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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
This is  an ongoing  discussion in my mail box.
 We  do not have a problem  with our  assessment method  but we had some problems,  many years back, when we tried  to use  a  NIRS trend  like tHb  or Hb Diff   or O2Hb  break points and tried  to correlate them with LT. Depending where we  would mount the NIRS,  we would have different break points when they showed  up, but same lactate readings. So one break point  may have  somewhat  showed up  with a  relative clear  increase in lactate  the other was  much earlier and an other  would be  later. Or in simple terms, it was  the " choice  " of the  tester to decide, which muscle may give you a real  timing  and   performance for the lactate threshold  zoning idea.???

  What we  can tell  from our uses  of NIRS  and MOXY is the following  trends.

1. The trends are  close  to each other when we look at  a  few  situations.
 a)  The initial increase in tHb  and SmO2  is  in  all muscles,  whether they are involved  or  a little bit involved or not involved  at t+-  the same  time.
 To find this reaction you have to avoid a " warm" up  as it happens there  and you have to include the warm  up in your assessment time.
 As well the initial 5  -  10 min have to  be  slow ,  very slow  30 % of your maximal performance you may be able to do.
  50 %  most often already misses  the  information on this topic.

 2.  The  "middle" section in a TIP  or  any step test  looks  very different  on the three options on involved , somewhat involved and not involved muscles.

3. The last part  , where we  go very hard  may   be again  close to each other as   in this phase, where we  go and push  hard  , where we push an intensity , where the  systems (  CG )  has to make a decision, whether to  reduce  O2  delivery  to protect  vital organs as  well to  avoid a  too low  ATP drop, we   see a drop in tHb  and SmO2  around the same time in all three  muscle involvement. The  not involved muscle  may create a centrally controlled  vasoconstriction ( drop in tHb )  and  the drop  of SmO2  is not due to utilization but rather due to reduced  O2 inflow.

 The   problem  with location is, when we go with the old idea of finding a LT  or AnT  or AT  or   VT  or any  kind of a break point   even in  the NIRS trend.
  At the moment where we  push hard ,  but not hard  enough  for survival  emergency,  we have  some very  different information depending on location where we mount the  MOXY.
 This may create some problems, when we  use  lactate  and  NIRS  to make  any kind of a correlation  with  a   NIRS break points   and  "lactate threshold."  concept
 As usual we  where looking  around  till we found  some papers  confirming  what looked   kind of  hard to defend  for us.
  Here a great part of a long paper  who shows, that when we  mount a  NIRS /MOXY on a  calf  we  may have a different break point than when mounting on a  Vastus lateralis  and    when we  think , that we take the lactate on the same place  ( finger ) than you can see, that there may be  some discussion on  which  muscle may give you the real LT intensity  and what  lactate value ??
 Here to enjoy  this part .
 By the way this is a  great example, that the lactate we test at the finger is the summary of an endproduct  of a  mixed  bag of muscles  either producing lactate, being just in a  MAX lass  situation or  actually consuming lactate.
 How  can we use  this    information of a mixed  bag  to actually design or use   a NIRS idea    of a direct measurement  and   correlate  this  to lactate taken  by the finger. True  if  you calculate  long enough  you will find   an algorithm of  some kind of.

