphate, which, depending on cellular pH, will ionize, releasing a
proton.  Thus, CrP hydrolysis is actually alkalinizing, and has been shown
to be such by 31P MRS.

  > There may be some mileage in considering pyruvic acid, the immediate
  > precursor to lactic acid.  Is that an even stronger acid than lactate?

Yes, but is is irrelevent, as pyruvate is already ionized!

  > Has nature hit upon lactic acid as a way to reduce acidity?  The issue is
  > complicated by the addition of two hydrogen atoms (not ions) to pyruvate
to
  > turn it into lactate: C3H4O3 + 2H -> C3H6O3.  Where those 2H come from is
  > interesting and no doubt deeply meaningful for something, but presumably
  > not relevant to the main issue that a molecule of glucose is effectively
  > isomerized into two molecules of lactic acid.

According to the organic chemistry of the reaction, one comes from NADH, and
the other is from a "free"
   proton.  Thus, lactate is a sink for protons.

  > Rob's presentation emphasized fluxes (rate of flow) of compounds through
  > biochemical steps.  I can't see the relevance of fluxes.  What matters is
  > concentrations, not fluxes.  For acidity to change, concentrations have to
  > change.

Yes, and No!  So long as ATP is regenerated by non-mitochondrial sources,
there is a net proton release that will not be detected from simply
measuring ATP and ADP.  This is why I state that flux through glycolysis and
metabolic rates are important.

Will, thanks for the stimulating query, and I hope to hear from other sports
scientists on this topic.

Rob Robergs

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Dear Sportscience colleagues

In my understanding, Dr Robergs was not the first to realize lactic acid
is not formed in significant levels in the human body. He and his
colleagues established which reaction was increasing acidosis.
Well, if lactic acid is really formed and accumulates in our body, like
we have been told for almost a century, why do we measure lactate?
Instead of trying to make simple stoichiometric calculations I would
like to point to the facts that we are not usually focusing when
studying biochemistry, not because we do not know, but because we
usually do not relate our basic knowledge of chemistry to the facts that
we know.

Lactic acid is one of the dogmas of exercise physiology. It is an easy
explanation for a complex phenomenon.

The first knowledge about it came from a study in sour milk, in 1780 by
Carl Wilhelm Scheele (1742-1786), who found an acid which he separated
by crystallizing a calcium salt. Scheele thought to have found a milk
component so he called it LACTIC ACID, But as a matter of a fact, it is
a fermentation product of rancid milk.

So we have been studying the so-called lactic fermentation based on
conditions related to the pH of sour milk. The pH of milk, is 7, which
is already lower that the plasma pH. The pH of sour milk is probably a
lot lower than that.

According to Lehninger (2000) p 542,  “ The dissociation of lactic acid
to lactate and H+ in the fermentation mixture lowers the pH, denaturing
casein and other milk products causing them to precipitate…..”
As we all know, the lower the pH, the more acid molecules will be found
in a solution.

So when Will asks:
There may be some mileage in considering pyruvic acid, the immediate
precursor to lactic acid.  Is that an even stronger acid than lactate?
Has nature hit upon lactic acid as a way to reduce acidity?
Well, this is the simplest answer of all!

Yes, pyruvic acid is more acidic than lactic acid! Therefore, even if
pyruvic acid was formed, which is not true and can be found in any
serious biochemistry book, it would be immediately deprotonated into
pyruvate at physiological pH.

And from pyruvate there is no formation of lactic acid, but if there
were, lactic acid also would be dissociated into its conjugated base:
lactate.

According to Maughan, Gleeson and Greenhaff(1998) p 148: “As early as
the beginning of this century lactic acid  accumulation was suggested as
being responsible for fatigue development during high intensity
exercise. At physiological pH, lactic acid almost completely dissociates
into its constituent lactate and hydrogen ions, and studies (not cited)
using animal muscle preparations have demonstrated that direct
inhibition of force production can be achieved by increasing hydrogen
and lactate ion concentrations. It would also appear that lactate and
hydrogen ion accumulation can result in fatigue independent of one
another, but the latter is the more commonly cited mechanism.

The Henderson-Hasselbach.equation is not that old and when we use old
stoichiometric calculations, we have to remember to use this equation…
Therefore if we wanted to know what would possibility be the cellular
concentration of lactic acid in the lowest possible cellular ph for the
muscle cell (6.2), we could calculate:

Let’s say that there were produced  0,01M of lactic acid: How many M of
lactate would be produced?.
6,2 = pKa + log [lactate][lactic acid]
6,2 = 3,86 + log[lactate][0.01]
6,2 - 3,86 = log [lactate][0,01]
2.34 -log 0,01 = log [lactate]
log [lactate] 0,34
lactate = 10 0,34
lactate= 2,18
2,18/0,01= 218
So for each  lactic acid molecule there would be formed 218
molecules of lactate
And if ph was 7 this proportion would be of 1380 lactates for onelactic
acid.
So lactic acid is not significant in acidosis, but the remaining
hyrogen ion is.

Well, for pyruvic acid, the numbers would be more impressive.
I know that you know this equation, but almost everybody forgets to
apply it

I hope to have contributed positively  in this discussion

Roberto Landwehr
Universidade Católica de Brasília

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Will

I hope I’m not too far off the mark from your original question with these
statements, but due to the lack of response, I thought I’d forward this
information.

During my undergrad degree I did an small assignment titled anaerobic
threshold – misnomer or fact. I decided to present the side of misnomer, and
while my research wasn’t exhaustive, much to my surprise I did find a fair
bit of info discrediting the anaerobic threshold concept. I’ll be the first
to admit that my selection of papers was bias towards my argument. I’ve
included several quotes from my short report along with the relevant
references – I’ll endeavour to pull these out and re-read them in the next
few days to see if I can get any more info.

While these don’t answer your question directly, they may give you a few
more places to look???

---------------

It is believed that the continuous development of acidosis during
progressive exercise results directly from carbohydrate oxidation (Dennis et
al 1992). Dennis theorises that metabolic acidosis is due to increased
glycolytic ATP turnover as workload increases and unlike creatine phosphate
and oxidative phosphorylation, protons produced via glycolytic hydrolysis
are not re-consumed and thus accumulate regardless of oxygen status (Dennis
et al 1992).

It is now known that type IIb fibres steadily release H+ and produce lactate
regardless of PO2 (Myers et al 1997) further supporting this theory.

It has also been observed that under certain conditions H+ efflux from
muscle cell is up to fifty times higher than lactate efflux (Walsh et al.
1988).

It has been demonstrated that ammonia may also contribute to metabolic
acidosis (Longhurst et al. 1986).

References

Dennis S C, Noakes T D, Bosch A N Ventilation and blood lactate increase
exponentially during incremental exercise Journal of Sports Sciences 10:
437-449 1992.

Longhurst K, Blundell N Anaerobic Threshold and Endurance Performance
National Sports Research Program - State of the Art Review No. 9 Australian
Sports Commission 1986.

Myers J and Ashley E Dangerous Curves: A Perspective on Exercise, Lactate
and the Anaerobic Threshold Chest 111: 787-95 1997

Walsh M L, Banister E W Possible Mechanisms of the Anaerobic Threshold - A
Review Sports Medicine 5: 269-302 1988.


David Driscoll
BEFITting Image Training and Nutrition Service
B Sc - Ex. Sci. & Nut.
M Sc - Exercise Rehab. and Nut./Diet. (in progress)
RFL
Sydney, Australia.


