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[RC] Field trials - part three - Ridecamp Guest

Please Reply to: Bill Proctor oasisarab@xxxxxxxxxxx or ridecamp@xxxxxxxxxxxxx
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Next a few email exchanges

Tom?s response to his consulting Vet as I mentioned above.

<< Is glucagon release during exercise linked directly to blood glucose levels
or can it be triggered by epinephrine regardless of blood glucose levels? 
From other papers, looks pretty consistently like gluconeogensis is linked
more to blood glucose than to exercise level per se and the liver is not
going to produce more than what is needed to maintain normal blood glucose.
 In the absence of an exogenous supply of glucose, glucose is maintained at
normal levels throughout exercise until or unless the animal gets into
trouble (e.g. hypoglycemia at end of endurance race).  In Smokey's case, I
would propose there was little, if any, gluconeogenesis going on.
 >>


You make some good points, xxxxxx, but remember, only 9 ounces of AGL was 
given before and during the ride. Nine ounces total per day. Is six ounces of 
what will be come glucose after digestion enough to oversupport a 26 mile 
effort? For there to be no liver support of the blood glucose, that 6 ounces 
would have to account not only for the exercise energy but for the rise in 
blood glucose observed.  

To be sure, it appears we have supercompensated muscle/liver glycogen over 
the three days, but once the ride starts, you have a closed energy 
system--whatever's in the blood, muscle and liver is what you get, other than 
the fast-absorbing sugar in the gut. There is no question that muscle 
glycogen will be used, and that the faster the horse works, the more muscle 
glycogen will be used. And as muscle glycogen is burned, the body will 
attempt to refill the tank. It will use blood glucose to do so. 

If glucose is drawn from the blood pool, but blood glucose levels rise 
according to a normal glucose response curve from a feeding of AGL, then 
there is a net gain in blood glucose from another source. And we're stuck 
with the liver as the source. 

On "normal" blood glucose: as a diabetic, I can tell you that this is a 
somewhat flexible parameter. If you were to spend the Christmas holidays 
eating everything in sight, then, temporarily, your "normal" fasting level 
blood sugar would rise over that week. It would likely take several days of 
lowered calorie intake for it to settle back to 100.  Because I am a 
diabetic, if I were to do something like that, with out a major change in 
insulin injections, my "normal" would hover around 200 and when I'd drop to 
150 I'd get the same "shockey" symptoms as if I'd dropped from 120 to 70. The 
set point for "emergency situation" goes up and down depending on food 
intake. 

So, as far as the liver is concerned, Smokey may not have been as 
hyperglycemic as the absolute numbers would indicate. Combine that fact with 
what we can assume to be a liver saturated with glycogen and you have good 
incentive for the liver to seek homeostasis at a higher absolute blood 
glucose level during increasingly intense exercise.  

Tom Ivers, President
Equine Racing Systems, Inc.

Second email exchange with his consulting Vet 

<< This resulted in a small (12 g) but significant (P < 
0.05) increase in glucose uptake without influencing carbohydrate
oxidation, 
muscle glycogen use, or time to exhaustion (CHO: 68.1 +/- 4.1 min; Con:
69.6 
+/- 5.5 min). 

***This is the part that really got my attention first time around.  Tom,
you said to note use of endogenous glucose over exogenous glucose.  The
only organ where that change appeared was in the liver.  According to the
sentence above, there was no change in the amount of carbohydrate
burned/oxidized, no change in muscle glycogen use.  What happened to the
extra glucose that was taken up?>

The muscles aren't the only organs using glucose. 

Decreases in muscle phosphocreatine content and increases in 
muscle inosine monophosphate and lactate content during exercise were
similar 
in the two trials. Although endogenous glucose production during exercise
was 
partially suppressed in the CHO trial, it remained significantly above 
preexercise levels throughout exercise. 

***Gluconeogensis slowed down because of the steady supply of exogenous
glucose.  Note that there was not an additive effect (at least they didn't
mention one) - i.e. at this rate of supplementation, the liver slowed down
gluconeogensis to allow for the glucose being provided exogenously so that
glucose production did not "overshoot".
 >>

Right. That is why we're seeing the "normal" glucose response curve to fed 
carbs in Smokey despite the hard work. The "additive effect" is the onslaught 
of glucose from the gut. We've got the hard exercise drawing down substrate, 
we have a loaded-to-the-gills liver trying to achieve homeostasis, we have 
stacked muscle glycogen/PC/IMTGs and then we have glucose bombs from the gut. 
As Bill said, this horse was good for two more 26s on available fast-acting 
substrate alone. 

My guess is that another 26 miles at this point, with no furnther feedings of 
AGL, would have depleted some of the excess to the extent that the liver 
would then get to work full time. 

And then another 26 would have brought the horse into the realm where most 
endurance horses operate. Somewhere in that loop, Bill would have felt Smokey 
start to lug. Bill would have to ease up a little and let the horse sort out 
its substrates--coming into the vet check at that point, he'd probably have a 
slower recovery. Bill would lose some of the 24 minutes he'd gained in the 
first 50. Then, with ANOTHER 26, and no carbs, would come the crash. Big 
shift to fats, higher HRs, higher body temp, and glucose at the finish 
somewhere around 70--typical rider finishing in this condition would put the 
horse on a "jug".  


Tom Ivers, President



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