Sign up Latest Topics
 
 
 


Reply
  Author   Comment  
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
Here a great formulated  question  from a  future MOXY user  from South Africa:
 I like to pick  the different sections from the question  you can see in red in the  text below.
 
Hi Roger
 
Thanks for the update on shipping.
I also had a couple of questions on the Moxy last week in an email and have included again below:
I read with interest your blogs, more from a layman's point of view, as I will be setting up the business and hiring the necessary skills in performance testing and coaching. I certainly see the benefit of the Moxy for the serious cycling and running crowd, but one of the markets I am looking to tap is the female weight loss market, through indoor cycling (using PerfPro) and metabolic testing.
Is weight loss and targeting the fat burning zone during exercise an area you have looked into?
Also would there be any contradiction in the studio utilizing FTP% workouts as the principle training methodology and then saying that the potentially differing results from the Moxy are a more accurate reflection of a customer's intensity zones? I don't see this as an issue for the majority of customers, but maybe for a few of the more serious customers.

You will see  in this answer as usual a fundamental difference  , when comparing on what we all learned  and use  from the "classical" school of exercise physiology. Yes  it may be controversial, but we have a lot of   fundamental datas  supporting our ideas  from  many different studies  you can find  on this forum.
 So let's start here  directly with the  thoughts:
 
 
1. I  do not believe, that we have  this nicely looking zones, where we  can  argue  : Now you burn  Fat, now  you switch to glucose  and now    you are " anaerobic"

True, it looks  impressive as  does the  %  calculation of a   so called VO2 max test.
 The question  simply is: Does mathematics  works in a physiological system?

Remember  the situation, that when we look at VO2  max  or   peak we  only get the sum of all systems  looking for VO2. So  if we  do not know    who is using how much VO2  and  whether we actually   delivery  or utilize  O2 in certain   body parts, we as well only speculate  and make a nice picture  of a Fat burning idea, when in fact we may not even be close to the  bodies ability to use O2   to burn actually fat.
 Any physiological system is  always using  energy in a  mixed  version.
 It will choose the  energy most efficient  at certain  activities  and it has to choose  the energy the body is able to convert  to ATP.
 
That means, that  even very slow intensities  considered  "Fat burning " activities may in fact   be hypoxic  ( O2  independent) as the muscle  does not has the ability (  lack of mitochondria )  to actually burn  the   O2  with  fat due to lack of O2  utilization.
 This  can be an actual utilization limitation  and or  it can be a " delivery / utilization" limitation.
 Example:
  Many overweight people   have as well respiratory limitation.
  We have  tested over   hundreds of    clients    and   the majority of overweight people have something called. CHRS (Chronic  hypocapnic respiratory syndrome ).
 When we  do a so called RRA  ( resting respiratory assessment)  than we see, that their  resting respiration rate is  very high  ( above  14  often )    , with this they often as well have   very high VE  even if the show a  Norm TV ).
 When we than look at  gas exchange  we see a very high FeO2  %  18  +  and a very low EtCO2  value  ( often below 32 mmHg  and lower)
 In simple  terms:
 Their CO2   is  out of balance  and they tend to shift the O2  Disscurve to the left. This means, that they actually load  O2 very nicely ( SpO2  looks ) great, in fact often higher than in top athletes   ) but they   can't  utilize the  O2  due to the O2  diss curve  and the  affinity of O2.
 So they load great, but they can't use   O2  very nicely.
 So even over night  they tend to be  low  of O2 utilization  and as such  they tend to   look for glucose  for energy supply during the sleep instead of    preferably Fat.
 In the morning the  blood sugar is relative low , they feel  not optimal  and they get their  coffee double double  and feel a burst of energy. Not that  it is true,, they do not have more energy  but form bad  to  go back to normal feels  great.


  So when we  go back.
 The   idea  to be able to  assess in a 3 min step test  metabolic  zoning based on RER ( RQ) is  discussed  to  the death and we  all know, that three minuet  and high activity    does not  gives  as  RER = RQ  as the respiration will change the  RER values dramatically.
  Solution:
 We have to see, whether we  actually  :
 a) load O2   ( SmO2  is increasing )
 b) maintain  O2 levels  ( SmO2  is flat )  and or  utilize more O2  than we  can deliver  ( SmO2  drops)
 Based on the dynamic  of the O2   ( SmO2  trend ) we   can  argue, that we  have an activity level, where at least the body uses  O2  for energy supply  and therefor we will have   metabolically   a feedback on what can be u used.