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This discussion is great. More proof that "if you ever think you understand
something, it is only because you don't know enough about it"

When I was doing my PhD, my supervisor (an ICU MD/physiologist) had begun to
investigate strong-ion differences. He said it changed the way he treats
patients with acid-base imbalances because the cause is not acid-base
imbalance but excess/deficiency of other ions (I think it was chloride but
it was 8 years ago and I just don't remember). I don't know much about this
area but could this (i.e. strong-ion differences, not necessarily chloride)
be the source of protons in exercise?

Ian Shrier MD, PhD, Dip Sport Med, (FACSM)
Pres-Elect, Canadian Academy of Sport Medicine
check out the Canadian Academy of Sport Medicine website
http://www.casm-acms.org

Address:
Centre for Clinical Epidemiology and Community Studies
Lady Davis Institute for Medical Research
SMBD-Jewish General Hospital
3755 Cote Sainte-Catherine Rd
Montreal, Qc  H3T 1E2
FAX:514-340-7564
Tel:514-340-8222 (ext 4562)

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The Architectural Association in London is planning to host a conference
on the topic of sport, which will be published as an MIT book in the
next year. [Below] you will find the draft concept, and I am writing to
ask you if you can recommend somebody from your research team who would
be willing to present a paper on one of the topics. Please let me know
if you are interested in contributing or if you could make some
recommendations, so that we can discuss this further. I look forward to
hearing from you.

Katharina Borsi
Histories and Theories of Architecture
AA Graduate School
++44 20 78094097


SPORT AND ARCHITECTURE

The conference Sport and Architecture is organised as a set of themes that
identify the shifts the relation between sport, architecture and the city
has undergone in the recent decades. New material technologies result in
different forms of spaces;  shifts in the cultural context bring forth a
diversification and  hybridisation of sports and its buildings, and the
emergence of mega events results in new design typologies and effects urban
restructuring.


1. The Space of Play - material technologies

The relation between the movement of the human body and the space, surface
and enclosure has given the parameters by which to define the spatial
limitations of the game. New material technologies imply a changed relation
between the capacities of the human body and  the tools, surfaces and
enclosures of the space  - the space of the game can change, new games
invented, new strategies of play can evolve due to different surfaces.
Additionally the increased use of digital technology, such as  transmitter
screens, armchair screens and digital advertisement have changed the nature
of the space and the experience of the event.

1.1  spatial history of games
1.2 relation movement - surface - space (kinesiology)
1.3 space of play - change of strategies due to new materials (football
strategy research, game theory)
1.4 new technologies: surfaces + materials (NIKE research team)
1.5 impact of digital technologies & simulations


2.  Constructing the Sporting Subject

  From the emergence of mass sport in the late 19th century, sport has
frequently been used to serve ideological purposes. From its employment in
totalitarian systems as the organisation of massed bodies, its connotation
to  rationality and hygiene in modernism to an individual lifestyle demand
in the present, the cultural and social role of sport has invariably been
linked to its architectural formulations.

2.1  social history of sport
2.2  sport and ideology - the organisation of massed bodies
(nazism-communism)
2.3  sport and modernism , (Le Corbusier and hygiene)
2.4  typologies - the gym, the swimming pool etc.
2.5  sociological analysis today and new emerging forms of sport
2.6  brand space



3. Sport and the City

The increasing role and scale of sport mega-events  has two simultaneous
effects on architecture and the urban fabric. On the one hand, the
specificity of specialist forms of sports design shifts more and more to an
hybrid architecture of festivities and entertainment. Not only does the
building have to accommodate multi-functional programmes, it has to cater
to an all around entertainment spectacle to provide new typologies of
experience.  Additionally the building functions as signature branding, in
which the building type has to single out its identity. Traditionally
sports architecture had been governed by specialist firms, which now gives
way to their co-operation with architects providing a more specific
iconography. For the city the implications of this emerging scale of
economic investment in these projects serves as a marketing strategy in an
increasing inter-urban competition, equally they are launched as catalysts
for urban planning and redevelopment.
Another aspect pertains to the limitations of the urban fabric  to
accommodate the space and scale necessary for various forms of sports. A
variety of hybridised and miniaturised versions are the result : indoor
artificial landscapes, climbing walls, roof garden golf course simulators,
skate boarding parks and indoor skiing slopes to name but a few.

3.1 Olympics and the city
3.1  Mega events and the urban fabric
3.2  Mega events and new typologies (branding/theme park)
3.3  new spaces: artificial and interior landscapes




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I have a student who asked me why his maximum heart rate varied so much from
one test to the next.  On a one-off occasion his heart rate reached 217 bpm,
since, he has ranged between 188-196 bpm.  The method he used involved
performing 10 x 200 m sprints followed by 200 m recovery jogs.  Can anyone
explain the variation?  Could it be his polar heart rate monitor?

I would also be interested in the various field methods used for determining
maximum heart rate and people's experiences.

Thanks in advance

Chris Lorenzen

B App Sc (Hum. Mov.)(Hons)

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Hello,

I am pondering over some issues related to interval training
prescription.  From that pondering a couple of questions have emerged
which I do not have sufficient data or references to answer with
confidence:

Let us assume a well trained athlete is performing intervals at an
intensity equal to their maximal aerobic power or vVO2max (plus/minus
5%).  The interval bouts last 1 to 4 minutes.

Upon cessation of an interval:

1.  How much has creatine phospate concentration declined?  Assume
resting levels are equal to 35-40 mmol/kg dry muscle

2.  What will the creatine concentration be after 1 minute of passive
recovery?


I have a second-hand reference suggesting a half-time for CP resynthesis
of 170 seconds.  Do I hear a second on that?

What I want to be able to say is that the modest declne in CP levels at
the end of an interval performed near
100% MAP (and well warmed-up)  will be basically restored after 1 minute
of rest.  Anybody got data to support or refute that assumption?


regards,

Stephen Seiler Ph.D
Institute for Sport
Agder College
Kristiansand, Norway

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this is a rather basic question but different sources are offering
different explanations:during a given aerobic activity,let's say at
70%mhr,carb.stores are used to produce energy until depleation,fat
stores being next in line for energy production ,)then protein;another
source says carbs. first,then protein,then fat;another says
simultaneous but disproportional use but did'nt mention the
proportions),yet anothes asserts that at this intensity after 30 mins.
the prortion is 50% carb.calories burned ane 50% fat calories and no
mention of protein.HELP

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GSSI Members:

Hello! Many updates have been added to the Gatorade Sports Science
Institute website during the past couple months. Please take a moment to
check out a few highlights including three new articles. Also available in
this message are GSSI 2001 Conference highlights and a "Member Quote" contest.

NEW ARTICLES:
1) GSSI Hot Topic - "Childhood Obesity: A Worldwide Epidemic"
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2) Sports Science Exchange #81 - "Anemia and Blood Boosting"
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3) SSE Roundtable #44 - "Conditioning and Nutrition for Football"
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GSSI 2001 CONFERENCE
The "GSSI 2001 Conference: Optimal Training And Nutrition for Fitness and
Sport" was a great success last week in Phoenix. Thanks to all the speakers
and participants! Whether or not you were able to attend, you
may still benefit from the presentations. A CD-ROM with the visual
PowerPoint presentation material synchronized to live conference audio is
available for purchase. Click here for further information and to order
on-line.
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Stay tuned also for a "post conference news" section that will soon be
added to the website.

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I've thought a lot more about the question of the source of acid in
high-intensity exercise, and I have exchanged further messages with
Rob.  Once again, though, we have reached an impasse.

