Okay    here we are back with some more practical  questions and possible practical applications.
 I like to go back to one of teh MyPAHD case studies we go  sent from this group.
 Att 1  shows you one of the step test " classical " step test " where   the data collections show SmO2  as well as  lactate.
Now look carefully  and it is a nice example to show you , how SmO2 is a very direct information on performance and the needed of O2. We see nicely at what step the client starts to use more O2  than it can bring in.
 This does NOT mean , that she is

" anaerobic" nor does it means, that she will show lactate in the system as of yet.
 This can be easy seen in the lactate curve.
 The lactate values run slightly one or 2 step behind the SmO2 trend.
. Why ?
 Lactate is an indirect information  and the4rfor  we have a lag time.
 The lag time is the time between the production of the lactate in the working muscles and the place, where we test for lactate ( ear or finger). The second problem is the concentration in the blood versus the concentration in the working  muscle ??
 and the third clear point is the  " recycling" of lactate  as an energy source from muscles between the production site and the test site.
All this plus more factors ( some possibly unknown as of yet ) will clearly influence and change lactate values. If it is this lag time, than you can see, why any change in lactate sampling in a  step test 2 - 4  or more minutes step will show a very different lactate curve, and where we  may only increase by 0.6 mmol in a 3 min test we may increase  by adding 2 more minutes to the step by 1.6 mmol  and therefore would  reach the criteria for a  step increase and  would define this as lactate threshold.
 Same is true for 2 and 4 mmol ideas and even more true for any mathematical  calculation based on  angle ( 45 degree  and so on ) on this lactate curve.
 There is no  physiological justification out there, why  a test suppose to have 3 min steps or why we would increase by 20 or 30 wattage. But all of this has a profound influence on the lactate curve.
 True  it as well will have an influence on a  SmO2 step Test.
 This is an other argument for the IPAHD idea.
 Now back to the  test result of  att. 1


 One part you look  is lactate trend and SmO2 trend.
 The more interesting section is at the end of the test. See how SmO2 starts to  flattened out as a sign of reduced use of O2 and how the lactate at that stage increases, as a sign of much bigger integration of O2 independent  energy supply.

Questions?  Why does this client has this incredible great  SmO2  value  but simply has a problem to actually use the Oxygen.
 She is completely saturated with O2  but can't get it to be used. 9 Bio availability of oxygen.
 When we  look in this case at the VO2 data's and there more at the VE ( RF x TV ) as well as at the EtCO2 values  we could give some better answers here.
 In this case 2 main open questions.
 a) Limitation  from the muscular system  to limitation from the bio availability of the   metabolic  trends ( CO2 trends.
 If we have a muscular limitation 9 Flat  SmO2 on a high  SmO2 level than we  have to look at vasuclarisation and  to mitochondria density.
 The first is needed to improve the second.
 If we have a deoxygenation limitation , than we have to look at  the respiratory system.
 With IPAHD n the   advance level we  assess this as we go along , by challenging in the second 5 min of the same load exactly this 2 systems.
..
 Once we have the reason of the  deoxygenation situation  we than can design  her a proper and specific  workout plan to try to improve this weak link.
 Here 2 att who show you what I mean.
 Two workouts.
 att 2. deoxygenation workout where we try to drop SmO2.
 and att 3  where we do the opposite, we stop deoxygenation to create a hypoxia to stimulate  vasuclarisation  and  therefor later  mitochondria density production.
The last one is a practical  load on the ice with first complete possible deoxygenation  followed by a section of hypoxia load ( no further drop  in SmO2 )