Post Number: 2
|Posted on Saturday, June 07, 2008 - 02:08 pm: |
I was just reading this article on a ski website and found it pretty interesting.
PARK CITY, Utah (June 4) - Olympian Kris Freeman (Andover, NH) could have easily given up his dreams when a doctor told him that he was a type 1 diabetic and would no longer be able to be an endurance athlete.
"I was devastated and I was crying, but I also went out and trained that afternoon," Freeman says of his diagnosis at the age of 20. "I wasn't going to give up after that."
And Freeman did not give up. He refused to. In fact, it was his determination, which led him through two Olympics, made him the first U-23 World Champion, and helped him to set a SuperTour record with 23 wins as the only endurance athlete with diabetes competing at an elite level in skiing.
But, with the recent advancement of insulin delivery devices and glucose monitors, Freeman is capitalizing on a unique opportunity he has to test his performance at different insulin levels.
"As an endurance athlete, you're always trying to keep lactic acid out of your system," Freeman said. "We've seen a correlation where if my blood sugar is too high, which is caused by low insulin, my lactate level spikes. So having high blood sugar causing you to make more lactic acid is not a good thing."
Freeman has worked with Eli Lilly, a company that produces insulin for diabetics, and the U.S. Ski and Snowboard Association's sport science department to find how best to be an elite athlete with diabetes. Recently, Freeman spent two days under the observation of USSA physiologists. Each day, they simulated an impossible-to-finish cross country race on a treadmill while testing his blood for lactate and glucose levels. On day one, he was given his normal amount of insulin, and on day two, he was given twice the amount.
"We're trying to figure out how much insulin I can race on to help me buffer that lactic acid," Freeman said.
On day one of his testing, Freeman straps into a pair of boots that attach at the front to a rod with two wheels on it - a cross between a rollerblade and a cross country ski. He wears a harness attached to the ceiling of USSA's training facility and begins to race on the treadmill.
After 20 minutes and 30 seconds of pumping his legs uphill, Freeman goes stiff and the spinning treadmill throws him back. The harness catches him as he slumps, pulling him onto the treadmill. His blood sugar levels and lactate levels are high, as was expected.
Day two looks and feels the same, but he has twice his regular insulin level in his blood. He races, looking just as strong as he did the day before, but this time, Freeman is thrown from the mat at 20:45. As they calculated it, USSA's physiologists discovered Freeman's performance was increased by nine percent from the day earlier - a large difference for a cross country athlete.
"It was very clear that I've been racing on too low of an insulin level. When we raised the level, my lactate was lower, my perceived effort was lower, and I was able to go further," Freeman said. "What we're doing here is on the cutting edge of what's possible."
Freeman plans to use what he learned from his summer testing for next season as he continues to push himself to be the best in his sport despite his illness.
"I'm hoping to be able to race as fast as I can and this is a tool that I have," Freeman said.
First off, I don't think this skier is very well educated with modern lactate theory. I was wondering if you could comment on what is happening in this study? I suppose insulin doesn't buffer the "lactic acid" like Kris says, and I'm thinking that all that the study showed is that insulin aids in the body cells' ability to utilize glucose, thus affecting sugar metablism and changing lactate readings. Is this right? Can you guide me in the right direction? What would the acidic situation be in both tests?
Post Number: 476
|Posted on Saturday, June 07, 2008 - 08:59 pm: |
Veyr interesting article,
First I think you are more on the "right" side than the article.
Yes Insulin will not buffer the lactate at all.
What happens may be more like that.
Insulin is not just here or perhaps not here at all to keep the blood sugar down as per see. Insulin is needed to move bloodsugar
from the blood into the working cells, and as well as a anabolic steroid to move it into the liver. ( the opposite hormone would be glucagon.
So when Insulin levels are relatively low you have more problem to move the glucose into your working muscle cell, and the energy production from oxygen dependent glucose delivery will be low or lower, and the delivery ( production) of ATP will be in a certain intensity not good enough anymore and you will start to add and or lock for some help from oxygen independent ATP production. This than will start to reduce pH ( increase H+ ) and we will see an increase in lactate in the blood stream due to this action and the lactate may in fact be of some nice help of partially buffer the H= as it helps to move some of this H= out of the cell into the system.
Now what we will actually see is an increase in blood sugar out of 2 possible situations.
1) the athlete may feed glucose of liquid or other supplements.
The liver releases some additional glucose. Now because of too low Insulin levels , the glucose will be not moved into the cell.
I did some testing with my son ( who is diabetic I ) and we see exactly what Freeman explains. A very fast rapid increase in blood sugar reading and a fast increase in Lactate readings, but they may have missed the parallel readings of keton bodies as well , as they go fast up as well , as an indication of lack of delivery of glucose into the cell..