Rob wants fluxes to be important.  For example, the continual breakdown
(hydrolysis) of ATP to ADP and Pi releases H+, says Rob.  Ah yes, say I,
but the regeneration of the ATP by whatever process consumes the H+ again,
and at intensities of exercise that evoke 5-10 mM lactate, ATP falls
little, so there is little nett acid production from ATP.  Perhaps it will
clarify the issue if I state that you cannot calculate the pH change from
the rate of breakdown and resynthesis of ATP and other substances, but you
CAN calculate the pH change from the changes in concentration of those
substances.  Therefore it all comes down to concentration changes, not
fluxes.

It's actually quite easy to calculate the relative contributions of the
various substances, including lactic acid, to the increase in
acidity.  That's the substance of this message.

To do the calculation, you need the changes in concentration between rest
and exercise.  Rob sent me these concentrations and comments, for all-out
sprinting:

               concentrations (mM)
                rest    exercise
-------------------------------
pyruvate       0.1          15
NAD+, NADH     We do not know these yet due to the difficulty in measuring
                 cytosolic components vs. mitochondrial vs. total cellular.
lactate        1            25
ATP            8            5
ADP            0.003        0.1??? (this is a tough one due to assay
insensitivity!)
creatine-P     26           3
creatine       3            26
Pi             3            26
-------------------------------

Let's start with pyruvate.  The fact that it has risen by about 15 mM means
that some glucose has been converted to pyruvate.  The process (again,
thanks to Rob) is as follows:

C6H12O6  +  2 NAD+  -->  2 C3H4O3   +  2 NADH  +  2 H+
glucose                pyruvic acid

I don't know much about NAD+ and NADH, but I will assume that NAD+ is a
strong cation, like Na+ or K+, and that NADH is a neutral, non-dissociating
substance, like glucose.  Therefore any change in concentrations of NAD+ or
NADH don't contribute to acidity, even if the change in their
concentrations is in the mM range.

Notice that this conversion of glucose to pyruvic acid has produced one H+
for each molecule of pyruvic acid.  Therefore, with an increase in pyruvate
of 15 mM in the muscle cell during a sprint, there is a contribution of 15
mM of H+.

What about the pyruvic acid itself?  It's a relatively strong acid: it
would be half dissociated to pyruvate and H+ at a pH of 2-3 or so (I forget
exactly--that's the so-called pKa).  So at cellular pH it has to be
virtually completely dissociated to pyruvate and H+.  In other words, we
get another 15 mM of H+ from the dissociation of pyruvic acid!  The H+ gets
buffered in various ways, but that's not an issue.

Now let's tackle the lactate.  The process for formation of lactic acid
from glucose is as follows:

C6H12O6  -->  2 C3H6O3
glucose       lactic acid

Sure, there's a lot of missing steps involving transfers of H+ and H and
whatever.  But there is no nett production or loss of H+ in the missing
steps.  These missing steps will therefore matter only if one or more of
the intermediate compounds is a strong acid or base, AND if the
concentrations of these intermediates change by mM amounts.  Rob tells me
the intermediates are not strong acids or bases, so these missing steps and
intermediates are irrelevant.  Period.

But let's return to the lactic acid.  Like pyruvic acid, it has to be
virtually fully dissociated at physiological pH.  The change in lactate is
24 mM.  Therefore the dissociation of the lactic acid releases 24 mM of H+.

Next, the ATP.  This one is tricky.  ATP has dropped by 3 mM, but the ADP
has hardly risen at all.  I presume the missing ADP ends up as AMP + Pi.  I
didn't ask Rob this one, and he is away for a couple of days.  The reaction
for hydrolysis of ATP to ADP is:

ATP  +  H20  -->  ADP  +  HPi  -->  ADP  +  H+  +  Pi

I'm not sure how strong an acid the HPi is, when you start off with ATP at
physiological pH, but let's assume it dissociates completely to H+ and
Pi.  Let's also assume the ADP is hydrolyzed to AMP  +  Pi +  H+.  So that
makes a total of 6 mM of H+.

Finally, the creatine phosphate, which by hydrolysis has dropped by 23
mM.  The reaction is:

creatine-P  +  H2O  -->  creatine  +  HPi

Now, the HPi in principle dissociates to H+ and Pi, but I presume it
depends on the original ionic form of the P in creatine-P.   Rob didn't
provide me with a satisfactory answer here.  The question is:  what happens
to a neutral solution of creatine-P when you hydrolyze it?  Does it go
strongly acidic?  Rob seemed to think that hydrolysis of creatine-P absorbs
rather than releases H+, but he might have been thinking of the way
hydrolysis of creatine-P is coupled to resynthesis of ATP from ADP.  That
coupling is irrelevant here.  If you try to bring coupling in, you have:

ATP  +  H2O  +  creatine-P  -->  ADP  +  Pi  +  H+  +
creatine-P  -->  ATP  + creatine  +  Pi.

In other words, you have hydrolysis of creatine-P, and no consumption of an
H+.  So my suspicion is that hydrolysis of creatine-P results in release of
more H+, but let's leave it out of the picture for now.

To summarize, in all-out sprinting, H+ comes from the following sources in
the following proportions:
    formation of pyruvic acid     15
    dissociation of pyruvic acid  15
    dissociation of lactic acid   24
    hydrolysis of ATP             6
    hydrolysis of creatine-P      ??

So, until we know more about the hydrolysis of creatine-P, lactic acid is
responsible for 24/60, or 40% of the acid in all-out sprinting.  I think
people generally recognized that pyruvic acid was also responsible for some
of the acid, but they may not have realized it was a bit more than the
lactate, 50%.  The other 10% is from hydrolysis of ATP.

A final point.  We've been talking about intracellular acidosis, which I
hope I have shown is partly a lactic acidosis.  There is also acidity in
the blood in exercise, but in this case it is entirely a lactic acidosis,
or more properly a lactic acidemia.  No other anion (and H+ with it) is
released from muscle in substantial amounts, as far as I know, unless
there's substantial loss of pyruvate.  There's no release of Cl- (and H+),
because there is some depolarization of the active muscle cell (from gain
of K+), and that favors entry of Cl- into the cell, not loss of it.

If you know any biochemical gurus, please run this stuff past them for
comment.  I'd like to know where I've gone off the rails.  Ian Shrier is
probably right: if you ever think you understand something, it is only
because you don't know enough about it.

Will

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They were APPROVED by me by mistake.  I meant to DISCARD them.  The person
who posted the asthma message should have done a lit search, and the person
who posted the website about weights belts should have said something
interesting, summarized the site, or whatever.

I suggest you don't respond to them until they have met our guidelines for
messages. I had already contacted them about it.

Will

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-aul Check needs to check his facts about American weightlifters.

An American won the 77 men's class at the Junior worlds and two women got
medals in Sdiney

Tara Nott - gold - 48kg
Cheryl Haworth - bronze - 75+ kg

There are a number of studies looking at the usufulness or not of a
weightlfitng belt - start with the recent review by Escamilla et al. in
Exercise and Sport Science (Garret and Kirkendall eds) Lipincott Willliams
and Wilkins.

mike stone


rpsport@...,internet writes:
>This would an interesting topic to discuss in the forum. Should weight
>belts be worn as a back support?
>Refer to the following link:
>
>http://www.chekinstitute.com/articles.cfm?select=16
>


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The National Strength & Conditioning Association has developed a
Strength & Conditioning Professional Standards & Guidelines document.
This document is posted online (in HTM & PDF formats) at the NSCA web
site:
http://www.nsca-lift.org/publications/standards.htm

The purpose of this project is to help identify areas of liability
exposure, increase safety and decrease the likelihood of injuries that
might lead to legal claims and suits, and ultimately improve the
standard of care being offered.  It is hoped that Strength &
Conditioning practitioners and the institutions employing them will
mutually benefit from applying this information, and in turn
significantly enhance the quality of services and programs provided to
their athletes.

