When we go through the started discussion with load 1 - 4 where we are stuck for the moment in load one you will see some potential indication what we see in your data collections here. Here just in short the load discussion graph
Now when you look your graph you can see, that in the short warm up you increase SmO2 nicely as an indication of better saturation and more intake of O2 than actual;ly needed at that load.
. Interesting is the relative minimal increase in tHb and just short before you stepped of there could have been a small trend in increase in tHb.
. Than at the 220 load you can see a slightly but steady increase in SmO2 and as well in tHb.
This in many cases is an indication , that your body was able to afford to sent more blood as well as in that blood good saturated Hb to a non involved muscle.. This would indicate , that 220 wattage is for your a load but not a critical load and you could go most likley for a nice duration.
. In fact this would be most likely for us in the STEI intensity , meaning , that you are not yet reached any system to a critical level of a limitation, just may be nipping on it.
Once you see a flat SmO2 and a flat tHb you are somewhere close but not over it. Once yous see in an non involved muscle a change you now know, that some of the vital delivery system have reached a critical intensity an you simply try to " survive" by regulating in the vascular region for your loco motor muscles the priority of O2 supply and as such as well the blood flow. This is what we mean with pyramid of Energy supply.
This may make now more sense for many. Now this is a great " theory " but as so often before we make a simple picture we do some cases studies and than hope and search for some back up from other groups. . Here is a nice one first.
A method for assessing heterogeneity of blood flow and metabolism in exercising normal human muscle by near infrared spectroscopy
IoannisVogiatzisHelmutHabazettlZafeirisLouvarisVasileiosAndrianopoulosHarriethWagnerSpyros G.ZakynthinosPeter D.Wagner
Heterogeneity in the distribution of both blood flow and O2 consumption (VO2) has not been assessed by NIRS in exercising normal human muscle. We used NIRS to measure the regional distribution of blood flow and VO2 in six trained cyclists at rest and during constant load exercise (unloaded pedaling, 20%, 50% and 80% of peak watts) in both normoxia and hypoxia (FIO2=0.12). Over six optodes over the upper, middle and lower vastus lateralis, we recorded: a) indocyanine green dye inflow after intravenous injection to measure blood flow (Q), and b) fractional tissue O2 saturation (StO2) to estimate local VO2/Q ratios. Varying both exercise intensity and FIO2 provided a (directly measured) femoral venous O2 saturation (SfvO2) range from about 10 to 70%, and a correspondingly wide range in StO2. Mean Q-weighted StO2 over the 6 optodes related linearly to SfvO2 in each subject. We used this relationship to compute local muscle venous blood O2 saturation from StO2 recorded at each optode, from which local VO2/Q ratios could be calculated by the Fick principle. Multiplying regional VO2/Q by Q yielded the corresponding local VO2. While six opt odes along only in one muscle may not fully capture the extent of heterogeneity, relative dispersion of both Q and VO2 was about 0.4 under all conditions, while that for VO2/Q was minimal (only about 0.1), indicating in fit subjects: a) a strong capacity to regulate blood flow according to regional metabolic need and b) a likely minimal impact of heterogeneity on muscle O2 availability.
Here a very short discussion s ection form an interesting wokr done in Japan.
There was no significant difference between MBP at 50 watts and that at rest. Since cardiac output
increases soon after the start of exercise, this unchanged MBP suggests vasodilatation in active muscles. After
ventilatory threshold (150 watts), the oxygenation level decreased. Since oxygenation level is a balance between
oxygen supply and since oxygen consumption is assumed to be constant in inactive muscle, the decrease in oxygen
level reflects a decrease in oxygen supply (Ogata
2002). At this power output, mean BP showed a higher level. Therefore, vasoconstriction may occur in the inactive muscle.
In other words. When we reach a critical intensity, where we can't afford to " waste" or sent O2 and blood to noninvolved muscels the body will react accordingly.
. So using a noninvolved muscle in an endurnace activity but as well during a strength workout or intervall can give you some fast and easy feedback, whether we reached a " delivery limitation of blood and of O2 from the vital organs like Cardiac system or respiratroy system.
This would go into the same thoughts of reflex reactions.
Here the full story in a picture and now for many again there may be a better idea why we use a MOXY on a noninvolved muscle. It gives you a relative fast feedback, whether the limiter is in one of the main delivery systems or whether we may have more a local limitation.
2 increased linearly after