I in fact believe that the increase of lactate is a nice help to "survive" this effort somewhat longer.
On the other side, yes, the high lactate level explains , that the race will be soon over, but not caused by lactate, in fact without lactate the race would be over earlier.
So that leaves us with the version of increase Insulin by much more and now deliver glucose in a much higher rate during the race or training , because we can deliver this way much more glucose to the working muscles , as a "normal" person ever could do.
So if we have a very good basic endurance and a high STF fiber situation, or a very good delivery system ( pulmonary as well as cardio system, increase the EPO and have a high but still allowed Hb, we have the advantage here, that the delivery of glucose is much less of a limitation than in a non Insulin injecting person.
There is one major problem to deal with . The situation after the race.
If the Insulin is too high , but there is a lack of glucose delivery after, we create a high risk of an after race hypoglycemia which is short term the much bigger risk than a high blood sugar , which is long term the big risk.
With the new Insulin pump system , where you can steady see your glucose level , this is now much smaller of a problem and you may have to "feed" enough glucose to keep this under control.
There are 2 major advantage as well.
There are 2 different Insulins , ( actually more ) but 2 which are very interesting in sport. (Levemir and Novo rapid )
Levemir is one of the newer generation of long lasting Insulins, which makes live but as well sport situation easier.
Novo rapid is a short fast reacting Insulin new on the market , which can be nicely used for sport.
Insulin is possibly one of the "drugs" which can give you some major advantages , if properly used and it is not or not yet on the banned substances , as it may always be a "therapeutical window" for athletes with diabetic I.
So to be the "devils" advocate.:
"continues to push himself to be the best in his sport despite his illness:
may be perhaps converted into , :Thanks to his illness he has the possibility to use a anabolic hormone to push certain situations ( metabolic) in his system far above and beyond the ability a "healthy " athlete actually has.
There are now "implants" on teh market for continues blood sugar testing in diabetic and with tis we have the ability to really work very accurate .
I did some very small case ideas with my son.
We can psuh surprisingly high intensity by increasing Insulin , but we have to "feed " steady glucose, and as long we are in balance with Insulin input and glucose input and the intensity is in a range where we still can go oxygen dependent , which means for us just on the LPB we can go with this situation much longer on this high intensity , than actually a "normal" person could go , as the delivery of insulin may have some problem over time as well , and the "artificial" delivery will take this control system out of the equation.
The problem if a healthy person would start playing with this , may be an overruling of the natural delivery and control process of the Insulin production and a potential risk of damaging your health.
How good and how smart it is on an already damaged person to play with this is an open question.
The increase of blood sugar with a sudden very high spike may have some long term damaging effect on the blood vessel system , and it is crucial to check with this athletes regularly the A1C test to assess the state of teh red blood cells.
The increase of Insulin will pretty much for sure be a clear advantage in races with duration up to 2- 2/12 hours for people with a weight above 50 kg , as the caloric output under normal situation can't be covered with glucose only . The additional help of insulin to deliver glucose in the cell with administration from out side will possible enhance dramatically the performance as this athlete will be able to maintain much longer oxygen dependent glucose metabolic energy production, compared with a heavy athlet without additional insulin.
( storage capacity in combination with delivery from the glucose into the cell.
The additional interesting fact is at least from our case studies, that we can see much higher lactate levels as usual, due to the fact, that lactate is produced as well in much higher dosage due to the high glucose delivery into the cell, and the lactate buffer ability seems therefor better as well.
This is another nice real example, that 2 and 4 mmol numbers just are out of now where, as we can see lactate levels of 8 - 12 over long time 1 - 2 hours with absolutely no "fatigue" as the H+ i seems to be even better buffered, as long the Insulin keeps moving glucose to the working area.
What we see additionally is an increase in respiratory rate , and this may be a reaction due to the higher CO2 production (RQ 1.0 ) and CO2 will stimulate the respiratory drive. Now you combine this with a very serious training of your respiratory system with Spiro Tiger , so you can use the CO2 out put due to the better respiratory action as well as a buffer idea and you may in fact see an athlete with this "illness" blowing away his competition.
Very interesting idea.
You take additionally Sildenafil and your race in altitude and you will be a very good personal best athlete.
The small blue pill is one of the possible more used drugs for the moment in races like a Giro or the upcoming Tour as soon they go into the mountain. And I don't think WADA as well as other agencies will be for the moment able to stop people from taking that , as the girl friend need some fun as well, and the daily steady sitting on a hard saddle can be used as an excuse for problem in that "plumming system :
Check the latest in the story of Geroldsteiner and the suspension of some of the racers from that team . ( Giro 2008 )
Post Number: 56
|Posted on Sunday, June 08, 2008 - 04:34 pm: |
I am a little surprised to see the very high lactate readings in the absence of insulin (as in the Type I diabetic).
