Actually the hct increases not your hb level as you lose water so there is no (significant) change in oxygen carrying capacity as you lose water. Hct is the thickness of your blood you don;t lose hb unless somethign pathological is happenning

Both Hct and Hb per deciliter of volume increase as fluid in the non-cellular component decreases. Consider how the Hb level rises when you've diuresed a CHF patient....

Certainly, the HB level in an individual blood cell doesn't change, but there are more blood cells per unit volume of blood. Total body HB hasn't changed, but the oxygen carrying capacity per unit volume has changed.

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

True but you are not changing the hb content in the blood by decreasing volume but increasing concentration... this would even out.

You have more blood cells per unit volume but you are decreasing the volume of blood. so the total o2 content of your blood does not change.

o2 content = (o2 binding capacity x % saturation) + dissolved o2

Dissolved o2 would decrease ever so slightly but this would not be a physiologically measurable amount

O2 binding capacity depends on the toal hb content of the blood.

I think the CT is a fantastic training tool. IMHO, the Spinscan function, while cool, isn't as fantastic. Ultimately, we train to improve performance. On the bike for triathletes, that would be an increase in sustainable power output (at various durations for different race distances). In other words...you want to go faster...you need to push harder on the pedals. Not necessarily rounder and harder...just harder. Spinscan can be nice in that it might take your mind off the pain in those long intervals. I agree with Stewart. KISS. Train (specificity, specificity, specificity), rest, eat, sleep, not necessarily in that order.

Also, another thing to consider, is that the Spinscan functions measures the "peaks" in the pedaling cycle without differentiation of the two different legs. Meaning, if you were pedaling on legged, you would still see 2 peaks, one when you push down, and one when you pull up. Using the Spinscan feature with both legs doesn't indicate the percentage each leg is contributing to that "peak". Granted, I can stomp on a pedal much harder than I can pull up with the other leg, but Spinscan still doesn't tell me IF I am or not.

Probably sounds a bit nitpicky, but if there's anything I learned in grad school...if you're going to measure something, make sure the tool you're measuring with is both valid (actually measuring what you're trying to measure) and reliable (is able to reproduce the same results).

Never been on a Powercrank, so the usefulness and limitations of that tool is up to someone else to comment on. :-)

Just my $.02., FWIW.

Dave

Doctor taku, O2 delivery is based upon Arterial-Venous content differences per unit of volume. If you increase the number of red blood cells in a deciliter , or raising the Hb (by removing plasma volume via sweat, or urination, or hemoconcentration as in dialysis), you have more O2 carrying capacity per unit volume.

O2 carrying capacity is: (ml of O2 /100 ml of blood) or: 1.34 X hemoglobin (gm%) + 0.003 X PaO2 (at normal body temperature). It's the "per 100 ml of blood" that is important here.

Someone with a cardiac output of 5 lpm with a A-V O2 content difference of (Y) and a Hb of 10; is not delivering as much Oxygen as someone with the same cardiac output, the same A-V O2 content difference of (Y) and a Hb of 12. The second person is actually utilizing more Oxygen...it doesn't matter if the total blood volume is 10 liters or 4 liters. It does matter what the Hb is, what the cardiac output is, and what the A-V O2 content difference is.

Oxygen content is how much O2 the blood is actually carrying expressed as volumes %.

Oxygen saturation is O2 content divided by O2 capacity.

Assuming you can maintain about a 99% O2 saturation on room air, you increase your O2 capacity by increasing your Hb.

O2 capacity therefore increases with increases in Hb...as when you sweat, urinate, etc.

I can only assume you are confusing O2 content with O2 capacity?

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

I've actually lost track of the original question.

here goes my feeble response.

Someone with a cardiac output of 5 lpm with a A-V O2 content difference of (Y) and a Hb of 10; is not delivering as much Oxygen as someone with the same cardiac output, the same A-V O2 content difference of (Y) and a Hb of 12. The second person is actually utilizing more Oxygen...it doesn't matter if the total blood volume is 10 liters or 4 liters. It does matter what the Hb is, what the cardiac output is, and what the A-V O2 content difference is.

yes as the fick principle states, CO = O2 consumption / V-A O2 difference.