This document is the result of a year-long project undertaken by the
NSCA Professional Standards & Guidelines Task Force.  Phase I, which
involved researching, authoring and reviewing the document, was
completed earlier this year.  The NSCA Board of Directors adopted the
final document in its entirety in January 2001, and in July 2001
approved the distribution and promotion plan which will comprise phase
II.  That effort is now underway, and is being coordinated through the
Education Department at the NSCA National Office.

Steven Scott Plisk, M.S., C.S.C.S.
Chair  •  NSCA Professional Standards & Guidelines Task Force
Director of Sports Conditioning  •  Yale University
P.O. Box 208216
New Haven, CT  06520-8216
tel: 203 432-2526     fax: 203 432-2495
e-mail: <steven.plisk@...>
http://www.yale.edu/athletic/Strength/strength.htm

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Lecturer in Sport and Exercise Nutrition
Department of Human Nutrition, University of Otago, Dunedin, New Zealand

An exciting opportunity is about to become available in New Zealand's only
Department of Human Nutrition.  Applications are invited for either a
confirmation path or fixed term (three year) position in sport and exercise
Nutrition, depending on the background and the attributes of the applicant.

The University of Otago's Department of Human Nutrition is the first
established academic department of its kind in New Zealand.  The department
has expanded rapidly during the past few years and there are at present
about 350 students enrolled in its undergraduate courses and 86 in post
graduate courses.  Post graduate options currently include Honours,
Masters, Post Graduate Diploma's and PhD programmes. Staff members have a
wide range of special interests and research activities. The department
also runs New Zealand's only professional dietetic education programme, the
primary function of which is to deliver the distance taught Post Graduate
Diploma in Dietetics which prepares students for dietetic registration.

The primary responsibilities of the position include student learning in
sport and exercise nutrition.  This area is well established within the
Department.  The appointee is expected to develop an independent or
collaborative research programme.

Key Tasks for the Position include:
Coordination of a 200 level Sports Nutrition paper.
Teaching specialist areas in other Sports Nutrition papers.
Teaching specialist areas in departmental undergraduate papers.
Research student supervision.
Develop and maintain an area of independent research.

Person Specification
Applicants should have a relevant post graduate qualification.
Practical work experience in varied areas of sports nutrition is desirable.
Work experience in sports nutrition education is desirable.
The lecturer will need to demonstrate commitment to and enthusiasm for the
area of sports nutrition.

Salary will be within the lecturer range NZ$46,350 to NZ$57,165 per annum
depending upon qualifications and experience. An exceptionally qualified
candidate may be appointed at the senior lecturer level.

Initial enquiries should be directed to Professor Jim Mann, Department of
Human Nutrition, University of Otago, P O Box 56, Dunedin, New Zealand
(Fax: +64 3 479 7958, E-mail: jim.mann@...).

Reference Number AG01/48   Closing date  Friday 28 September 2001

METHOD OF APPLICATION
Further details regarding this position, the University and the application
procedure are available from the Deputy Director, Personnel Services,
Univesity of Otago, P O Box 56, Dunedin, New Zealand (Fax No: 64-3-474-1607).

Applicants should send two copies of their curriculum vitae together with
the names, addresses and fax numbers of three referees, to the Deputy
Director of Personnel Services by the specified closing date, quoting the
appropriate reference number.

If an applicant is shortlisted for the interview, whanau support will be
welcome.

Equal opportunity in employment is University Policy.

===============================================================
Christine D.Thomson
Associate Professor
Department of Human Nutrition, University of Otago,
P.O. Box 56, Dunedin, New Zealand
TEL: 64-03-479-7943,  FAX: 64-03-479-7958
Email:christine.thomson@...
===============================================================

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Greetings from the Universidad de Costa Rica. This is to invite you to the
VIIIth International Symposium on Sports Sciences, Exercise and Health. This
event will be held in San José, Costa Rica, from November 7th to November 10th.
Please visit our web page to find out more information:

http://cariari.ucr.ac.cr/~edufiucr/congresos/simposio/viisimposioingles.htm

Thank you.

Jose Moncada, M.Sc.
School of Physical Education and Sports
School of Medicine, Department of Physiology
Universidad de Costa Rica
P.O.Box 239-1200
San José, COSTA RICA

Tel: + 506 207-3269
Fax: + 506 225-0749

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Apparently the NSCA's web server has been down for several days due to a
lightning hit over the weekend.  Until they get their system up and
running again, the Strength & Conditioning Professional Standards &
Guidelines document will be available at the following link:
http://www.yale.edu/athletic/Strength/Downloads/SCPSG.pdf

Apologies for any inconvenience - we won't let acts of nature keep this
information from anyone!

Steven Scott Plisk, M.S., C.S.C.S.
Chair  •  NSCA Professional Standards & Guidelines Task Force
Director of Sports Conditioning  •  Yale University
P.O. Box 208216
New Haven, CT  06520-8216
tel: 203 432-2526     fax: 203 432-2495
e-mail: <steven.plisk@...>
http://www.yale.edu/athletic/Strength/strength.htm

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I have been debating with myself on a topic that the applied sport
scientists and coaches interested in periodization might like to
discuss:  how do you set training pace?

One option is to set training pace relative to expected (predicted) race
pace. For example say you intend to run at 19km/hr in a triathlon in 3
months time. You include, in your periodised plan, training at this pace
starting in your first week with say 2x400m at this pace and build up to say
6-7x1000m. Now initially that might mean that you are working at higher
heart rates and lactate levels. The concept would be to show your body the
specific speed. In this model when you feel bad you stop, so you might only
do 5x1000m when you had 6x1000m planned, but it was all at race pace.

The other option is to work out what intensity you will be racing at (Heart
Rate, Lactate) and train the energy systems used in racing (Bompa
Periodization 4th edition p357-366).

In the above example you might start with 3x1000m with a Heart Rate average
over the last 400m of 165 and this might be 17.5km/hr and then progress
through the three months to 19km/hr. The concept is to show your body the
specific intensity from an energy system perspective. In this model you run
slower when you don't feel as good but still cover the distance.

Can anyone give a conclusive argument for one over the other? Are they
equally valid? What about published work looking at this issue?

Brendon Downey
Manager
Sport Science & Medicine Clinic
Sports Super Centre
Morala Ave, Runaway Bay 4216 Qld
AUSTRALIA
PH: 617-55 00 9830
FAX 617-55 00 9831
http://www.brendondowney.com
http://www.sportssupercentre.com.au
brendon@...

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Hello again;

The topic/saga of the cause of intramuscular acidosis continues yet again!

In noticed that Will had submitted another commentary based on some of my
input.  I need to clarify and correct some items that Will included in his
posting.

1. The regeneration of ATP does not consume a proton.
When ATP is regenerated in the cytosol there is no consumption of a proton.
The proton produced from ATP hydrolysis comes from water.  The transfer of a
phosphate to ADP does not require a proton, as there is no need for added
protons or electrons.  Whenever you have an increases in ATP turnover that
is fueled by the regeneration of ATP from the CK and AK (myokinase)
reactions, or glycolysis, you get an increase in proton release.  This is
why flux is so important.  ATP can be unchanged, but you can have a greater
reliance on the phosphagen system and glycolysis for ATP.  This situation
results in a tremendous increase in the rate of proton release!