I would have thought the lower insulin would have made it difficult to produce lactate due to the lack of glucose getting into the cell as a fuel. Likewise, I would have suspected that with the increased insulin being injected, and the subsequent increase in glucose being supplied to the working muscles, I would have expected a RISE in lactate, as a result of the increased glucose metabolism.
It begs the question...is insulin a hormone responsible for the functioning of the lactate shuttle in addition to what we learned in medical school (that it simply helps move glucose form bloodstream to cytosol across cellular membranes)?
Juerg, when your son is very low on insulin, do you see a rise or fall in lactate?
Perhaps the trends they are reporting are simply what happens at "regular" insulin levels compared to "supra-normal" levels.
Fascinating...I will expect many people will be asking how to use this information to "cheat" in the future, and hope that everyone recognizes the long history that Juerg has shown in supporting the athletic development of clean athletes, by using the training, recovery and nutrition rather than supporting athletes who wish to turn to drugs for the answer.
Post Number: 478
|Posted on Sunday, June 08, 2008 - 09:29 pm: |
Lactate and low insulin level.
This is an interesting situation and I can only talk from one single case here ( my son ) but it would be interesting to see other people and the reactions.
We actually can see three reactions . Lactate going very high and lactate is in a "normal " range, and lactate does not show up.
1. Lactate is very high. If we supply lot's of Insulin and feed lot's of glucose than we see, what would be expected a very high Lactate level and it is much higher than "normal" but no " fatigue " due to lactic acidosis , as lactate does not "fatigue " the muscle.
This is the case if we supply Insulin , which would lead to a very fast hypo if not feeding glucose.
2. Now we see a high lactate as well if we have go with an activity with only lower body muscle involvement, like biking on a trainer.
Lactate is in the normal range when we have a normal blood sugar level ( so proper Insulin supply )Now if we keep pushing the difference in here is , that the insulin level stayes up and when the blood sugar level goes lower there is no feedback working and the blood sugar level drops very low 2.1 and so. Now here is an interesting observation , but I need much more test to see whether that is always the case.
If we feed glucose , the blood sugar levl can go back up , depending what we take as carbs. ( it show , that there is a different speed in absorption of different carbs during work as some .
So if we take the "proper" carbs we see a increase of blood sugar and the performance can be maintained.
If we don't feed we have to quite, but the lactate here is in the expected range for the choosen intensity, while if we feed carbs the lactate goes immediatly up again.
In the third reaction we have a very strabge situation.
Low Insulin, but no Keton in the test.
Now we keep pushing and we will see an increase in blood sugar but as well an increase in lactate despite the fact , that we assume we can't get glucose into the cell.
What happens first here is the performance is good for app. 30 - 40 min and than the performance collapses completely. I have to mention, that we did a good refeeding the day before and before the test nothing on work.
Now here the hypothetical thoughts.
He uses the glycogen storage in the muscles and runs out of them after 30 - 40 min.
Now somehwere the gluco stat gives a feedback of low glycogen situation and triggers a release in the liver and the glycogen from the liver moves into the blood stream increasing the blood sugar.
Due to lack of Insuling it does not work as the blood sugar stayes up and the glucose in teh blood can't be moved into the demanding muscle.
The brain does not use so fast glucose and the too much release of the glycogen from the liver is the result to a high blood sugar.
Now for a short moment before we wuit the test the lactate is up as well and it goes up relatively fast and high.
Now here is the hypothetical speculation based on Brooks shuttle idea.
The low glucose situation in the leg muscles triggers a signal to demand more glucose, and the lactate shuttle may actually move still available muscle glycogen from the arms or other not involved muscles over the muscle glycogen - lactate conversion into the blood in the hope that it can moved with insulin into the working muscles.
Sounds very adventure full , but any specialist I asked for an answer just were shrugging the shoulders and had no answer to may question at all. This does not mean my ideas are the right answer , but it is a carefull try to have some ideas on what perhaps happended.
Now here what we tryed.
If you now give insulin you have an interesting situation , as normally with lot's of glucose and enough or lots of insulin you will see an increase in lactate.
Not here you will have two stages. First a reduction of lactate with still high blood sugar values followed by a normal lactate value and a drop in blood suagr to a increase in lactate with the drop in blood suagr.
This leaves the question open , whether the body will take as soon Insulin is available again first the lactate as an energy source, before moving over to glucose.