 So  can we use  MOXY  for weight loss.
  Well  based on what we  do or did in the past    MOXY is a  fundamental step forward in the  assessment  and  physiological feedback  during a workout in that direction.
  It clearly is a  physiological step forward  compared to the %  calculation based on statistics.. So   answer is simple:
 Yes  it is the  tool  for   weight loss ideas  and  control during a workout.
 Here a  assessment  from a beginner indicating  a problem  with  O2 utilization  and therefor a problem to actually loose weight in the long term as the structures  are simply not here to allow  and optimal efficient    energy production  with Fat integration. In simple term a great   assessment indication a  lack of  mitochondria density.


K SM tHb SmO2.jpg

We  all know the term ( heart rate drift )  we all  discussed this  since  any years. Is it really a  heart rate or  respiratory  of  SmO2  drift   or is it a performance drift.
  It all depends  on what we  try to keep  on the same level.
 If  we  as so often argue, that  performance (  wattage ) is the only objective feedback on performance ) than we  are  absolutely right.
 200 watt is always 200 watt.
 
But  it is not always the   same energy supply line  which helps us to maintain 200 watt.
Again we discussed  and showed that  so many times.
 1. Temperature.
 It is  warm outside  so  200 watt at the start  may be in the Fat zoning ) but as the time  gets up
 the  priority is not  to maintain 200 watt but rather the   priority will be to maintain core temperature.
 So we  shift blood  to the surface  to  cool down the   body. As  such we have a  reaction in   circulation of blood volume  and to maintain the needed  cardiac out put  with now a smaller  pre load ( SV  drops ) we have to increase heart rate ( heart rate  drift ??? )
 Due to the fact, that blood  now is   used  to cool down  and  O2  may be  not  as  readily available in the   muscles  we  have to see, how we  maintain the metabolic  demand  . The drop in available O2  will  force the body to find    energy supply  which may demand less O2  for the same amount of ATP production and we  may shift  from   preferred  FFA  to  more glucose involvement.
  Question:
 do we really have a heart rate drift or  do we  actually have  due to the fixed 200 watt a  shift in  metabolic  delivery  and utilization action.
 Or in other words.
 If we really like to stay in a relative  stable metabolic  supply idea, than we may have to reduce   wattage to maintain    stable HR  a stable respiratory rate  and a stable  oxygenation  trend ( MOXY).
 So we  may start out with 200 watt  and  may end  with 155 watt  after 2 hour  ride but we maintain a relative stable metabolic  demand  reaction.
 So we really have a  performance ( wattage ) drift  and not  heart rate  drift.
 This is  because wattage is   NOT a physiological  feedback   and it is NOT  usable  for  training intensity control. It is great to see   changes in performance as it is  an objective value.
  BUT   by   training on a fixed wattage  we may move   during a workout  through a set of very different physiological changes  and not even understanding why   we  not always see the same  reaction by the same  wattage.


Summary:
 With MOXY  combined  with  feed backs  like HR  and respiratory information  we now  have the first time the ability to actually see live   what and how we  use O2  for the current  activity or workout.


1.  I certainly see the benefit of the Moxy for the serious cycling and running crowd,

Interesting statement. Reality  shows  us, that exactly this group  is  completely stuck on  performance. The  majority of feed backs we    have form  Pro cyclists  and from coaches  working  with this group is a  feedback of a   incredible  lack of physiological  fundamental information.
 The majority of this groups  know  the tire  pressure of the bike, the gear ratio  and the   optimal wind resistance factores as well use  bio mechanical feed backs  fro  bike fitting.
 If you ask  what  the actual performance  part  ( the athlete ) has on SpO2  , RF  TV   SmO2  shift  and whether the bike position changes TV  or O2 utilization ) than  you  get big eyes   funny looks  and  end of the discussion. .

So we are  actually  surprised  how   little   interest  there is  to  at least    open a fair discussion on the fundamental steps of performance improvement.
 Instead we see further   steps in trying to find  allowed or  not yet banned ideas like certain gases to inhale  to increase the  delivery  ability of O2  to a great  trained  muscle system.
 The traditional  " classical" coaches  are  for the moment far of  to open a discussion on  physiologically sound  and  accepted  new directions.