2. There are no acid intermediates of glycolysis.
As I have stated before, when the first caroxylic intermediate of glycolysis
is formed - 3 phosphoglycerate, it is devoid of a proton on the carboxyl
functional group.  This means it is ionized.  Thus, every other carboxyl
intermediate that follows is also ionized - 2 phosphoglycerate,
phosphoenolpyruvate, pyruvate, and yes even lactate.  I do not know why Will
is so emphatic about the existence of pyruvic acid and lactic acid.

3. NADH accumulation is associated with an added proton.
It is not an issue as to whether NADH releases a proton.  When NADH is
formed from glyceraldehyde 3-phosphate being converted to 1,3
bisphosphoglycerate, NADH + H+ is produced.  Conversely, when using NADH to
reduce a molecule (pyruvate), and added proton is consumed.  Whenever there
is an increases in NADH (decrease in cytolosic redox), you also have an
increase in proton release.

4. Glycolysis phase 2 intermediates are ionized forms of strong acids
Will mentioned that I indicated that the intermediates after
3-phosphoglycerate were not strong acids.  However, what I really said was
that it was irrelevant, based on item 2, above.  These intermediates could
accumulate, but it would not change proton exchange as there are no protons
to release.

5. AMP is produced without a release of a proton.
AMP results from the adenylate kinase (AK) (or myokinse) reaction, where
ADP + ADP -----> AMP + ATP

6. There is no intracellular hydrolysis of CrP.
In-vivo, CrP hydrolysis is coupled to ADP phosphorylation, forming ATP.
Thus, there is no release of a proton, and no Pi as a product.
CrP + ADP + H+ -----> ATP + Cr
The reaction consumes a proton due to the need to complete the chemical
structure of Cr.  Unless Will wants to re-invent cellular biochemistry, this
coupling is totally important!!!!  Will's coupling equations are totally
wrong because he doesn't understand that the enzymatic coupling of two
reactions is not represented by the net combining of the two chemical
reactions.

7. Summary of proton sources
There are no protons resulting from Will's first 3 components, or the last.
The only protons that come from the catabolism of CHO in skeletal muscle
during muscle contractions are glycolysis and ATP hydrolysis.

8. Blood lactate and pH
Due to the lactate-proton transporter, there will always be an association
between increasing blood lactate and decreasing pH.  However, association
does not mean cause and effect.  Remember, we teach this concept to our
students!!

9. Biochemical gurus
I guess Will does not view my knowledge as coming from a biochemist!  If
no-one out there questions my view of the development of acidosis, then my
interpretation is that there is support for the biochemical basis for what I
am saying.  Maybe more of you need to mention this to Will!  Furthermore, I
have not been the only scientist to question the concept of a lactic
acidosis.  See the following for additional published support for my
arguments.

Busa WB, Nuccitelli R (1984).  Metabolic regulation via intracellular pH.
Am J Physiol 246, R409-R438

Dennis SC, Gevers W, Opie LH (1991).  Protons in ischemia: Where do they
come from; where do they go to?  J Mol Cell Cardiol 23, 1077-1086

Gevers W (1977).  Generation of protons by metabolic processes in heart
cells. J Mol Cell Cardiol 9, 867-874

Gevers W (1979).  Generation of protons by metabolic processes other than
glycolysis in muscle cells: a critical view [letter to the editor].  J Mol
Cell Cardiol 11, 328

Hochachka PW, Mommsen TP (1983).  Protons and anaerobiosis. Science 219,
1391-1397

Noakes TD (1997).  Challenging beliefs: ex Africa semper aliquid novi.  Med
Sci Sports Exerc 29,571-590

Vaghy PL (1979).  Role of mitochondrial oxidative phosphorylation in the
maintenance of intracellular pH.  J Mol Cell Cardiol 11, 933-940

Wilkie DR (1979).  Generation of protons by metabolic processes other than
glycolysis in muscle cells: A critical view.  J Mol Cell Cardiol 11, 325-330

Zilva JF (1978).  The origin of the acidosis in hyperlactataemia.  Annals of
Clinical Biochemistry 15, 40-43

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Dear Sir/Madam

We are very pleased to inform you that Iran's First International Football
Forum (IFIF'2001)will be held in Tehran on 12 and 13 November 2001 by
Football Union of Iran with supporting and presence of National Olympic
Committee, Physical Education Organization (A Governmental Organization
affiliated to Presidency of Iran), I.R. Iran Broadcasting as well as
Football Federation of Iran.
The Forum has adopted the theme and the mission of looking at "Past,
Present & Future of the Football in Asia". The main objective of the
Forum is to promote level of football in Asia by using of surveying
the professionals involved in the world football industry.
Beside of this Forum, a specialized Exhibition being held which
industries, domestic and foreignclubs and other authorities related
to football will be invited to participate at the said Forum.

Since the time for receipt of Papers is going to be finished, so we
hereby invite you to attend this important by presenting a paper
on Forum's Proposed Subjects. Closing date for receipt of abstracts
is 25th Aug. 2001 and for complete text is 30th Sep. 2001.

Please let us have your favorable response in order to enable us
to make necessary arrangements. For detailed information, such as
Call for papers, Sponsors, Registration and Proposed Two-day Schedule
visit Forum's website www.rahyar.com/football.

Thanking you in advance for your valued co-operation.



Regards,
M. Dehmeshki
Coordinating Manager of the Forum
Mobile: +98 911 215 0535

The Secratriate of the Forum:
Rahyar Bamin Co.
Tel: +98 21 753 2864, Telefax: +98 21 752 8354
Email: football@...

Forum's Proposed Subjects:
* Investment opportunities in Iran's Football
* The role and place of press, mass media & new media in respect of football
* Ethical aspect in football playing (Fair Play)
* Studying the problems of judgment and referees
* Surveying the experiences of the world's successful clubs
* The outline of development trend of football in Asia in comparison
	 with other part of the world
* The role of finance, marketing and sponsors in improvement of football
* The procedures of student's training with different ages in football schools
* The role and place of governments in development of football
* The role of football in acquaintance and friendship among
	 the nations and in the other hand dialogue among the civilizations

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I understand that it used to be thought that gastric emptying and absorption
of fluid from the intestine could occur only at a maximum rate of ~1 L/h,
but that this has been questioned recently. I have seen reference to a rate
of fluid uptake of ~2 L/h, but cannot now locate the reference.

If the lower rate is correct, it means that typical sweat rates associated
with fairly hard work in the heat (up to 2 L/h) will inevitably lead to
hypohydration. If the upper rate is correct, this implies that it is
possible to rehydrate at the same rate as water is lost through sweating,
unless the sweat rate is extreme (> 2 L/h) .

Can anyone provide references to the current position with regard to maximum
rate of fluid uptake, please.

Chris Forbes-Ewan

Task Coordinator, Nutrition
Defence Nutrition Research Centre
76 George St
SCOTTSDALE  Tas  7260
AUSTRALIA

Phone: Int + 61 3 6352 6607 (03 6352 6607 in Australia)
Fax:     Int + 61 3 6352 3044 (03 6352 3044 in Australia)

E-mail: chris.forbes-ewan@...

The opinions expressed in this message are those of the author and should
not be taken to represent the official position of the Defence Science and
Technology Organisation or of the Australian Department of Defence

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Dear All,

The following message is posted on behalf of the Department of Physiology at
the Australian Institute of Sport.

The Department of Physiology at the AIS has this weekend advertised two
positions (job descriptions below):

1. Senior Physiologist
2. Scientific Officer (available until April 2003)

Information and Job descriptions available at:
www.ausport.gov.au/asc/employment or calling (02) 6214 1427.

Contact officer is: Allan Hahn on (02) 6214 1564 or at
allan.hahn@...

Applications close on 3 September 2001. Applications should address at least
section G of Job Description.



