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DanieleM

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 #1 
I was reading this interesting research:

Effects of short-term endurance training on muscle deoxygenation trends using NIRS

J. PATRICK NEARYDONALD C. MCKENZIEYAGESH N. BHAMBHANI

This article would require different specific topics, anyway I would focus here on the 20TT.
After the training, most of these athletes showed ability to further (better) deoxygenate compared to the pre-training period.
This trend would mean better muscle utilization due to enhanced peripheral adaptation (capillaries/mithocondria).

I was surprised by another athlete who instead had a similar SmO2 profile (pre/post training), still managed to reach a better performance.
They suggested in this case a better central adaption.
My question is how would be possible to verify it with a Moxy trace? Overall better central adaptation (in this research, if I remember correctly, the hypothesis is an increase in HR/SV) should mean better delivery and consequently less drop in SmO2.

Daniele
Juerg Feldmann

Fortiori Design LLC
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 #2 
Here the abstract of the work in discussion .
 

Effects of short-term endurance training on muscle deoxygenation trends using NIRS.

Author information

  • 1Faculty of Kinesiology, University of New Brunswick, Fredericton, Canada. pneary@unb.ca

Abstract

PURPOSE:

This study examined changes in cardiorespiratory responses and muscle deoxygenation trends to test the hypothesis that both central and peripheral adaptations would contribute to the improvements in VO(2max) and simulated cycling performance after short-term high-intensity training.

METHODS:

Eight male cyclists performed an incremental cycle ergometer test to voluntary exhaustion, and a simulated 20-km time trial (20TT) on wind-loaded rollers before and after training (60 min x 5 d x wk(-1) x 3 wk at 85-90% VO(2max). Near-infrared spectroscopy (NIRS) was used to evaluate the trend in vastus medialis hemoglobin/myoglobin deoxygenation (Hb/Mb-O(2) during both tests pre- and post-training.

RESULTS:

Training induced significant increases (P </= 0.05) in maximal power output (367 +/- 63 to 383 +/- 60 W), VO(2max) (4.39 +/- 0.66 to 4.65 +/- 0.57 L x min(-1)), and maximal O(2) pulse (22.7 +/- 3.2 to 24.6 +/- 2.8 mL O(2) x beat(-1)) during the incremental test, but maximal muscle deoxygenation was unchanged. 20TT performance was significantly faster (27:32 +/- 1:43 to 25:46 +/- 1:44 min:s; P </= 0.05) after training without a significant increase (P > 0.05) in the VO(2) (4.02 +/- 0.52 to 4.04 +/- 0.51), heart rate (176 +/- 9 to 173 +/- 8 beats x min ) or O pulse (22.4 +/- 3.2 to 23.5 +/- 2.8 mL O(2) x beat(-1)). However, mean muscle deoxygenation during the 20TT was significantly lower after training (-550 +/- 292 to -707 +/- 227 mV, P </= 0.05), and maximal deoxygenation showed a trend toward significance (-807 +/- 344 to -1,009 +/- 331 mV, P = 0.08), suggesting a greater release of oxygen from Hb/Mb-O(2) via the Bohr effect.

CONCLUSION:

The significant improvement in VO(max) induced by short-term endurance training in well-trained cyclists was due primarily to central adaptations, whereas the simulated 20TT performance was enhanced due to localized changes in muscle oxygenation.


 It is an interesting case studie with lot's of hidden questions.
Now  you will see, that I look  at this type of NIRS studies very different.Whether it is  better or nor  is not the point here. It  is a question whether " traditional " thinking may inhibit the wider options  NIRS  my  give us, when looking  at the datas  from a different point of view.

1.
I  believe, that the difference in the  result in deoxygenation is  produced  by the " protocol"

 In a 3 min step test we have no chance  to see a  systemic  decent reaction  like  vasodilatation ( delivery  question ) as well as respiratory  adjustment  ( O2  diss curve reaction  )  and so on.
 In this case the step test , when you look at  O2  pulse  and VO2  shows  , that the  maximal tested HR  was  much higher than what we see in the TT .  190+-  to 175 +-   So a very different  CO.

We see than in the Step test  repeat the O2  pulse  increased nicley  as  an indication of  potential  bigger SV.
 Whether the SV increase was  a  structural real change  and  or a  reaction of plasma increase  due to the type of   load ? . We  do not know. The problem as well is :  was the 85 - 90 %  VO2  max load    the 85 - 90 %  VO2  max load  from what  kind of a VO2  max  result  . Step test or TT?.
If it was  from the  step test  than they  in a 60 min workout  where much closer  to 97 - 100 %  load  ( see  4.04  VO2 in the TT.
\
 Now here how  the SmO2  reactions paired with tHb reaction could look. 
In the step test   every step creates a   compression with  or without decompression depending on CO  and muscle tension ratio.