O2 delivery relys on pulmonary function, hematolgical function, renal function, cardiac function, and muscle/myoglobin function.

It is true that a person could theoretically live on a very small plasma volume but this would be very hard on the heart. The decreased ventricullar filling pressures would cause the heart to have to work very hard to maintain a BP to maintain organ perfusion. The difficult in pulmonary perfusion would also cause VQ mismatch which would make oxygenation of the blood more difficult, this would also cause increased stress on the renal system to maintain fluid levels. This in turn could lead to prerenal azotmia and a whole host of other things...

point being I disagree that it doesn't matter what the fluid status of a patient is. But you are right that the principle relating CO and O2 usage does not rely on the amount of blood.

I totally agree that oxygen capacity can only really be changed through increased redblood cells either artificially through EPO or through training.

Also another thought is that through training the myoglobin content of the musculature should also incease as well as the capillary density so you increase the amount of blood going through your muscles and you increase your ability to use that increased oxygen going through.

all said and done pulmonology and hematology were not some of my better classes and I would have to think about this more before I gave a better answer.

Either way this is a very interesting thread you have started...

I think we should also discuss the drawbacks to using such performance enhancing drugs, which would include how expensive these drugs are...I mean think of the bike you could build with a month's supply of pro-crit

Right, and let's don't go into the changes of buffering capabilities and changes of oncotic pressure from the fluid shifts, etc.

What the earlier comment was, stated more precisely is this:

Isn't it interesting that when the intravascular fluid volume decreases in longer "aerobic" (I know that word isn't an accurate description of all the minute mitochondrial events that are occuring at any given time, but, let's use the word "aerobic" here anyway) endurance events (due to sweating/urination/third spacing), thus increasing the Hb (measured in grams %) and therefore increasing the Oxygen capacity of a deciliter of blood, that the athlete's performance doesn't also increase? After all, the athlete now has a higher Hb (even if the change is only plus 0.5 gm%), and the cardiac output isn't diminished (as long as we haven't lost LOTS of volume), but the workload done by the muscles does diminish over time.

This tells me that cardiac output is not THE limiting factor in maintaining a long-term endurance (here's where people usually use that "aerobic" term again) workload, because Oxygen carrying capacity actually increases as we lose intravascular fluid. And an increase in Oxygen carrying capacity, at a stable cardiac output, would result in the availability of more Oxygen delivered by the blood to the muscles for power generation. This tells me there is another bottleneck, and it isn't cardiac output, which is limiting muscular function.

To explain this concept in a medical setting: if taku has a patient with a fixed cardiac output of 3lpm (due to cardiovascular disease, and the patient is on the correct drugs to increase the force of heart contraction, but, 3lpm is all this patient can put out) and this patient's venous saturation is low, and their Hb was 10 gms% but they had plenty of blood volume...their PA Diastolic was 20, CVP 18, taku could order lasix to get the patient to urinate some intravascular volume out, and the patient's Hb level would rise...let's say to 12 gm%. Now, their oxygen carrying capacity has increased, and their venous saturation will rise...even thought their cardiac output stays at 3lpm.

That's what I mean when I talk about Hb levels rising as we sweat, therefore oxygen carrying capacity increases, and at a fixed cardiac output (an athlete's cardiac output isn't fixed as this patient's was fixed, but, it cardiac output is limited to being most efficient at somewhere around 70-90% of max heartrate, so we "fix" ourselves at this ceiling during long endurance events) still, we don't see a gradual increase in our workload...therefore, there must be some other component that is THE limiting factor...such as local neuromuscular fatigue? This is such a broad term, it could include many different possibilities, but it ain't cardiac output that is creating the bottleneck.

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

I definately agree that CO is RARELY the limiting factor in atheltic performance. The only situation I could think abotu is if you had some valve or muscualr abnormality. There is a slight exercise induced cardiac hypertrophy but this is only seen in very long distance athletes, and not at all in most other athletes... point being you can be in good shape without structural changes in your heart. Which adds support to your statement that CO is rarely a limting factor. Athletes also have greater SV and greater EF with better shape, but even these can be overcome with increased HR to meet CO demands.

as to the other stuff I would have to think about it come more.

as in regards to neuromucular fatigue... neurons do not fatigue except under the extremes of circumstance.

