Tanks so much for the enthusiastic participation we had from whole set of experienced coaches all over the world . NZ, Switzerland USA and Canada.Andri compiled in Switzerland enough data's to see, whether further data collection is justified and whether we actually can do ahead to step 2 and 3
The information n part one should be by now in you drop box for review and discussion.
2 information's in part one we where looking for:
1. Can an equipment with this affordable price really be used for coaches and people on the street for the same as we use the great tool ( Portamon ) ( price difference over 10-000 $.
2. Second objective was to see, how NIRS information will show up , when using a classical accepted 3 min step test. Question of trend information , when looking at information like VO2 ( indirect blood gas information ) or VE ( direct respiratory information or lactate ( indirect metabolic information)
Same here, we found some great directions and information's.
Now this leads to part 2 and 3.
In short : Part 2. Simple question :
Does the classical 3 step test protocol forces the physiological reactions to be incomplete for a full ability to see the trends. Or in other words, does the Physical protocol we decided to use many years back with 3 min steps dictates the outcome or not.
If this may be the case , what can we try to change with the new generation of equipment o understand possibly more on LIMITER and COMPENSATOR and how the different system may work together.
Questions like : VO2 max = total O2 use from the whole " team " body.
but who uses how much , or who may run out of ability to contribute to the overall performance.?
Question like VE or CO ( Dempsey's metaboreflex idea or T. Noakes CG idea )
Can we see this as a better trend by changing the protocol idea.
Question : Can we find a homeostasis disruption or rebuild after a stimulus.
Is NIRS a potential early information , who leads us to a better understanding on load and deload in strength ,interval and endurance workouts.
Last but not least :
VO2 = CO x (a -v O2 Diff )
Now classical idea is , that VO2 is influenced by CO but very little by a-v O2 difference.
NIRS will perhaps help us to see, whether O2 can be around but not available ( BIO -Availability of O2 ) and what and how may change the ability to deload ( drop SmO2)
Key words , who may at least open a discussion on the above claim of a-v O2 diff.
are O2 diss. curve shift due to respiration ( TV change ) hypo and hypercapnia. , key word vasoconstriction and dilatation due to CO2 influence.
Why do we see in real life athletes with relative low CO compared to same level competitor , but an incredible low SmO2 compared to the same competitor.
Is important CO and a-v O2 difference. .
Is one limiting the pother or compensates for the other . Does respiration may be completely underrated due to the "classical" idea, that ventilation never reaches its limit. Think about that and think somewhat further.
Example MMV ( maximal minute volume is never reached n a race so there for the ventilation is never a limitation ?
How about VO2 max is never reached in a triathlon iron man so VO2max is never a limitation.
Or 1 min all out run time is never reached in a 10 km race so speed is never a limitation.
Or maximal HR is never reached in a marathon so HR is never a limitation.
Or wattage max in a Wingate test is never reached in a race so wattage is never a limitation. ?
True many many stupid questions , but all started out by a very common question or statement.
Part 2 . Introduction of UrPAHD and analyzing , whether we find not just with NIRS /MOXY but as well with other data's like VO2 and VIE data's a better answer as well as with lactate trend.
Part 4 will be an ongoing study to show , what classical workouts influence and change NIRS information as a functional reaction immediately or as a structural change over a longer period of time. Do classical ideas who promise certain changes really hold up to what we promise our clients.