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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
Here is a very interesting study.
 The conclusion of the study would  support us, but I have a major problem with the idea and the point, that lactate  can be used to validate NIRS.  just because we are stuck in the tradition that 4 mmol lactate would work and that there suppose to be a lactate break point  does not mean we  use that to validate  NIRS. It is rather the opposite. NIRS information will show  that lactate  can have a  direct connection with NIRS  as a trend information  but not the other way around.
 Lactate has in many cases a  severe lag   compared with NIRS.
 The best examples are information post  workout   of interval ls  and you can as well see in any NIRS graph how fast the SmO2 is going up and is reaching a maximal level.  and you can see in the pic  below how   the lactate result is directly  correlated to the intensity on one side and to many other factores like MCT   ability   as well as respiratory ability to help to balance H +. The second picture is a trend of SmO2  and lactate from the case study we showed from Brian KOZAK.
 We as well can show many many  studies we did , where it is very easy to show how lactate and SmO2  are not timed the same way but lactate  lags behind in  many of the cases.
 Look at the BPR  graphs , the group who uses LBP in the second stage  how different SmO2 and lactate can be in any case depending on LIMITER and Compensator.

 Here the  article 
 

Using near-infrared spectroscopy to determine maximal steady state exercise intensity.

Snyder AC, Parmenter MA.

Source

Department of Human Movement Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53201, USA. acs@uwm.edu

Abstract

Maximal steady state (MSS) speed can be determined from blood lactate concentration (HLa); however, this method is not optimal. The purpose of this study was to determine whether near-infrared spectroscopy (NIRS) technology could be used to detect a breakpoint in percent oxygen saturation (StO2) of the muscle and whether the determined breakpoint exercise intensity could be used to determine MSS exercise intensity. Sixteen distance runners and triathletes (men = 9, VO2max = 64.9 +/- 4.9 ml x kg(-1) x min(-1), women = 7, VO2max = 50.8 +/- 7.0 ml x kg(-1) x min(-1)) completed an incremental exercise test. A change from linearity when plotting StO2 or HLa vs. running speed was defined as the breakpoint. The subjects then completed constant speed runs to determine maximal lactate steady state (MLSS). In 12 subjects, breakpoints were identified for both HLa and StO2 values. Predicted MLSS velocities from HLa breakpoint (12.76 +/- 1.63 km x h(-1)), StO2 breakpoint (12.84 +/- 1.58 km x h(-1)), and 4 mM HLa (13.49 +/- 1.71 km x h(-1)) methods from the incremental test did not differ from MLSS speeds (13.04 +/- 2.03 km x h(-1)). A Bland and Altman analysis of agreement between the MLSS and the StO2 breakpoint speeds resulted in a mean difference of 0.14 +/- 0.36, whereas the mean difference between MLSS and HLa breakpoint speeds was 0.19 +/- 0.43. During the incremental test, no StO2 breakpoint was determined in 2 subjects, whereas 2 subjects had no HLa breakpoint. The results of this study lead us to conclude that the NIRS determination of StO2 is a noninvasive technique that is comparable with HLa in determining MSS intensity and therefore appropriate for use in determining exercise training intensity.

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Here another nice study with some questions.
 1. O2 Disscurve  shifts to the right  due to different reasons :
 pH drop, H + increase  , Co2 increase to name some  points in this  discussion.
 It does not shift doe to lactic acidosis  but the explanation shows how   this is just stuck in the literature.
 When O2 Diss sifts  in this combination it is due to H + increase . The lactate itself  will not influence the O2 Diss curve directly but indirectly by  helping to buffer H +   as does respiration by helping to release CO2.
 Nice is , that they honestly write 
   A ‘‘point of inflection’’ of [La]b vs. w˙ was arbitrarily

identified at the lowest [La]b value which was .0.5

Blood lactate accumulation and muscle deoxygenation

during incremental exercise

BRUNO GRASSI,

 

1 VALENTINA QUARESIMA,2 CLAUDIO MARCONI,1

MARCO FERRARI,

 

AND PAOLO CERRETELLI1

 

1

 

 

 

Istituto di Tecnologie Biomediche Avanzate, Consiglio Nazionale

 

delle Ricerche, I-20090 Segrate (MI); and

 

2Dipartimento di Scienze e

 

Tecnologie Biomediche, Universita` di L’Aquila, I-67100 L’Aquila, Italy

 

Grassi, Bruno, Valentina Quaresima, Claudioarconi,

 

Marco Ferrari, and Paolo

Blood lactate accumulation and muscle deoxygenation

during incremental exercise

BRUNO GRASSI,1 VALENTINA QUARESIMA,2 CLAUDIO MARCONI,1

MARCO FERRARI,2 AND PAOLO CERRETELLI1

1Istituto di Tecnologie Biomediche Avanzate, Consiglio Nazionale

delle Ricerche, I-20090 Segrate (MI); and 2Dipartimento di Scienze e

Tecnologie Biomediche, Universita` di L’Aquila, I-67100 L’Aquila, Italy

Grassi, Bruno, Valentina Quaresima, Claudioarconi,

Marco Ferrari, and Paolo Cerretelli. Blood lactate accumulation

and muscle deoxygenation during incremental exercise.