There are however lots of interesting changes which happen in the msuculature in response to exercise including increased capillary density and increased myoglobin which will get more O2 there and increase the ability to remove it from the blood and into the tissues. Is this what you are referring to

in regards to CHF... CHF is the condition where there is a left heart failure, this leads to impaired left heart contractility, this will lead to increased LA pressure and in turn increased pulmonary venous pressure. at pulmonary venous pressure above 20mm Hg you get transudation of fluid into the interstitial space which in turn leads to decreased gas diffusion from the alveoli and decreased lung compliance and decreased bronchiol diameter all of which leads to dyspnea. Through a combination of higher cortical centers and J receptors in the lungs will lead to rapid shallow breathing. In addition the decrease perfusion pressure of the renal system due to the decreased CO from the ventricular dysfunction will lead to activation of Agiotensin aldonsterone system which leads to increase fluid retention and so on and so forth.

The big reason you would want to diurese such patients is to shift the frank starling relationship to a better funcitoning part of the curve, to decrease the pulmonary congestion to increase their pulmonary function...


in regards to your example, if CO stays the same, O2 consumption satys the same according to the fick principle the difference between [O2] pulmonary v and [O2] pulmonary a should stay the same...


If I was going to venture a guess with what the bottle neck would be it would be muscular, your muscles wear out long before your heart does. Neural would not be my first guess. Pulmonary capacity would be my second place bottle neck the ability to exchange O2 adn CO2 to meet the O2 needs of the muscles would be a big limiting factor. unfortunately this is something not really changable... unless you are talking about making it worse (ie. smoking) Cardiac would be a distant 3rd.

Taku, Thanks for taking all the time.

I used the term "neuromuscular fatigue" simply to include everything that happens from from the neuron firing (which I previously stated, just as you noted, is almost unfatiguable) to the muscle moving...it is just a catch-all phrase.

Anyway, you certainly have come to the same conclusion I have, that Cardiac Output isn't THE limiting factor in long-term endurance.

I really wasn't trying to delve into any complexities of CHF (which, by the way, could be due to either the right or left ventricular failure, or Biventricular...different set of clinical findings, but, ventricular failure nonetheless, that's why we sometimes use Right ventricular assist devices, and sometimes use Left ventricular assist devices, and sometimes us biventricular assist devices), I was just trying to get you to more clearly see what I was talking about in regards to the role of Hb level in Oxygen carrying capacity by using a clinical example.

BTW, since you brought it up; in these patients, if the cardiac output remains fixed (because they have no more ability to generate more work than they are currently generating) and you have a gradually dropping venous saturation (to below 65%), by raising the Hb level (however it is done, either by diuresing or infusion of packed red cells), you will see their venous saturation rise in minutes...since they now have a higher oxygen carrying capacity per deciliter of blood. If you shoot a thermodilution CO, you will see that this increase in venous sat wasn't because of an increase in cardiac output...it is because more oxygen is carried per deciliter of blood with a higher Hb, so the patient's mild tissue hypoxia can be relieved by increasing the Hb. (Again, let's ignore all the minutiae about 2,3, dpg levels being low in packed cells and all of that, I'm talking about looking at the forest, not the trees.) Also don't get side-tracked by the pulmonary venous-arterial saturations in the Fick principle...we're assuming we can bring the saturation up to "normal" with a single pass through the lungs.

This relationship between cardiac output, oxygen carrying capacity, and oxygen delivery to the tissues (A-V O2 differences) is perhaps the main focus of what I have done for a living the past couple of decades. It's what I do.

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

Ktanlon/yaquicarbo

Thank you for taking all of this time also... it is a very interesting question and a fundamental one also. As more light is shed on this i think it would has the potential to impact the direction of training... much like the friel has you focus on your limiting factors in his training bible this could be done on a physiological level.