To our surprise we see  the  openness  for changes  coming form game sports  like Ice hockey, soccer, Basket ball and than the huge  field of   health and fitness sport  areas.

looking to tap is the female weight loss market

Yes this is the big  market. This  market  in the past  got  not very well served  despite all the gadget.
 We still use  220 - age ideas  and or  activity ( accelerometer )  to tell them  what is optimal instead of actually looking  how their  physiological systems use  and deliver O2  for the current  performance and or activity.
 This  market here is where you will see   an incredible interest  as  it is  the first time we  can use an individual  feedback  ,simple , non invasive  and clear to understand  for the client  what he or she has to adjust to   maintain a stable utilization  activity.

utilizing FTP% workouts

I do not see this as a contradiction but  why would I stay in the past  using a  interesting idea of a 1 hour all out  load to than use a calculator    and hope , that the 1 hour result is repeatable every day  otherwise  my calculation is off, when I can use a simple tool  and see daily, when  and how I have to adjust intensities..


 Physiological bio feedbacks  when using equipment  is now possible by combining  clever idas  and using MOXY as the real feedback on what is actually happen.
 Look at the  growing behind the scene   integration of this equipment.
 We  have  many   groups and teams   starting to work with ideas, but   most of them keep it  as a  " secret"   instead of sharing the great  benefits  and progress we  all could  make  and learn  from each other.


SOCCER SPIRO.jpg

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Woww got a  very fast great response.
 Wattage is not always the same  physiological performance.
  Yes we have many  nice examples, how  performance  changes  due to  certain influences.
  Here a nice summary from a presentation  we gave.
 It shows  the FTP changes  due to temperature  changes  and due to metabolic  (Glucose changes).
 When you follow  our ideas  than you can see, that the change in physiological reaction will change the  $  load  of the FTP. As  such  the same  FTP % is not the same  stimulus on your body.
 If we like to create the same stimulus or  at least   if  we like to know  how we  stimulated the  body, than we  have to look at the physiological changes  rather than the stable wattage load.

heat  and  glucose.jpg 

As  you can see in the temperature  reaction,   we will have a different  stimulus  and will try  to get  the O2  from different options  rather than just  from Hb  unloading.
 One of the options is  using  O 2 from  Mb. This will show up in a very nice  way in MOXY  SmO2 trend information by dropping the level of SmO2  but still   may be balanced in O2 intake  and output. The temperature  not only shifts the O2  diss curve of Hb  but as well   from Mb.

myoglobing diss curve horses.jpg

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
And here is  an independent answer to the above question  from Europe .
 Andri  who runs Swinco   is  the real deal and all in English.

Nice  to see how South Africa moves  ahead  with open mind  and new  ideas outside the BOX.

I will give you my best attempt at an answer for your questions.

1.)Is weight loss and targeting the fat burning zone during exercise an area you have looked into?

Weight loss is not something that I focus on, as much as athletic performance; however the two can have an important relationship depending on the person and the activity. Firstly, as you may know, weight loss effectiveness is much more tied into diet than exercise. Numerous review papers show that diet as an intervention for weight loss alone is only slightly less effective that diet and exercise, meaning diet makes up the majority of weight loss. Health is a different, issue, as exercise correlates very high with exercise. Secondly, resistance or high intensity training also shows better results for weight loss than endurance training; even if this sounds counter intuitive. The applied reasoning for this is that high intensity training burns more calories (as endurance is much more about efficiency), and secondly high intensity training results in greater muscle build up and therefore increased metabolism. It is correct that you burn more fat per se in endurance training, but in order to effectively lose fat during endurance training, especially for untrained individuals, we are looking at very large amount of hours. Something to discuss and think about when focusing on weight loss as a goal.

However, there is some good news apart from this. Yes, I believe that using Moxy you can determine fat burning zones, and much more effectively than using other measures. The effect increased oxygenation has on energy production and supply is nicely outlined in this paper; Hyperoxia decreases muscle glycogenolysis, lactate production, and lactate ,efflux during steady-state exercise. Stellingwerff et al.

In essence when increasing oxygenation you decrease the usage of so called oxygen independent energy pathways, and for this reason or vice versa you have an increase in oxygen dependent energy pathways (electron transport chain, beta oxidation, etc.) and thereby have increased FFA- FAT utilization for energy, meaning you burn more fat. Based on these findings it is logical and reasonable to assume that at the maximum performance that yields that maximum oxygenation level you should have the maximum fat burring ability. This can then be discerned from Moxy, by identifying the fat burning zone as the top of the STEI zone (yellow), or at the maximum intensity that allows maximum SmO2. Does this make sense?