Muscular differences in breakpoints of muscle oxygenation changes

Considering that the VL and GL were mostly studied independently in previous NIRS studies, we tested the VL and GL simultaneously to compare the two muscles, as the VL and GL are involved as a knee extensor and a knee flexor/ankle stabiliser, respectively, during cycling. The BpVL appeared earlier than the BpGL (p < 0.001), indicating that the oxygen supply-consumption balance in the VL was broken earlier than that in the GL during cycling IET. Furthermore, the BpVL had higher assessment ability (indicated by the higher R2a and lower RMSE, Table 2) for the aerobic capacity indices than the BpGL. One reason for the differences in the Bp of OI between the VL and GL might be the differences in anatomical and histochemical characteristics. Sufficient evidence has shown that the percentage of type I (slow twitch) fibres in the VL is lower than that in the GL (Edgerton et al., 1975; Houmard et al., 1998; Staron et al., 2000). Additionally, the activity of oxidative enzyme (citrate synthase) was previously reported to be lower in the VL than that in the GL (Houmard et al., 1998). Due to the lower percentage of type I fibres and lower activity of oxidative enzymes in the VL, the fast twitch fibres would be largely recruited earlier in the VL when the workload continuously increases, resulting in more anaerobic metabolism in the VL during moderate and high intensity exercise. The earlier accumulation of acidic metabolic substances in the VL might result in more H+ and a lower pH. Due to the Bohr effect, the accelerated dissociation of O2Hb would occur earlier in the VL due to the earlier accumulation of acidic metabolic substances; this result is indicated in our data by the earlier breaking up of the oxygen supply-consumption balance in the VL (BpVL). Another reason for the differences in the Bp of OI between VL and GL might be different usage patterns of the muscles during cycling. The mono-articular muscles (e.g., the VL) are primarily involved in the generation of positive work, whereas the biarticular muscles (e.g., the GL) are responsible for regulating force transmission during cycling (So et al., 2005). Additionally, the VL is thought to be one of the most active muscles during cycling (Hug et al., 2006) and seems to produce more muscle work than the GL over the crank cycle (Neptune et al., 2000). Therefore, the contribution of the VL is most likely higher than that of the GL during cycling, which might account for the earlier occurrence of the BpVL and the higher assessment ability of the BpVL for the aerobic exercise capacity indices. In summary, the differences in the BpVL and the BpGL might be mostly associated with the muscular differences in the percentage of muscle fibres and the usage patterns during cycling. However, further research with muscular biopsy and/or sEMG is needed to confirm this type of association.


Bangde Wang,1,2* Guodong Xu,3,4* Qingping Tian,1,2* Jinyan Sun,1,2* Bailei Sun,1,2* Lei Zhang,1,2* Qingming Luo,1,2* and Hui Gong1,2*


1Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics


2Key Laboratory of Biomedical Phototonics of Ministry of Education, Huazhong University of Science and Technology, Wuhan, China


3School of Physical Education, Jianghan University, Wuhan, P.R.China


4College of Health Science, Wuhan Institute of Physical Education, Wuhan, China


Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, China


Received May 9, 2012; Accepted July 17, 2012.


Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Got  some nice  mails after this topic.
 One  statement was intriguing.
 In short.
Statement was;
 NIRS  will  simple to read and predict reactions.Therefor it does not need  complicated systems  and does not need  expensive equipment. Simple  trends  and correlation to  lactate will do it.
 NIRS will simply  show :
  When SmO2  drops , than  O2Hb  will drop and tHb  will drop.
 When  SmO2  goes up than O2 Hb  will go up and tHb will go up.
 So no need  for any other  info  than just a SmO2  ( SpO2 ) trend  and it will  correlate to lactate.  SmO2  drops  lactate goes up   and SmO2  up  and lactate goes down. Simple as that.
That is   frustrating.( Smile ) I work  since over 30 years on this and learn in one simple email how easy it is.
Here a suggestion.
  Bike  with your MAX Lass   for 10 min (  to be more correct rid on Max lass  actually for 16 min. [wink] So we are sure you are stable . Check  with any NIRS the level  of SmO2  which most likely could be stable

 Than  for 3 to5 min  breathe   much faster than you would need to breathe  at this performance so you actually  create a slightly  hyperventilation ( more  breathing than needed ) which by definition will drop your EtCO2.
 Initially  you actually will see an increase in EtCO2   before it will start to drop. To be  relative sure that your EtCO2  is  close to PACO2  and  PaCO2  you have to try to get this going  for  5 min+..  For people  NOT respiratory trained  you may have to drop your  load  by about 20 %  . So if you  know your FTP    drop by  about 20 %.  In this intensity you should be able to  breathe  as suggested. ( There are reasons  why some can't  do it  on MAX LASS  and or  on FTP.)
 Now  observe  what happens  with your SmO2  and take  lactate  after the 15 min MaxLass or FTP  load  and than  after 3, 6 ,9 min   in  and after the hyperventilation.