J. Appl. Physiol. 87(1): 348–355, 1999.—Near-infrared

spectroscopy (NIRS) could allow insights into controversial

issues related to blood lactate concentration ([La]b) increases

at submaximal workloads (w˙ ). We combined, on five welltrained

subjects [mountain climbers; peak O2 consumption

(V˙ O2peak), 51.0 6 4.2 (SD) ml ·kg21·min21] performing incremental

exercise on a cycle ergometer (30Wadded every 4min

up to voluntary exhaustion), measurements of pulmonary gas

exchange and earlobe [La]b with determinations of concentration

changes of oxygenated Hb (D[O2Hb]) and deoxygenated

Hb (D[HHb]) in the vastus lateralis muscle, by continuouswave

NIRS. A ‘‘point of inflection’’ of [La]b vs. w˙ was arbitrarily

identified at the lowest [La]b value which was .0.5

mM lower than that obtained at the following w˙ . Total Hb

volume (D[O2Hb 1 HHb]) in the muscle region of interest

increased as a function of w˙ up to 60–65% of V ˙ O2peak, after

which it remained unchanged. The oxygenation index

(D[O2Hb 2 HHb]) showed an accelerated decrease from 60–

65% ofV ˙ O2peak. In the presence of a constant total Hb volume,

the observed D[O2Hb 2 HHb] decrease indicates muscle

deoxygenation (i.e., mainly capillary-venular Hb desaturation).

The onset of muscle deoxygenation was significantly

correlated (r2 5 0.95; P , 0.01) with the point of inflection of

[La]b vs. w˙ , i.e., with the onset of blood lactate accumulation.

Previous studies showed relatively constant femoral venous

PO2 levels at w˙ higher than ,60% of maximal O2 consumption.

Thus muscle deoxygenation observed in the present

study from 60–65% ofV ˙ O2peak could be attributed to capillaryvenular

Hb desaturation in the presence of relatively constant

capillary-venular PO2 levels, as a consequence of a

rightward shift of the O2Hb dissociation curve determined by

the onset of lactic acidosis.

lactate threshold; near-infrared spectroscopy

 

Cerretelli.

 

 

 

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Here is another great accepted study.
 

Muscle oxygenation trends during dynamic exercise measured by near infrared spectroscopy.

Source

Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Canada.

Abstract

During the last decade, NIRS has been used extensively to evaluate the changes in muscle oxygenation and blood volume during a variety of exercise modes. The important findings from this research are as follows: (a) There is a strong correlation between the lactate (ventilatory) threshold during incremental cycle exercise and the exaggerated reduction in muscle oxygenation measured by NIRS. (b) The delay in steady-state oxygen uptake during constant work rate exercise at intensities above the lactate/ventilatory threshold is closely related to changes in muscle oxygenation measured by NIRS. (c) The degree of muscle deoxygenation at the same absolute oxygen uptake is significantly lower in older persons compared younger persons; however, these changes are negated when muscle oxygenation is expressed relative to maximal oxygen uptake values. (d) There is no significant difference between the rate of biceps brachii and vastus lateralis deoxygenation during arm cranking and leg cycling exercise, respectively, in males and females. (e) Muscle deoxygenation trends recorded during short duration, high-intensity exercise such as the Wingate test indicate that there is a substantial degree of aerobic metabolism during such exercise. Recent studies that have used interestingltiple sites, such as brain and muscle tissue, provide useful information pertaining to the regional changes in oxygen availability in these tissues during dynamic exercise.


An interesting section is :
 "lactate (ventilatory) threshold   )
. You may recall the discussion, where we  showed, how VT is not equal to AT and LT.  Well it is  as it seems a pretty common idea, even though we know it is not that case in most of the test situation ( exceptions of  respiration as the LIMITER )

2 another interesting part is,. what confirms what we  explained somehwere before. Wenn doing a basic MOXY  MYPAHD assessment it  may not matter, where you  attach the senore.
 ( It has some small influences we  will explain in the handout to MOXY whether you work with trend of SmO2 or with actual  numbers.

"There is no significant difference between the rate of biceps brachii and vastus lateralis deoxygenation during arm cranking and leg cycling exercise"

   In the next month  we  will do a major datacollection of  possibly hundreds of test to  actually get this right for us to have a perfect information for beginner buying a MOXY in a sport store or where ever.
 Stay tuned for that section comming up.
 The key is  to have  a few hundred   datas instead of  5 - 10 , as so often.

   3. This last section is  even nicer.
About  10 years ago we started on the FaCT Forum a   long discussion on " anaerobic power and  test lenght. ( again and again  the  fact , that a physical protocol design will create an answer  you look for rather a physiological response.)
 
 The question why a Wingate test suppose to be a great test for anaerobic power.??
.  
 Here from an accepted  place an interesting statement , which may reopen  partially the discussion .

 " Muscle deoxygenation trends recorded during short duration, high-intensity exercise such as the Wingate test indicate that there is a substantial degree of aerobic metabolism during such exercise.  "

So what MOXY really will do is  to answer exactly that question  from a Wingate test, whether the athelet really has a good aerobic or anaerobic  ability.
 It is  NOT the wattage you push it is the question on the doexygenation trend.
 Do you see a  nonstop deoxygenation or do you see a "plateau" and in the doexygenation and how long is the plateau there befroe we have a stop in the test.
 The lenght of the SmO2 plateau will inform us on the "anaerobic " power  and not the wattage level.
 I will show you some test we did many years back  where we exactly looked at that  possibility  with NIRS.


 This is the difference between an IPAHD and an IPAHR.
 In the IPAHR we look at the deoxygenation  trend and the  plateau and than the recovery.
 So in other words  IPAHR is the individual assessment of homeostasis recovery rather than disruption.
 In endurance sport you need an IPAHD as you look to stay in a homeostasis for ATP production.
 IN an acyclic sport like Icehockey you know you will distroy ATP homeostasis ,so the  key is to look how  long can you go all out  and how long does it take you to recover.   Look at IPAHR example in this forum.

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