AUSTRALIAN SPORTS COMMISSION

JOB DESCRIPTION

Position Title: Senior Sports Physiologist
Position No:  654
Grade:  Sports Officer Grade 4
				 $63,000 - $66,000 per annum plus
superannuating and other employment benefits
Division:  Sports Sciences
Program:  Physiology
Manager:  Head of Physiology
Date amended: 9 August 2001
___________________________________________________________________


A.   Primary Job Purpose

	 To provide high level physiology services to a major AIS sport and
to assist with the development and operation of scientific programs for a
variety of other sports.


B.  Major Responsibilities

	 * To be the primary physiology consultant for a major AIS
sport.
	 * To assist other AIS physiologists in the design and
implementation of effective scientific services to a range of sports,
including those visiting the AIS under the various arrangements.
	 * To plan and conduct applied research in consultation with
coaches and the Steering Committee of the AIS Physiology Department
	 * To provide supervision and guidance to at least one PhD
Scholar working with the primary sport.
	 * To assist in the development of new measurement techniques
and facilities (including equipment) that can improve the quality of
information provided to athletes and coaches.
	 * To participate in and contribute to the activities of a
Cooperative Research Centre (CRC) for MicroTechnology, of which the AIS is a
member.
	 * To co-ordinate and conduct high quality physiological and
anthropometric tests on athletes.
	 * To present the results of physiological  tests to coaches
and athletes and provide practical recommendations based on test outcomes
	 * To assist with the administration of the AIS Physiology
Department, including the formulation of departmental policies.
	 * To contribute to the development of a national network in
sports physiology through regular liaison with colleagues in State Sports
Institutes, Academies and Universities.
	 * To disseminate information through participation in
appropriate conferences and through publication of articles in coaching and
scientific journals.
	 * To assist in developing a co-ordinated National approach to
the provision of Sports Science services.

C.  Issues and Challenges


	 * To maintain a balance between the leadership, servicing and
research aspects of the role.
	 * To develop a close working relationship with AIS and
national coaches, particularly in the primary sport.
	 * To oversee and facilitate a working relationship between
coaches and PhD Scholars that is conducive to high quality research and
servicing of athletes, resulting in the development of practical solutions
to problems limiting the performance of athletes.
	 * To liase effectively with University and Industry
colleagues.
	 * To obtain internal and external research grants.
	 * To contribute toward a national approach to the provision of
Sports Science services.
	 * To be familiar with the operation of a wide range of
laboratory and field testing equipment.
	 * To conform to strict Quality Assurance standards in the
conduct of all laboratory and field tests, and to provide leadership in
ensuring the AIS laboratory meets these standards.
	 * To develop new and innovative approaches to the monitoring
of athletes.
	 * To keep up-to-date with physiological literature that may
have relevance to sport, and to critically evaluate this literature.

D. Decision Making and Accountability

To be responsible for:
	 * co-ordinating physiological support to selected AIS and NAP
sports.
	 * determining the most effective testing programs for
monitoring of athlete performance.
	 * designing and conducting applied research projects that
yield practical benefits to AIS and national athletes.
	 * supervising and guiding at least one PhD Scholar.
	 * contributing effectively to the activities of the CRC for
MicroTechnology.
	 * setting-up and calibrating equipment, and conducting tests
in accordance with rigorous internal and external Quality Assurance
standards.
	 * timely preparation and interpretation of test results and
literature reviews for presentation to coaches and athletes.
	 * evaluating external research findings for possible
applicability to AIS programs.


E.  Job Dimensions

E.1. People Management

	 * Supervising PhD Scholars, work experience students, research
assistants and other staff involved in physiological testing and research.
	 * Providing a primary point of contact for coaches, athletes
and administrators from selected sports.
	 * Liasing with external contractors, research collaborators
and industry colleagues in relation to specific projects.

E.2. Financial Management

	 * Operating within the budget for laboratory consumables
allocated to specific sports.
	 * Maintaining an awareness of departmental and research budget
constraints.
	 * Administering research grants and any funds provided by
National Sporting Organisations for specific purposes.

F.  Key Performance Indicators

	 * Feedback from coaches on the effectiveness of physiological
support to specific sports (particularly the primary sport).
	 * Feedback from other physiologists and the Physiology
Department Laboratory Manager on the quality of support provided.
	 * Accurate set-up and calibration of testing equipment
	 * Effective conduct of laboratory and field tests.
	 * Involvement in research projects of a highly applied nature
	 * Participation in professional conferences and publication of
articles in coaching and scientific journals.
	 * Effective supervision of a PhD Scholar.
	 * Effective participation in the CRC for MicroTechnology.


G.  Job Holder Requirements

G.1.Qualifications

	 A postgraduate qualification at PhD level in Physiology or a related
area is essential.

G.2. Experience

		 *  An equivalent of at least 3 years full-time
experience in a Physiology testing laboratory or closely related facility is
required.
		 *  Experience in working with elite coaches and
athletes is desirable.
		 *     Experience in strength, power and neuromuscular
assessment of athletes is considered advantageous.


G.3. Specific Technical Skills

Requirements include:
		 *       Demonstrated ability to conduct independent
research, and to apply the findings in practical settings.
		 * Demonstrated ability to take a leadership role in
the scientific and managerial aspects of laboratory and/or field work.
		 * Familiarity with basic physiological testing
equipment and procedures.
		 * Good computing skills, including familiarity with
Microsoft Office and various statistical packages.
		 * Excellent oral and written communication skills.

G.4. Personal Attributes

		 *  Love of sport
		 * Enthusiasm, reliability and creativity
		 *  Good interpersonal skills.
		 * Ability to work effectively as a member of a team.
		 * Ability to work independently where necessary.
		 * Willingness to work unconventional hours, including
some weekends.
		 * Willingness to travel with teams for up to several
weeks per year.
		 * Ability to articulate a "vision" concerning ways in
which Sports Science may contribute to improvement in the performances of
Australian athletes in the coming years.

H. Organisational Framework

The occupant of the position will report directly to the Head of the
Physiology Department, and will be a member of the Physiology Steering
Committee that is responsible for the planning and monitoring of general
Departmental activities. He/she will be responsible for the activities of a
"staff stream" consisting of Scientific Officers, Technical Officers,
research assistants and sport-based PhD scholars.



AUSTRALIAN SPORTS COMMISSION

JOB DESCRIPTION

Position Title: 	 Scientific Officer
Position Number: 	 187
Grade: 			 SO3
					 $44,000 - $46,000 per annum plus
superannuation and other employment benefits
					 Job available until April 2003
Division: 			 Sports Sciences
Program: 			 Physiology
Manager: 			 Head of Physiology
Date amended: 		 13th August 2001
___________________________________________________________________________

A.  Primary Job Purpose

		 To provide physiological support to selected AIS and
national sports programs.

B.  Major Responsibilities

		 *       To assist senior scientists in their work with
high-priority AIS and national sports squads
		 * To be the primary Physiology consultant for several
other AIS and national sports programs
		 * To set up and to calibrate equipment required for
laboratory and field monitoring of athletes
		 * To conduct appropriate physiological and
anthropometric tests on athletes from a wide range of sports
		 * To process test results, carry out statistical
analyses and prepare reports
		 *       To assist in conducting applied research
projects

C.  Issues and Challenges

		 *       To work in close cooperation with senior
scientists to ensure an effective team approach to the implementation of
scientific support programs for        specific sports
		 * To develop and administer appropriate programs of
physiological support for other sports
		 * To be familiar with the operation of a wide range of
laboratory and field testing equipment.
		 * To maintain the highest standards in equipment
calibration
		 * To conform to strict Quality Assurance and OH&S
standards in the conduct of all laboratory and field tests
		 * To effectively summarise scientific literature on
specific topics
		 * To present results to senior scientists, coaches and
athletes in a clear format

D. Decision making and Accountability

	 To be responsible for:
				 * coordinating physiological support
to selected AIS and national squads
				 * setting up and calibrating
equipment required for athlete testing
				 *    successfully conducting laboratory and
field testing
				 *   timely preparation of test results
and literature reviews for presentation to senior scientists, coaches and
athletes





E.  Job Dimensions

	 E1.  People Management.