2, )Also would there be any contradiction in the studio utilising FTP% workouts as the principle training methodology and then saying that the potentially differing results from the Moxy are a more accurate reflection of a customer's intensity zones? I don't see this as an issue for the majority of customers, but maybe for a few of the more serious customers.

In the end you have to do what is commercially viable for you. This is the issue I have FTP. Functional Threshold Power as it is called is based on lactate threshold. Now I do not want to get into a physiological debate about the existence, accuracy, or usage of lactate threshold, the point is FTP assumes that it is somehow working in accordance with a physiological measure of oxygen supply and utilization (which is at its basic what lactate threshold is supposed to be). So having defined what FTP is you know have to consider what you are doing by using FTP and then complementing FTP workouts with Moxy. You are taking a very questionable and at best indirect measure of oxygen supply and utilization and decide to, if needed, to complement this with an actual real measure of oxygen supply and utilization. Do you understand what I am trying to get at? If you believe that Moxy works, and believe that oxygen supply and utilization is an underlying factor in performance (as you do otherwise using FTP makes no sense either, or VO2), it makes very little logical sense to use FTP rather than Moxy data directly. And Moxy is easy to use, has very very little cost associated per use, and has not effect on the athlete.

 I hope this helps! If you have more questions please contact me, or Roger.

 

Andri

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #4 
Now  some nice emails :
 Here what is open for discussion.Lactate inhibits fat metabolism.

 So the idea of using strength or HIIT for loosing fat is discussed for the group of people looking at  endurance slow workouts to increase fat metabolism.

They seem to have a point.
 What I like to show you over the next few days is on the other side the suggestion Andri  throws out there on strength and high intensity, which  may or may not be " anaerobic alacticid  but it may be  super  aerobic  and  intracellular lacticid. ???
 So stay tuned  as we will go back to the "classical " discussion of interval  length  and reps  and   show how MOXY  actually opens a lot of interesting questions  but as well  many   critical  answers  to the traditional thinking  of interval and its  stimulation.


doi:10.1074/jbc.N806409200

Lactate Inhibits Lipolysis in Fat Cells through Activation of an Orphan G-protein-coupled Receptor, GPR81*

  1. Changlu Liu1,
  2. Jiejun Wu,
  3. Jessica Zhu,
  4. Chester Kuei,
  5. Jingxue Yu,
  6. Jonathan Shelton,
  7. Steven W. Sutton,
  8. Xiaorong Li,
  9. Su Jin Yun,
  10. Taraneh Mirzadegan,
  11. Curt Mazur2,
  12. Fredrik Kamme3 and
  13. Timothy W. Lovenberg

+ Author Affiliations

  1. Johnson & Johnson Pharmaceutical Research & Development, LLC, San Diego, California 92121
  1. 1 To whom correspondence should be addressed: Johnson & Johnson Pharmaceutical Research & Development, L.L.C., 3210 Merryfield Row, San Diego, CA 92121. Tel.: 858-784-3059; Fax: 858-450-2090; E-mail: cliu9@its.jnj.com.

Abstract

Lactic acid is a well known metabolic by-product of intense exercise, particularly under anaerobic conditions. Lactate is also a key source of energy and an important metabolic substrate, and it has also been hypothesized to be a signaling molecule directing metabolic activity. Here we show that GPR81, an orphan G-protein-coupled receptor highly expressed in fat, is in fact a sensor for lactate. Lactate activates GPR81 in its physiological concentration range of 1–20 mm and suppresses lipolysis in mouse, rat, and human adipocytes as well as in differentiated 3T3-L1 cells. Adipocytes from GPR81-deficient mice lack an antilipolytic response to lactate but are responsive to other antilipolytic agents. Lactate specifically induces internalization of GPR81 after receptor activation. Site-directed mutagenesis of GPR81 coupled with homology modeling demonstrates that classically conserved key residues in the transmembrane binding domains are responsible for interacting with lactate. Our results indicate that lactate suppresses lipolysis in adipose tissue through a direct activation of GPR81. GPR81 may thus be an attractive target for the treatment of dyslipidemia and other metabolic disorders.

GPR81 (1) is an orphan G-protein-coupled receptor that is highly homologous to GPR109a and GPR109b. GPR109a and GPR109b were recently identified as receptors for niacin (also known as nicotinic acid) (2, 3) and subsequently characterized as receptors for the endogenous ketone body β-hydroxybutyrate (4). Niacin has been used clinically for a half-century as an effective treatment for dyslipidemia (5); however, its utility is somewhat hampered by a target-related effect on dendritic Langerhans cells, which release prostaglandin D2 in response to GPR109a stimulation, resulting in a cutaneous flushing response (68). GPR81 is highly expressed in fat, similar to GPR109a, but is not expressed significantly in spleen; nor is it highly detected in any other tissue, and it has thus been hypothesized to be a potential target for the treatment of dyslipidemia that would be analogous to GPR109a/niacin but without the potential side effects (9).