 Than come back  and we  review  your  great  and  short summary with the data you collected.
  To add some  more to this point  see the 2 pictures.

Pic  1
 Yes you are right see in green TSI %  or   SmO2  reaction  it goes up  and with it the red  trace which is the O2Hb.    No tHb  on this here  to stay simple and not be too confusing.
Pic 2
  See  second picture     yes  O2Hb ( red ) goes up as above .  Small problem here TSI    (SmO2  drops )

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now here  some positive feed backs  , a  study sent to me.
 This is a nice  study supporting our idea on  actually suing trends versus absolute numbers  as well the  interesting idea that people think they can  add an actual lactate number  to a  NIRS trend.
. This   study as well shows, that when using  MOXY  not just for assessments  but even better for actual  live  feedback during workouts   you have   the first time an actual control to be sure  you  loading the  zone you have planned to load. Non of the existing  ideas  from VO2  Max %  to lactate    zoning calculation to  FTP  % to  max watt %  will do this.
 The interesting part is  that possibly the Borg scale is   most accurate   from all of the zoning  and  paired  with MOXY you have the feedback.  Take your    Garmin watch   and see SmO2  and  tHb trends  there as you  run bike    or do anything.  Take  your PC  and use  a simple software  for live info  and you see  HR  and    MOXY info live in front  of you when you run  on the e treadmill or use  a  stair climber  a Versa climber   a  rowing  equipment.
 Here to enjoy the read.

Regional muscle oxygenation differences in vastus lateralis during different modes of incremental exercise

Michael D Kennedy1*, Mark J Haykowsky1, Carol A Boliek1, Ben TA Esch2, Jessica M Scott2 and Darren ER Warburton2

Author Affiliations

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

2 Cardiovascular Physiology and Rehabilitation Laboratory, University of British Columbia, Vancouver, British Columbia, Canada

For all author emails, please log on.

Dynamic Medicine 2006, 5:8 doi:10.1186/1476-5918-5-8

The electronic version of this article is the complete one and can be found online at:

Received:28 April 2006
Accepted:3 July 2006
Published:3 July 2006

© 2006 Kennedy et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.



Near infrared spectroscopy (NIRS) is used to assess muscle oxygenation (MO) within skeletal muscle at rest and during aerobic exercise. Previous investigations have used a single probe placement to measure MO during various forms of exercise. However, regional MO differences have been shown to exist within the same muscle which suggests that different areas of the same muscle may have divergent MO. Thus, the aim of this study was to examine whether regional differences in MO exist within the same muscle during different types of incremental (rest, 25, 50, 75, 100 % of maximum) exercise (1 leg knee extension (KE), 2 leg KE, or cycling).


Nineteen healthy active males (Mean ± SD: Age 27 ± 4 yrs; VO2max: 55 ± 11 mL/kg/min) performed incremental exercise to fatigue using each mode of exercise. NIRS probes were placed on the distal and proximal portion of right leg vastus lateralis (VL). Results were analyzed with a 3-way mixed model ANOVA (probe × intensity × mode).


Differences in MO exist within the VL for each mode of exercise, however these differences were not consistent for each level of intensity. Comparison of MO revealed that the distal region of VL was significantly lower throughout KE exercise (1 leg KE proximal MO – distal MO = 9.9 %; 2 leg KE proximal MO – distal MO = 13 %). In contrast, the difference in MO between proximal and distal regions of VL was smaller in cycling and was not significantly different at heavy workloads (75 and 100 % of maximum).


MO is different within the same muscle and the pattern of the difference will change depending on the mode and intensity of exercise. Future investigations should limit conclusions on MO to the area under assessment as well as the type and intensity of exercise employed.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Now here a nice  mail I got from our  friends  and study group  from Norway.
 Here the abstract  fromm a work  from Norway.