		 * Supervising work experience scholars and research
assistants involved in physiological testing and research
		 * Providing a primary point of contact for coaches,
athletes and administrators from specific AIS and national sports programs

	 E2.  Financial Management.

		 * Operating within the budget for laboratory
consumables allocated to specific sports
		 * Maintaining an awareness of departmental and
research budget constraints

F.   Key Performance Indicators

		 * Feedback from senior scientists and the Physiology
Department Laboratory Manager on the quality of support provided
		 *    Accurate set-up and calibration of testing equipment
		 * Effective conduct of laboratory and field tests
		 *    Feedback from coaches on the effectiveness of
physiological support to specific squads

G.  Job Holder Requirements

	 G1.  Qualifications.

			 A postgraduate qualification in sports physiology or
a related area is essential.

	 G2.  Experience.

				 * An equivalent of at least 12 months
full-time experience in a scientific laboratory or closely related facility
is required.
				 *    Expertise in the physiology of motor
skill acquisition is considered advantageous.

		 G3.  Specific Technical Skills

	 Requirements include:
				 * Familiarity with basic physiological
testing equipment and procedures
				 * Good computing skills, including
familiarity with Microsoft Office and various statistical packages
				 * Excellent oral and written
communication skills

	 G4.  Personal Attributes

				 * Love of sport
				 * Enthusiasm, reliability and
creativity
				 * Good interpersonal skills
				 * Ability to work effectively as a
member of a team
				 * Ability to work independently where
necessary
				 * Willingness to work unconventional
hours, including some weekends
				 * Willingness to travel with teams for
up to several weeks per year


H. Organisational Framework

			 * This position is accountable to the Head of
the Physiologist and to various senior scientists according to the sport
under assessment. For certain duties the position is also accountable to the
Physiology Department Laboratory Manager.
			 * No staff members report directly to the
occupant of this position, although in some circumstances the occupant will
be responsible for overseeing the practical work of research assistants,
sport-based PhD scholars and visiting students.





Rebecca


Rebecca K Tanner
Laboratory Standards Co-ordinator
Australian Institute of Sport
PO Box 176
Belconnen  ACT  2616

Phone: +61 2 6214 1563
Fax:  +61 2 6214 1603
E-Mail: Rebecca.Tanner@...
Web site:      www.ais.org.au/lsas


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The Department of Sport & Exercise Science at the University of
Portsmouth, England seek to appoint a Senior Lecturer to help
establish a new degree programme in Aquatic Sports Science and
act as Course Leader.  The successful applicant will have a first
degree and higher degree in Sports Science or a related discipline,
have contacts within the water-based sport network and possibly
be an active participant in an aquatic sport.

For further details please contact the Head of Department, Alun
Rees on 023 92 842659 (email alun.rees@...)

Closing Date:  7th September 2001

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Last week I sent a message requesting advice on current beliefs about
maximal rates of gastric emptying and intestinal absorption of fluids.

The relevant sections of all replies I received are below my signature block
in the order in which I received them.

In addition, the following is a summary of my understanding of the present
state of knowledge in this area, based on the information provided by
subscribers to Sportsci and some of the references they provided:


The importance of determining the maximal rate at which an athlete can
absorb water is illustrated by the sweat rate of 3.7 L/h reported by
Armstrong et al [Phys Sportsmed 1986;14:73-81] for Alberto Salazar at the
1984 Los Angeles Olympic Games. Other (anecdotal) reports of ~3 L/h sweat
rates suggest that Salazar may not be alone. If the commonly applied 'rule
of thumb' is right--that fluid can be absorbed only at a rate of about 1
L/h--then some athletes clearly cannot avoid a high level of hypohydration
within two hours of commencing very vigorous activity in the heat.

Although such athletes may not be able to replace all the water lost as
sweat through drinking, there are other factors of significance to hydration
status. Muscle glycogen is stored with water (which is released as glycogen
is mobilised) and the amount of metabolic water produced by the catabolism
of carbohydrate and fat (to H2O + CO2) also needs to be considered. Rogers
et al [Med Sci Sports Exerc 1997;29(11):1477-1481] found that
ultra-endurance athletes who had engaged in 21 km canoeing, 97 km cycling
and 42 km running were approximately in water balance despite drinking a
quantity of fluid equivalent to only ~80% of their sweat losses (mean value
of sweat rate was 940 mL/h).

Also, the common belief that fluid can be emptied from the stomach and
absorbed from the intestine at a rate of only about 1 L/h may be incorrect.
Gisolfi and Ryan [In: Buskirk ER, Puhl, SM, eds. Body Fluid Balance:
Exercise and Sport. Boca Raton, FL: CRC Press, 1996:19-51] discuss papers
reporting that both emptying and absorption can occur at ~2 L/h. Combined
with release of water from glycogen and the generation of metabolic water,
this should allow for water balance even if sweat rate is slightly in excess
of 2 L/h (perhaps up to ~2.5 L/h, extrapolating from the findings of Rogers
et al, 1997).

Nevertheless, Noakes [Exerc Sport Sci Rev 1993;21:297-330] states that "...
high rates of fluid intake (> 1 liter/hr) are achieved with difficulty
during exercise, especially when
running, and are likely to lead to feelings of abdominal discomfort,
possibly due to the accumulation of unabsorbed fluid in the small bowel or
colon."

It may be that the action of running leads to abdominal discomfort if large
quantities of fluid are consumed, while the same problem may not apply (or
not to the same extent) for athletes such as cyclists and canoeists. Gisolfi
and Ryan (see reference above) seem to imply that GE is not impaired during
cycling compared to resting when they state that "Cycling has not
consistently been shown to enhance GE ABOVE (my emphasis) resting values.
Data on other modes of exercise does not exist."

My (current) belief is that at least in theory, sweat rates of ~2 L/h or
even slightly more should not be incompatible with maintenance of
euhydration for several hours, through a combination of ingested fluid,
water released from glycogen mobilisation and the production of metabolic
water. This may be harder to achieve when running than when cycling. The
practicality of drinking at a rate approaching 2 L/h (from the point of view
of discomfort due to excessive stomach distension and/or accumulation of
water in the small intestine or colon) needs more research.


I would be pleased to receive constructive criticism of this (very brief)
summary.

Chris Forbes-Ewan

Task Coordinator, Nutrition
Defence Nutrition Research Centre
76 George St
SCOTTSDALE  Tas  7260
AUSTRALIA

Phone: Int + 61 3 6352 6607 (03 6352 6607 in Australia)
Fax:     Int + 61 3 6352 3044 (03 6352 3044 in Australia)

E-mail: chris.forbes-ewan@...

