Hct/Hgb levels and power

Originally Posted by Fday

I would expect very little change from this. There would be a difference but it should be less than you would expect looking at the oxygen carrying capacity alone. The reason for this is lower hct/hb levels is associated with lower blood viscosity, so it is easier for the body to deliver more cardiac output to make up for the lower oxygen carrying capacity and harder to deliver high cardiac output when the oxygen carrying capacity is high.

Originally Posted by Urkiola2

I may be wrong because maybe you did not explain yourself properly, but if you did so, your assumption seems to be wrong. Please explain yourself in a more scientific way or however you think. I am sorry but your hypothesis is not understandable to me. Thanks

Originally Posted by Fday

In a prior life I was an anesthesiologist. Believe it or not, anesthesiologists worry about xoygen delivery to the tissues under all sorts of conditions, especially regarding the effects of hemodilution from blood loss and polycythemia (too many red cells, a pathologic condition). We worry especially about when it is really necessary to transfuse to prevent complications like heart attack from the inability to deliver oxygen to the heart when blood loss has occurred. Hence, this has been pretty well studied. You could probably pick up any basic anesthesia text and this will be discussed.

Anyhow, how much fluid one can push through a pipe of any given size depends on the pressure gradiant and the viscosity. The lower the viscosity the more flow there will be. Lower viscosities occur with lower HCT. I did a little search and here are a few links that while not directly related to this discussion, goes to the gist of what I am trying to say.

Summary paper

mice study

bypass study

book extract

Compensation is not total

Originally Posted by Urkiola2

Great to talk/discuss with an anesthesiologist. That is very impresive, as I personally have high respect for your field for the huge knowledge of general medicine and physiology involved.

Maybe we are not making our points across.
I know that anthesthesiologists are very concerned always with oxygen delivery since it is a crucial part of your job. Especially important as you better than I know, dealing with hypovolemia and hypovolemic shocks is one of the situations anesthesiologists deal with the most and plasma expanders like Hidroxiethyl Starch (HES), albumin, Gelofusine (Gelatin) or Dextran (branched polysaccharide) are widely used by anesthesiologists under hypovelemic situations. So I understand that from your point of view and your experience hypo and hypervolemia are terms and situations that you control very well. I have no doubt about your knowledge about oxygen carrying capacity and delivering to the tissues.
I believe that what you claim has to do with viscosity and in situations like the one you mention (polycythemia vera) the blood flow will be decreased due to the increased viscosity as we can apply Poiseuille's Equiation.
However the situation in which anesthesiologists work is different than the situation we can observe in athletes like it is the case of the post by rmur17. In general medicine and especially during surgery a Hct of 40% or 50% as you know is pretty much irrelevant since the patient is perfectly stable and oxygenized. However in terms of exercise situation a decrease from a physiological normal Hgb levels of 14g/dL to 13g/dL you could have some consequences in terms of performance. An average citizen will probably not tell such a small decrease but an athlete will defenetely tell it. In that situation we are dealing with neither hypo/hypervolemia but dealing with exercise performance and oxygen delivery to the cells. Since O2 is bound to Hgb, if your Hgb levels decrease your O2 carrying capacity will be drecreased to the tissues and especially important this will be during high intensity exercise. An increase in Cardiac Output will not have an effect to compensate the lower Oxygen carrying capacity since during maximal exercise you will reach your Maximal Cardiac Output with low or high Hgb levels. To me the only thing that can change to compensate the decrease in oxygen carrying capacity is 2,3 DPG (2,3 diphosphoglycerate) which could increase in order to increase the unload of O2 bound to Hgb. However and something that it is my day-to-day thing when an athlete decreases his/her Hgb and Hct they can defenetely tell a decrease in their performance. When these athletes bring back their normal physiological Hgb/Hct their performance goes back to normal.
Same thing happens with EPO or blood transfussions. Even when you can be dealing with a hypervolemia the oxygenation to the tissues will be much larger increased due to a higher levels of Hgb and therefore oxygen carrying capacity.

Cheers.

Originally Posted by Fday

I didn't say there would be no effect from changing the hct but that it will not be as great as many might think as many different things affect oxygen delivery to the tissues. A 10% increase in hct does not result in a 10% increase in capability and vice-versa. And, there is a point where increasing hct further will not result in an improve performance. There are so many variables it is almost impossible to say what the optimum hct for optimum performance would be. You suggest that maximum cardiac output is fixed and not dependent upon hct. There is no evidence to support that view.

I personally think that filling pressure is a much bigger deal in affecting how an athlete performs than the normal variations in hct. For instance, if an athlete exercises and does not replenish fluids lost through sweat the hct will go up but the filling pressure will go down. Wonder if the potential of the athlete goes up or down as the hct goes up under the situation of dehydration?

The capillaries do not care if the oxygen demand of the tissue is due to athletic demands or some other reason. In fact, the two major areas of concern regarding medical research look at delivery of oxygen to the brain and to the heart. The heart is nothing more than an exercising muscle so what is learned there can be applied directly to what happens in the legs. The major difference between exercising muscle and non-exercising tissue is blood flow can only occur in the muscle when it is relaxed, not during contraction. The physiology of this is pretty well understood and the current best understanding be found in any cardiac anesthesia test. Otherwise, the physiology of blood flow through the capillaries (the only part of the vascular system where oxygen can leave the vessels to get to the tissues) is pretty much the same for all the tissues.