 What is shows is  interesting  and supports  many of our  points  we   discuss on this Forum.
  Placing a  NIRS   during cycling on a calf  has  little or less information  as the reactions are   not  as clear.
 We did  a similar comparison   in running, as   you would think in running the calf  may be a great placement.
  Problem here is. If you run on  a treadmill it may work okay , but as well some problems.
 If you run  or start slow you may be a heel striker   than you may move to mid foot  and finally you may end upon  the  fore foot.
 When you use the equipment outside  you run   downhill ???  flat  and   up hill?  What can you expect  may happen in the calf  with this  and how  can you calculate  any idea  based on NIRS feedback and potential lactate threshold.
 ?? here  thanks  to this mail.


Oxygen Consumption in Cycling:

The Relationship between Whole Body Pulmonary O2 Consumption and Muscle Oxygenation in Different Muscles During Constant-Load Cycling


Introduction: Oxygen consumption during prolonged cycling exercise has been extensively studied at different work rates and durations, but with the focus primarily on pulmonary oxygen consumption (pVO2). The purpose of this study was to use near-infrared spectroscopy (NIRS) to investigate the relationship between pVO2 and local oxygenation responses in six active leg muscles during prolonged constant-load cycling at different intensities. Methods: 26 recreational male cyclists performed a constant-load high-intensity cycling test at 75% maximal aerobic power (MAP) for 30 min duration or until exhaustion. Of the 26 subjects, 14 performed a constant-load low-intensity cycling test for the same duration as well, at 50% of the work rate found to elicit blood lactate levels of 4 mmoll-1during incremental exercise. Pulmonary gas exchange (pVO2, RER, VE), heart rate, and NIRS measurements of the muscles vastus lateralis (VL), vastus medialis (VM), biceps femoris (BF), gluteus maximus (GMax), gastrocnemius lateralis (GL), and tibialis anterior (TA) were obtained continuously through both tests, while blood lactate and RPE was measured at specific time intervals. Results: Local oxygenation measurement for all the muscles collectively behaved in a similar manner as pVO2 at both intensities with an increase in O2 utilization only found in the initial phase, and additionally showed a surprisingly homogenous response. However, differences were found between the muscle groups with heterogeneity in regard to the amount of desaturation at low- and high-intensity. Discussion: Although the local responses were similar to each other and that of pVO2, differences were found between the muscles with heterogeneity in regard to the amount of saturation. The distal muscles TA and GL showed less difference in saturation between low-intensity and high-intensity than the more proximal muscles (VL, VM, BF, and GMax). Also the BF and GMax muscles were found to behave different with a lack of TSI steady-state during high-intensity
. Conclusion: The use of NIRS might provide a noninvasive and direct way of measuring local oxygenation responses in muscles and provide an indication of the work contribution of various muscles during cycling exercise. Although local oxygenation responses across the muscles were in agreement with pVO
2, difference in amount of saturation was found between muscle groups in the present study. Also peripheral differences were found between the subjects able to complete 30-min constant-load high-intensity cycling and those who did not.

Key words: Near-infrared spectroscopy, NIRS, cycling, constant-load, VO2, local oxygenation, tissue saturation, SmO2, muscle, muscle groups.

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
In this study is a perfect section,  and for regular readers it makes perfect sense, when you look how we    use lactate.  In this study  they where somewhat surprised.
  Here the small section. Lactate has little    to do with  4 mmol  and or  lactate threshold.
 They where in a perfect  balance with VO2  and stable  but lactate increased  still. Why?.   So  the so called  VT  or  the   information we take where  O2  crossed  CO2  as the  other option for indirect lactate threshold  is thrown out here as well  as  VO2  was stable.
  How where they able to  sustain a steady  increase in lactate ?