The opinions expressed in this message are those of the author and should
not be taken to represent the official position of the Defence Science and
Technology Organisation or of the Australian Department of Defence

FIRST REPLY
You make a good point. I think that GE can reach rates higher than 1 l/h,
but don't have a reference that shows that . Indeed, Coyle and Montain
(1992) state that 1 L/h may be the limit, but I know that ultraendurance
athletes generally consume 1 to 2 L of fluid per hour depending on the
athlete's sweat rate and the temperature (Laursen and Rhodes, 1999; Clark et
al., 1992; Noakes, 1992). Personally speaking, as a former ultraendurance
triathlete, I'm pretty sure that I consumed greater than 1 l/h during
ultraendurance performance in high temperatures. Don't forget also that this
rate would also likely be affected by the physical size of the athlete, with
larger individuals likely having a larger pylorus.
Coyle EF, Montain SJ. Carbohydrate and fluid ingestion during exercise: are
there trade-offs? Med. Sci. Sports Exerc. 1992; 24(6), 671-687.
Clark, N, J Tobin, C Ellis: Feeding the ultraendurance athlete: Practical
tips and a case study. Journal of the American Dietetic Association. 1992,
92(10), 1258-63.
Noakes TD: The hyponatremia of exercise. International Journal of Sport
Nutrition. 1992, 2, 205-228.
Laursen, P.B., and E.C. Rhodes: Physiological analysis of a high-intensity
ultraendurance event. Strength Cond. J. 21(1):26-38, 1999.

SECOND REPLY
Nancy Rehrer did a good review on this in 1995 in MSSE?
The GSSI site has all the references on fluid absorption. One of the
references must reference the basic research.

FYI when I was training for Ironman, I rode in a heat chamber for 5 hours at
30C and 50-60% humidity at 270 watts on 4 occasions over 4 weeks. I measured
temperature, sweat rate, urine production and body weight. I drank 1.1 L per
hour of a 7% CHO solution with 30 mmol NaCl with a 300 ml start. I found
that in the first week my stomach was full and very uncomfortable. In the
second week it felt full but comfortable, in the third week it was fine and
in the 4 week I could have drunk a lot more.

Additionally if you are exercising you liberate H2O stored with Glycogen and
also produce metabolic water. There are equations on this. But I seem to
remember that 600g Glycogen has 1.2L of H2O and will also produce 1/2L of
water, but don't quote me on that.

So you do not need to equal sweat rates with fluid replacement (read emptied
from the stomach into your body's ECF and ICF).

Also check out the Ironman Nutrition article on the sport sci web site.

THIRD REPLY
I remember reading somewhere that elite marathon runners such
as Alberto Salazar had a sweat rate of more than 3 Liters per minute during
the
Los Angeles olympic marathon, but I cannot find the reference.


FOURTH REPLY
I've always been taught to use the 1L/h rule of thumb, but lately this has
been
shown to be inaccurate, so I've changed my thought.  Teaching sport
nutrition
I've found a reference to a much higher level of gastric emptying in the
text.
In the text book, Sport Nutrition for Health and Performance, by Melinda
Manore,
they reference that rate to be approximately 40 ml per min translated to 2.4
L/h.  This is referenced to Gisolfi and Ryan , 1996 (Ref follows).
Gisolfi CV, Ryan AJ.  Gastrointestinal physiology during exercise.  In:
Buskirk
ER, Puhl, SM, eds.  Body Fluid Balance: Exercise and Sport.  Boca Raton, FL:
CRC
Press, 1996:19-51.


FIFTH REPLY
I don't know the references, but I do know two of my friends who have done
triathlons and gained weight over the 3 hours.


SIXTH REPLY
Greater rates of fluid ingestion had no measurable effects on plasma volume
and osmolality and did not improve 2-h running performances in a 25 degrees
C environment: 150 or 350 mL x 70 kg(-1) body mass (approximately 130 or
300 mL) every 15-20 min, or 20 fluid ounces vs 40 fluid ounces per
hour....[Daries HN, Noakes TD, Dennis SC, Med Sci Sports Exerc 2000
Oct;32(10):1783-9.] Fluid intake of 20 fluid ounces/hour were satiating and
adequate.

I have not read anything indicating a faster fluid loss from sweat rate
than -1.2 liters/hr.

Noakes wrote: "At low sweat rates (< 1 liter/hr), it is probable that all
of the lost fluid can and should be replaced; rates of fluid ingestion
needed to offset higher sweat rates may exceed the maximum intestinal
absorptive capacity for water. Furthermore, high rates of fluid intake (> 1
liter/hr) are achieved with difficulty during exercise, especially when
running, and are likely to lead to feelings of abdominal discomfort,
possibly due to the accumulation of unabsorbed fluid in the small bowel or
colon." [Exerc Sport Sci Rev 1993;21:297-330]

Circulatory fluid shifts were studied in MIDDLE-AGED MARATHON RUNNERS (6
males and 5 females, ages 32-58 yr) during a 42.2-km marathon race run in
mild weather (dry-bulb temperature = 17.5-20.4 degrees C). Running times
for the subjects were 3:12-4:40 (mean values were 3:34 for males and 4:10
for females). Venous blood samples were taken without stasis in all
subjects seated at rest before the start of the race and within 3 min of
finishing; eight of the subjects also paused for samples at 6 and 27 km
during the race. At 6 km, body weight loss averaged less than 1%, whereas
plasma volume (PV) had decreased by 6.5% in male subjects and 8.6% in
female subjects. By the end of the race, hypohydration had reached 3.2% in
male subjects and 2.9% in female subjects, but PV in both groups remained
stable. SWEAT RATES DURING THE RACE AVERAGED 545 and 429 g X m-2 X h-1 for
male and female subjects, respectively, with ad lib. water intake replacing
21-72% of fluid loss. [J Appl Physiol 1985 Aug;59(2):559-63.]

At this point, I do not know how to rationally explain hyperthermic
exercise fluid balance by drinking in enough to replenish losses.
Other than slowing down the pace to a crawl, taking long walk breaks,
the rehydration problem during competitive exercise is not possible. If
rehydration is possible beyond the 21-72% observed, please inform me.


SEVENTH REPLY (FOLLOWUP TO SIXTH)
I have a file full of athletes who have suffered from muscle cramps, gastric
stress, from either dehydration or related hyponatremia. Their common report
include a fluid intake above 30 fluid ounces, a caloric intake above 300
calories, or a sodium intake below 300 mg each hour during hyperthermic
conditions in events lasting longer than 3 hours duration. When the fluid
intake is kept in the range of 16-30 fluid ounces, calories reduced to under
280, and sodium electrolyte increased to 300-600 mg/hour, 19 out of 20
resolve symptoms in follow-up similar conditions. Most of those who report
either hyponatremia or dehydration from any and all combinations of the
above were doing events in excess of 5 hours duration, with the bulk of them
doing triathlons in the 11 hour range or ultramarathon trail runs in the
50-100 mile range [9-29 hours].

If there is an exact position determining fluid replacement rate beyond 1
liter per hour, beyond 280 calories per hour, or one that gives sodium
electrolyte loss replacement beyond 600 mg. [2000 mg are lost per hour, but
the kidney recirculates cooperatively on less intake], I would be extremely
keen in participating in establishing reference range intake for endurance
athletes in hyperthermic exercise applications, basing the ranges on loss
vs repletion rate.





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Hello,

In our laboratoriumprotocol for measuring physical fitness we use the
Wingate-test. The Wingate-protocol starts with a warming-up for 5 minutes
with a load of 75 Watt. The last three seconds of the warming-up we
countdown and then the person on the bike has to cycle for 30 seconds as
hard as possible. On the moment the person has to cycle as hard as possible
the load increases dependent on the bodyweight.

The originaly Wingate-protocol from Barr-Orr starts three seconds before the
increased load with maximal cycling. I wonder why that is en what it tries
to measure. Can anyone explaine.

Regards,

Drs Jason van der Burgt
Human Performance Laboratoy Royal Netherlands Air Force
Soesterberg, The Netherlands


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