In this report, we demonstrate the initial identification of the ligand activity for GPR81 from the rat tissue extracts, the purification of l-lactate from porcine brain as the source of the ligand activity, and the pharmacological characterization of l-lactate as a ligand for GPR81. In addition, we show that in its physiological concentration range, l-lactate effectively inhibits lipolysis in adipocytes from humans, mice, and rats. Adipocytes from GPR81-deficient mice lack responses to l-lactate, indicating that the antilipolytic effect of l-lactate is mediated by GPR81. Despite a long history of being considered as waste or a by-product of metabolism, l-lactate has maintained some attention as a potential signaling molecule (10). As early as the 1960s, researchers have demonstrated significant effects of lactate on adipocytes (11); however, the mechanism by which this occurs has remained unknown. Our finding in this report provides a molecular basis for the ability of lactate to modulate lipolysis in adipocytes and establishes a new target opportunity for the treatment of dyslipidemia.

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #5 
A very interesting point to consider in this  more and more popular  research directions  is the  ability of the physiological systems  to sent " messages" signals   over different feedback loops.

This  is one of the main reasons of the discussion  between peripheral  governor  and  the central governor  idea.
  The discussion is"
  If we do research in VITRO, can we than make conclusions on feedback and reactions, which would go over central feedback loops which are not  "connected" anymore.
 If    feedback's  go over  circulation  and or over other options  of messaging  and we  DISCONNECT" this  options, doe we than have the same reaction in the discontent  sample as we would have in a connected  sample.

 Here  an interesting case study.
 If  we  create  an occlusion over a tourniquet in the fore arm or leg  we have a nice local occlusion information  without  any central or systemic  reaction.
 If we  create an occlusion over  a muscular contraction like a venous occlusion trend, than we  do have a systemic  delayed  reaction in the way that the physiological systems  start to shift O2 to the needed area and we see a vasoconstriction ( drop in tHb )  and a drop in SmO2  ( no delivery of O2 ) in a non involved muscle area.
 An artificial  limb occlusion does not create this reaction.

 So the above  research  pushing us into the believe, that  lactate  inhibits  lipolysis  can be assessed as well from a different point of view.



Now here  the interesting point. If we use MOXY  and we create a  hypoglycemic situation, which we can do easy in diabetic  1  people  but as well in endurance  athletes  and  due to nutritional manipulation in any person.
 We  see suddenly  changes in  SmO2  trends  and we have to adjust  performance   ( reduce performance to keep SmO2  in balance.
 This indicates  a change in metabolic  delivery  and the need of  more O2  for a lower intensity.
 Normally we would shift  from    Lipid   to glucose   when increasing in a test the steps  as   glucose  will need somewhat less O2.  How about shifting   back  from glucose to lipids  to survive  with the disadvantage  of  actually  slowing down performance. ???
 Here  a  paper supporting our observation.
 

Role of Lactate in Lipid Metabolism, Just Always Inhibiting Lipolysis?

1.   Hai-jun Xu1

+ Author Affiliations

1.    Department of Chemistry and Life Science, West Anhui University

1.    1E-mail: xhjflying@yahoo.com.cn

I appreciate the mechanism underlying the role of lactate in lipid metabolism proposed by Liu et al. (1). They found that lactate suppresses lipolysis in adipose tissue through a direct activation of GPR81. However, the argument that lactate suppresses lipolysis might be worthy of further consideration. Several studies have shown that there exists a substrate cycle or futile cycle in skeletal muscle as well as in adipose tissue, which dissipates redundant energy as heat via the cycle of synthesis, hydrolysis, and oxidation of triglyceride (2, 3). Furthermore, Hagström-Toft et al. (4) found that hypoglycemia increases both lipid and lactate mobilization in skeletal muscle and adipose tissues. It is well known that hypoglycemia will promote lipid hydrolysis to release fatty acids for providing energy by oxidation. I also found that lactate concentration was positively correlated with glycerol concentration in skeletal muscle and adipose tissues (unpublished data). Therefore, it is possible that lactate produced by anaerobic glycolysis might relieve the inhibition of glucose aerobic oxidation on fatty acid oxidation or adjust intracellular redox state via lactate shuttle in skeletal muscle and adipose tissues and thus promote fatty acid oxidation.