3.1 Whole Body (Systemic) Response

Individual pVO


2 and [La-] responses during CL-HI for both group 1 and 2 are presented in Fig. 4. After an initial increase in pVO2, no further increase after the 6th minute was seen in any of our subjects (n = 26), suggesting that the intensity of 75% MAP was below the MLSS threshold. This is, however, in contrast with the increase of blood lactate levels in some of the subjects. High levels and continuous increase of [La-] were present in several of the subjects unable to complete 30-min cycling, with the highest increase of lactate from the 10th minute to finish being 4.21 mmoll-1. Nevertheless, the Δ[La-] (i.e. Δ[La-] = [La-]end MAP – [La-]end CL-HI)

Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Wowww fast  email , must have  waited  for this ( Smile )  yes I can show the VO2 respond  and lactate in a graph.
 It is another great example  how VO2  is  just an overall  view on the O2  use  form the whole body. What we  do not know is  how during this load the cardiac system  and the respiratory system got  either more or less efficient or who  was  the limiter in this person.
 The  lactate  shows  as a metabolic marker , that  despite a stable VO2   the way the O2  was used  to create  ATP  was very individual. When we  would have not just  SmO2  but as well tHb  we  would have  a much deeper information on  how the delivery  may have changed  and or  how the delivery change may  have affected the utilization.

 Here  the pic  graph

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Again  for all readers  a  feedback on a mail just coming in.
 How  do you explain, that despite increase In lactate they where able to go ?
  Short answer, as we discussed this to  the never end   many times.
 1. Lactate is not an indicator  of fatigue or the reason of fatigue.
 1.1  Lactate is a bio marker, that  energy is  produced in certain body parts  like here in cycling  with  some O2 independent help, as  well as glucose is  used in a high rate.
 Therefor  in some body parts we may  have  an increase in H +    production and in this areas the body will try to maintain a H + balance  as long as possible . As long lactate helps there to shuttle H + out of the hard working muscle  and   than gets rid of it to be used in other muscles ,   we can maintain  the H + balance and  can get going.
 The increase in H +   in the blood will be compensated  as well  and one  path way will end up with an increase in CO2. This part can  get  controlled over an increase in ventilation  VE  up. So as long the respiration can  move enough VE  and CO2  out  and we  can  maintain H +  by using lactate as a buffer   as longer we  can go and lactate can increase to  levels  far above the famous  4 mmol and  can increase more than 1 mmol  so   above what would some  use  as  an indicator of the famous  lactate threshold???

  The  main  problem here is in people, where the respiratory system is a limiter. Here we will run into  problems with an increase in CO2  as we  can't  get rid of this .Now balance is gone  and the  exercise is over.  Is this  a nice theory  or is   it possible . You are the judge  see pic  and summary of the   data's.

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Juerg Feldmann

Fortiori Design LLC
Posts: 1,530
Here an abstract I got mailed  to  me yesterday. Unfortunately no   info on  the  group who did this interesting work.
  If  I can remember  good enough  ( the nice part in getting older is , that you always  can claim  you know everything  you simple  can't remember it anymore , always a great excuse   )  This study  was  possibly  form the UBC study group. Here the nice abstract.


The purpose of this study was to determine which upper-limb muscle exhibits the greatest change in muscle deoxygenation during arm-cranking exercise (ACE). We hypothesized that the biceps brachii (BB) would show the greatest change in muscle deoxygenation during progressive ACE to exhaustion relative to triceps brachii (TR), brachioradialis (BR), and anterior deltoid (AD). Healthy young men (n = 11; age = 27 ± 1 y; mean ± SEM) performed an incremental ACE test to exhaustion. Near-infrared spectroscopy (NIRS) was used to monitor the relative concentration changes in oxy- (O2Hb), deoxy- (HHb), and total hemoglobin (Hbtot), as well as tissue oxygenation index (TOI) in each of the 4 muscles. During submaximal arm exercise, we found that changes to NIRS-derived measurements were not different between the 4 muscles studied (p > 0.05). At maximal exercise HHb was significantly higher in the BB compared with AD (p < 0.05). Relative to the other 3 muscles, BB exhibited the greatest decrease in O2Hb and TOI (p < 0.05). Our investigation provides two new and important findings: (i) during submaximal ACE the BB, TR, BR, and AD exhibit similar changes in muscle deoxygenation and (ii) during maximal ACE the BB exhibits the greatest change in intramuscular O2 status

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