A few of the recent posts have made me think about THb, and have come up with some thoughts that i thought would possibly stimulate some discussion
I am going to use a hypothetical example to try to illustrate, but to do this i think it would be useful to highlight key formula/concepts that i am going to use:
Peak recovery, loosely means a point where oxygen utilisation would be very low but delivery would still be high from a previous interval
Peak work, loosely means a point where oxygen utilisation and delivery would be at their peaks
O2Hb = oxygenated hemoglobin = Sm02% x THb
HHb = deoxygenated hemoglobin = (1-Sm02%xTHB)
MaxO2Per (new metric for the purposes of the discussion) = Maximum oxygen available and used to support the given performance = = HHb (@Peak Work) - HHb (@Peak Recovery).
This is because we are assuming that delivery during peak work, and immediately after peak work during peak recovery are close enough to consider equivalent. So then oxygen available and used to support the performance required in the interval is the difference in utilisation during Peak Work (i.e. full utilisation) and Peak Recovery (i.e. "no" utilisation).
Consider 2 athletes, athlete A and athlete B.
Suppose for hypothetical athlete A their cardiac output and muscle strength is such, that their THb is perfectly balanced for a given performance level, as shown in the graphs below.
So we can see, for Athlete A:
HHb (Peak Work) = (1-20%) x 12.5g/dl = 10g/dl
HHb (Peak Recovery) = (1-80%) x 12.5g/dl = 2.5 g/dl
MaxO2Per = 10g/dl - 2.5g/dl = 7.5g/dl
HHb (Peak Work) = (1-20%) x 12.0g/dl = 9.6g/dl
Now consider Athlete B. Assume that this athlete has the same utilisation capacity, but whose cardiac output and/or muscle strength is weak leading to THb being pushed down during the given interval. Suppose the change in THb peak recovery to peak work THb is 12.5g/dl to 12.0 g/dl (note: this would be a fairly substantial change based on observed changes we tend to see in THb on case studies on the forum). Again see the graph below.
So for Athlete B
HHb (Peak Recovery) = (1-80%) x 12.5g/dl = 2.5 g/dl
MaxO2Per = 9.6g/dl - 2.5g/dl = 7.1g/dl
Thought 1: what is the "cost" of the limitation.
We could calculate this as the difference in Max02Per between Athlete A and B. Therefore the "cost" of the limitation of Athlete B = 7.1 g/dl - 7.5 g/dl = -0.4 g/dl (or approximately 5.3% lower MaxO2Per than Athlete A).
Thought 2: what increase in oxygen resaturation or desaturation would be required for Athlete B to "offset" their THb limitation
If Peak Recovery Sm02 for Athlete B was just 83.2% (instead of 80%), and still desaturated to 20%, then Max02Per = 7.5 g/dl which is equal to that of A.
If Peak Recovery Sm02 stayed 80%, but Athlete B could desaturate slightly further to Sm02 = 16.6% (instead of 20%), then they would match Athlete Aâ€™s 7.5g/dl MaxO2Per
In short, the changes in Sm02 don't seem that significant.
If relatively â€œbigâ€ differences in THb only lead to minor changes in MaxO2Per; and if
Relatively â€œsmallâ€ changes in 02 saturation or desaturation (i.e. Sm02 changes) are required to offset these "big" THb differences;
Then this raises questions:
1. Why do we place a big emphasis on THb trends if they don't seem to account for that much difference?
2. How big an issue are cardiac limitations really? This is the oxygen transport system, but overall oxygen availability seems much more sensitive to oxygen load and unload dynamics than it does to the efficiency/strength of the transport system?
After thinking about it, i think the following may be the answer:
There is some kind of â€œleverageâ€ effect because THb only operates in a â€œtrueâ€ range that does not run from zero. For the sake of example lets say it operates in the range of 11-14 g/dl, say. So if in reality THb could only go down to 11g/dl, then we might need to define new oxygenation and deoxygenation metrics. Let's say say O2Hbâ€™ and HHbâ€™ that only consider oxygenation/deoxygenation information for the part of THb above its minimum possible value. So
02Hbâ€™ = 02Hb â€“ 02Hb @ minimum possible THb value = Sm02% x (THb â€“ minimum possible THb value); and
HHb' = HHb â€“ HHb @ minimum possible THb value = (1-Sm02%) x (THb â€“ minimum possible THb value)
If we then relook at the hypothetical example, calculating Max02Per, using these adjusted HHb values
Athlete A Max02Per = HHbâ€™ (Peak Work) â€“ HHbâ€™ (Peak Recovery) = (1-80%)x(12.5-11) â€“ (1-20%) x (12.5-11) = 0.9 g/dl
Athlete B Max02Per = (1-80%)x(12.5-11) - (1-20%)x(12-11) = 0.5g/dl
So in this sort of â€œleveragedâ€ view Athlete Bâ€™s Max02Per is only 55% that of Athlete A's. Viewing it in this fashion helps resolve why THb trends are important, and why cardiovascular/hemoglobin transport system is a potential big limiter.
I understand that the problem here is that we won't know a reasonable minimum THb value - however the purpose here is to be a conceptual model.
THb changes are normally fairly small. This is partly because we view them in the context of the absolute THb value, and implicitly run the hemoglobin scale from 0 g/dl. When viewed in this context, it might seem that THb changes have only a small impact on the oxygen available and to be used to deliver a given performance. However in reality, THb values operate in a fairly narrow range. When THb changes are viewed in the context of this much smaller range of values, particularly the notional lower bound of the range , "small" THb changes start to be much more significant. Viewed in this way we might better appreciate the sensitivity of oxygen delivery and utilisation dynamics.