 smo2  tHb.jpg  
So the  " delivery " in the step test ( here 5 min steps ) will create a different reaction due to the step lenght  compared to the  delivery (tHb reaction ) in a  stable    or relative stable  TT  performance( see below .)
mark workout thb smo2.jpg So the SmO2  desaturation  can be different due to better utilization ( mitochondria  volumina ( which is hard to believe in 3  weeks workouts as a structrual change )  but it  can be different due to a change or Fatigue of a  weak respiratory system, which would increase  in a TT  the CO2  level   and or  metaboreflex  or both.  so drop in SmO2   ( right shift )    or drop in SmO2  reduction in delivery  due to   higher muscle contraction, or lower tHb  due to vasoconstriction ( metaboreflex )  so less O2   and blood delievery by a similar performance so higher CO2 production towards the end and so lower SmO2.
 In this cases it would be fun to have RF and TV as well and see, whether they reacted similar in step test  and  TT.
 The higher VO2  in the step test   may be simply due to a higher demand of  O2  from the cardiac system  which showed a higherr HR    than in the TT  and that would create a higher  MVO2 due to  much more contraction per minute  than in the TT.  ( This  why we use  Physioflow  when doing this type  of   studies )
This would be the  basic  question we always  wonder. VO2  is the summary of all O2 used  from all the systems involved  .
 So a training %  based on VO2  max tested  does not help us  to understand , what may have limited the  better performance  or what may have  helped  to see a better performance. As long we do not know  limiter  at the beginning of a  study  or training period , as more we simply have to compare  and than  speculate  like in this case. Having a limiter and than repeat the assessment and look upon changes in  the limiter we than have a feedback  why SmO2  changed in one  but not in the other.
 The limiter in a step test may be different than the limiter in a TT.

 That's  why an  assessmnt has to be sport specific  and there as well race  specific. To find a limiter in a TT you have to make a TT.
The weak part of my points is: The SmO2  change in the TT   to a lower one, but not in the step test  . But how high was the SmO2  in the step test  first tme  compared to the TT  first time. ?


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
I was looking in my  papers to see  whether I had a study in this direction. meaning that  the   protocoll  may change the results.
 Here  an interesting one  from far back.

J Sci Med Sport. 2003 Dec;6(4):422-35.

Comparison of W(peak), VO2(peak) and the ventilation threshold from two different incremental exercise tests: relationship to endurance performance.

Bentley DJ1, McNaughton LR.

Author information

  • 1Department of Human and Health Science, University of Westminster, United Kingdom.

Abstract

This report presents data comparing the peak rate of oxygen consumption (VO2(peak)), peak power output (W(peak)) and the ventilation threshold (VT) obtained from two different incremental cycle exercise tests performed by nine well trained triathletes (Mean +/- SD age 32 +/- 3 yrs; body mass 77.4 +/- 4.9 kg and height 185 +/- 3 cm). Furthermore, the relationship between these variables and the average sustained power output (W) during a 90 min cycle time trial (TT) was also determined. The two incremental exercise tests involved a 'short' test, which commenced at 150 W with 30 W increments every 60 s until exhaustion. The second ('long') incremental test commenced at a power output representing 50% of the W(peak) obtained in the short test. The subjects were then required to increase the power output by 5% every 3 min until exhaustion. The results showed the W(peak) (W) in the short test was significantly (p < 0.01) higher than in the long test. However, there was no significant difference in the VO2(peak) (1 x min(-1)) between the two tests. There was a weak but significant correlation between W(peak) (W) and VO2(peak) (l x min(-1)) (r = 0.72: p < 0.05) in the short (60 s stage) test but not the long (3 min stage) test (r = 0.52). There were no significant differences and good agreement between for the heart rate (HR) (b x min(-1)) and oxygen consumption (VO2) corresponding to the VT. In contrast, the power output (W) corresponding to the VT was significantly different and not comparable between the long and short incremental tests. The cycle TT performance was most correlated to the W(peak) (W) (r = 0.94; p < 0.01) and the VT (W) (r = 0.75; p < 0.05) from the long test as well as the VO2(peak) (l x min(-1)) obtained from the short incremental test (r = 0.75; p < 0.01). These data suggest that the length of stages during incremental cycle exercise may influence the W(peak) and in turn the relationship of this variable to VO2(peak).

 

DanieleM

Development Team Member
Registered:
Posts: 264
 #4 
I agree that there are quite a few unsolved questions from this research.
First of all, as you also pointed out, I argue that the training procedure was a 60 minutes at 85/90% VO2Max which is basically what they managed during the 20TT.

To focus the attention to the TT and the guy that performed better even with a lower desaturation, if I understood correctly your points, this could be due to a better delivery (more O2 availability), or improved respiration (better removal of CO2/less shitf to the right). 
liversedge

Development Team Member
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Posts: 15
 #5 
Hi Juerg,

I know this is not the purpose of this thread, so a quick "side" question.

In your chart you show tHb +/- from 0 .. do you feel it is best to chart it as a difference from the average ?

I wondered if it would be helpful to plot the delta also ?

Thanks,

Mark
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #6 
Mark,  hmm you ask the wrong guy. I  just simply use  it  so  coaches  can see what we can read out. You   have to discuss  with Roger  about  what you   propose here. What I need  live is a picture  for my clients    so they can see as they work out, what   quality of contraction they reach  and   I have to see, whether they  do what we try to do. For example an endurance strength workout  for  ice hockey player  over 3  x  20 min  so we have    open blood flow  so the  load  or performance is not  limited  due to outflow restriction 9 H +  accumulation ) or even worse  due to in  and outflow restriction so limitation     of local O2    storage. )  In the case  of an interval  we may use  SmO2  as a guide  but  the tHB will most often  set the amount  of  sets  or duration I can do  again  due to physiological limitation of  supply and demand  due to utilization limitation ( Mitochondria density ) or  due to  delivery limitation which  I can pick up   with tHb trends.
 Hope this helps a little bit   other wise  Roger is getting   nearly to good   to understand  on what we look for  and how we like to display this.
 Cheers Juerg

 PS  it may help usefull you sent me  for example  a data collection form you form a Wingate    as csv file  form the moxy app.  or  you can sent me an interval you did  same feed backs  or a  VO2  " max " test or what ever  and I can show what we can see  and are pretty confident it   tells  us something decent. 
Here a fun  example from a  cycling interval
col train.jpg 

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