My point is that it is complicated. Changing one thing may have adverse influences on another thing. Many things affect oxygen delivery to the tissues including all the variables that can affect maximum cardiac output, the blood pressure, and all the things that can affect the oxyhemoglobin dissociation curve, and how much right left physiolgic shunting is occuring in the lungs, and how easily the blood flows through the tissues, beyond the simple question of how much hemoglobin is in the blood. And then, exercise can affect other variables like electrolyte concentrations that can adversely affect the ability of the muscles to contract optimally that has nothing to do with hemoglobin concentraiton but everything to do with performance. Wishing it to be simple does not make it so.

It is possible to say if I increase hemgolbin concentration the expected tendency is going to be to improve performance but it is not going to be possible to predict how much.

Originally Posted by Urkiola2

I defenetely agree that it is quite impossible to predict an exact performance or a %gain in performance solely based on Hct%. To me there is no way you can do that and I agree with you. However, and please don't get offended, as this is a friendly argument I always have with cardiologists and also anesthesiologists because they look more at the big picture and hemodynamics than at the cellular level. There are many studies showing that a decrease in Hgb levels (from a physilogical individual homeostasis) and therefore Hct will result in impaired exercise performance due to a decreased O2 carrying capacity. Otherwise the term "anemia" or "pseudoanemia" would not exist. As a matter of fact, it is thought that Anemia is the no.1 disease in the world...However in the vast majority of cases is not disgnosed simply because to carry a regular life a person would not tell unless it is a severe anemia. I have seen people as you as well for sure with Hct's of 30% and barely feeling it for the day-day activities...or others with 25% and just feeling a bit tired...something that it is still amazing to me (used to work with athletes) and you may be right due to the increased cardiac output to make it up for the lower "viscosity". However this is not the case of athletes, that I can tell you for sure. If your Hct is 45% and you decrease it to 38% you bet you will be decreasing your performance and you will struggle more on the races. As I mentioned that is one of the many "features" of overtraining and I see that everyday. You can tray it yourself. Withdraw 2 bags of blood (roughly 1L). Filter the contents except the erythrocytes and reinfuse the plasma with the rest of elements in it back so that you will recover your plasma volume and electrolyte and other elements to achieve homeostasis. The only thing you would be missing would be the packed red blood cells. Then go on your bike and go racing or a high intensity training. Regardless of the efforts of your heart, arteries, arterioles and any other vessels as well as any hemodynamic mechanism ossible to "save your butt" you will hurt on the bike like yoiu never had before, that is for sure.
About Cardiac Output, yes there is a limit. THat is the endocardium. Your heart can try to increase it but there is an anatomical self-defense mechanism by the one your Cardiac Output cannot increase more and that is the endocardium. That is a typical question of residency/medical/physiology exams to "trick" you.

Anyways, I am tired of writing too much today...I think I may bee anemic.. ..Just kidding!.

Cheers.

Originally Posted by Fday

Don't take my objections to some of what you are saying as my thinking you are attacking me. This is more of an academic discussion and we are in general agreement except for one or two small points that are worthy of further discussion. I am not offended. I appreciate your tone.

First, I think you meant to say that CO is limited by the pericardium, not the endocardium. I would agree with this if we are talking about acute changes, but not if we are talking the chronic ability to adapt.

You are not the only one to believe the heart is the limiter to our ability to exercise but, IMHO, there simply is no physiological limit, except as our ability to stress the cardiovascular system to effect the increases. If we can figure out a way to regularly exercise more muscle mass the heart will adapt to the stress, whatever it is. There is zero evidence that there is an absolute maximum yet the evidence to support the cardiovascul system is adaptable is several and compelling. First, our hearts grow as we do. They don't grow simply because we get bigger but they grow because, as we get bigger, there is more demand placed upon it. Those who push the stresses even more than the average, the endurance athlete, ends up with a bigger heart than average, affectionately known as "the athletes heart". Further evidence exists in the form of other mammals. All mammals have pretty much the same cardiovascular physiology. Cardiac output and heart size is related to the mass of the animal (which also relates to the surface area which corresponds with how easy or hard it is to maintain temperature) with a high degree of precision yet all mammals are starting with essentially the same cardiovascular physiology, these cardiovascular systems are the size they are because they have adapted to the daily stresses they see. There is no physiological reason, that I am aware of, the human heart could not become the equivalent of the elephants heart in both size and pumping capacity if it were subjected to the same ongoing daily stresses (and if there were room in the chest for it to expand).

Originally Posted by Urkiola2

1st of all....I have to apologize because I can't believe I said Endocardium!!! . How embarrasing!. I had a long ride today and have been with a cold this week and I think tyhat my brain is not recieving too much glucose...What a dummass. Sorry about that mistake. I meant pericardium!.

2nd, I think we agree in all the terms you say and we could keep talking for hours about cardiac physiology and pathophysiology, especially if we get into hypertrophic cardiomyopathies and defenetely getting out of the post. I just was pointed out about the fact (seen and suffered by thousends and reported in scientific literature widely) that a decrease in Hgb/Hct due to, not a hemodilution nor hemodynamics situation, but an erythrocytopenia either acquried due to lack of iron, B12, folate, hemolysis...or idiopathic will elicit a decrase in exercise capacity, especially in a competitive athlete regardless of CO or any other hemodynamics compensations. But again I agree it is to me, at least, abosultely impossible to predict performance based on hct level to a such a specific degree of accuracy as posted here. There are just way too many players to just isolate one. However I still believe not only from literature but from every-practice and experience by me and other collegues that a decrease in carrying oxygen capacity to the muscle cells and therefore a lowr O2 avaliability is seen in people whose Hgb is decreased by either an acquired or idiopathic condition as mentioned before.

Cheers.