The reason why we see in Diabetic I a so fast drop in blood sugar ( hypo ) is because the Insulin level will not drop under exercise as we see in "healthy " people , but in fact Diabetic I burn sugar in a high intensity exercise as well as the insulin stayes up and moving much faster than normal the blood sugar into the working cells and where ever there can be sugar stored.
Now to create ATP out of lactate needs less O2 than out of Glucose, so it is more efficient and faster to get to ATP, which will explain perhaps , why the lactate is first used.
The other interesting thing is , that if we have a high lactate level after the workout it seems that the re-fuelling of the liver is much faster than in healthy people and you very rarely see high lactate levels after breakfast even after extreme hard workouts, as in opposition to healthy people.
So the recovery due to the Insulin of the storage levels is much better and woyld allow a much higher intensity in a row of races like a Tour.
Now here a very bad speculation.
You ad to the high Insulin level T3 ( a thyroid hormon ) and you are Mr. perfect in recovery but may kill yourself very fast.
Some may remember a Tour winner just in a Tour lately , who was allowed to take thyroid medications due to "health " reasons.
I was always and still be surprised , that this was never discussed in that case.
Due to very unfortunate situation we have 2 Guinea pigs in our group ( My son and myself with grave disease ) but believe me do not even think off trying one or the other as you play with the most important part of your self your health.
The reason why I play around or did , was very simple , I just could get not good enough information when we went to look for help so we started to do testing on our self to find the proper dosage for a good feeling and a healthy body.
Thanks for the question and all of the above are speculations based on a case study .
Post Number: 57
|Posted on Tuesday, June 10, 2008 - 01:38 pm: |
So the lactate rises as a result of teh small amount of available glycogen, or the glucose that was able to enter the cell while there was still circulating insulin. The drop in lactate with teh addition of more insulin is a result of teh body using first the lactate over the available glucose? If so, then insulin is a key component to lactate transfer in and out of cells...
I thought the scientists were looking for a new lactate shuttle. Have they not ruled out insulin in the research before?
Post Number: 481
|Posted on Tuesday, June 10, 2008 - 06:16 pm: |
hmm interesting idea , with the question:
If lactate is "the faster " or more efficient way of using lactate plus O2 to create ATP than glucose and O2 to create ATP, and the "empty " , depleted muscle in search for an efficient oxygen dependent energy source to "survive" is desperate to get that done , than Lactate with help of one of the MCT proteins , may be "faster " and more efficient and therefor kick in , and in the meantime the now available Insulin will move the glucose back into the muscle to be prepared and working on oxygen dependent energy production over that metabolic pathway.
If this is the case , we should be able to get the body going , by seeing a lactate increase even though the blood sugar is going very low and the lactate would be relative high even in very low intensity , as the body may try to move glycogen from the arms to the legs.
Now after a very long hard race in normal people we use to check lactate and glucose at the end of the raise to see , whether there was possibly still enough glucose available in the body.
The protocol has a long history and is used since many years.
You take lactate and blood sugar immediately going through the finish line , and than you follow up after 3 - 6 - 9 min after.
Some schools do a 90 sec all out again after the finish line and take it than , but normally the end sprint of the athlete is already the all out.
Same can be used in a FaCT when we have a problem to see lactate increasing in the second part.
Important is do see , that after 90 seconds , we may no have a much higher lactate at all , but see the increase after 3 and 6 min post all out work.
Now in most cases, if the blood sugar is very low 4 and so in normal people we often see , that the post lactate levels are not climbing , because there is a problem of lactate production, even though there is still a level 4 in the blood.
Question of glucose stat protecting a minimal level as long as possible for the brain "feeding".
Now in nearly all the cases , where we thought the blood sugar is low , because the athlete is "empty " we see a very small , if no increase of lactate after the all out.
In our case person this was never the case.
Even with blood sugar of 2.6 the lactate was relative high 3 - 5 mmmol and by pushing somewhat harder it would climb. So the question was. :
Is that as a result of the metabolic pathway of glucose or, is this lactate coming from other areas and is moved towards the working muscle to try to survive , and keep a bit glucose for the brain.
Would be nice to push longer, but there is a moment , where the case person starts to feel
Usy and shaky and that's the end of the test.
So I am not sure ,whether insulin is a shuttle for the lactate or whether lactate is a "savior" of the ATP production , due to the "delay " of efficiency the glucose -ATP pathway.
The beauty would be if Universities would take an aim of ideas like that , as we just have not enough cases to actually see a trend , as it is one case with possible very different reactions from case to case . There needs to be some major numbers going through this testing ( 100 + ) to see a possible trend in this direction.
The rest is speculation and nice ideas in a strange world of hypothetical informations, but still fun to play with the different available models and see which one can make some sense out of many open questions.