Summary:
  Now you can see that the question of  " fat" zoning  and other metabolicc zoning based on the current ideas of indirect   testing has more than a few open questions.
 True  the ability to use a calculator makes it very nice  for business purposes  but does it actually tell us the   reality of  each individual client.
 How  about opening the mind  and  at least try to use  a direct feedback over  the abiltity to actually track  and see oxygenations trends  live ? True , it is hard  to changee traditions but we are well underway. If  you think, that it took the catholic  church 500 years to accept  Galileo's  point that the world is not the center of the universe.
 And it took the british admirality 150 years to accept that Vit  C  has to be substituded on ships  traveling over  longer distances , than we are doing pretty good   of looking at  25  + years to accept , that lactate  may  not be the reason of fatigue  and similar amouint of years that NIRS is a direct  information with  a much smaller delay on information , than  VO2    or lactate ????





Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #6 
Just got  a chatt going after my above  information. I like to answer  the chatt question on here.
  Yes  there  are great studies  proving our  " adventures  " theory.
  The body in an all out   load  will show different options  if   tested in VIVO on  shift  abilities of  energy substrate.
 We  will  see shifts in a few options. Glucose shift  , O2  shift  but as well  lactate shift as one option  to move already stored  gluocse  from the upper body  to the more demanding and  more important  leg  muscles  over a lactate shuttle.
 This explains  sudden  high lactate readings in the circulatory system during a long  race or a long workout  despiet  same or lower  intensity.
 As well this explains  shifts in the SmO2 trend.
 In sports  like  Ice hockey or  triathlon or cross country skiing ,this shifts  are very common , just  the problem was, than in the past we never  looked at them.
 ( reasoning is that most studies are done in a lab )  now  with MOXY we  can  follow this  live  where ever we like to  assess it.
 Before we show  some own studies  we like to back this  idea up  with some  studies accepted  and done by  real " classical"  accepted  research groups.
 
 

       Submitted 20 June 2002.

       accepted in final form 5 September 2002.

 

Next Section

Abstract

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72–76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 ± 17 μmol · kg−1 · min−1) but a low arterial lactate concentration (∼2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ∼2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ∼45% at rest and ∼95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged

 

Now here our  very small  feedback  form a live  case  situation.
 Blue is leg  main  involved muscle, red is  arm  less involved muscle.
 "  Warm up " or better oxygenation phase  followed by  an abrupt  high demand of  energy like an all out  ice hockey  load.
 SmO2 in leg muscle  drops immediately  and arms have a delayed  reaction. as soon we  shift O2  from arms  to legs  tHb  drop as well ) we  ' rebound a  short moment tin the legs  and " collapse in the arms The short  stability in the  legs allows  a slightly rebound in the arms  plus a settle in  a given intensity  with a  reaction of  closing again in the arms.
So  for  coaches using cricket workouts  this is  an interesting trend to be considered  when  creating a  circuit  in duration as well as in intensity set ups.  This will allow  coaches now to plan individual load  time as well as individual recovery times  as well as  recovery times  for  local recovery only  or recovery times  for systemic  recovery as well.

2 drift.jpg 

Etiennebest

Development Team Member
Registered:
Posts: 34
 #7 
From what I've been picking up, there are some limitations regarding NIRS when it comes to doing measurements through fat layers. For athletes (unless they are Sumo wrestlers or involved in competitive hot-dog eating) I suppose this is not a problem.

The question - how/where would one place the Moxy to get a sensible/usable reading?
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #8 
Sure  there are limitations  and yes  Fat  layer is one of them. If you get  your  MOXY look the  distamce  between the red  light  and the  furthers  opt ode  receiver  half the distance is the depth penetration  . So  you can make a  caliper  assessment with  the fat  and  you  see,whether the place  you choose is   a good one.
 In  most  endurance athletes  the leg  VL is  a  good  one.   front  and back. Abdominal is often a problem  so is  trunk if you look  for intercostal muscles . Arm       normally not  problem in average   people.  So in many cases it work  nearly anywhere   with the above  exceptions.
Ruud_G

Development Team Member
Registered:
Posts: 279
 #9 
Maybe this one can add to the weightloss reply: http://bmjopensem.bmj.com/content/1/1/e000047.full
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #10 
Just  some loud thinking  ot  Ruud's  great  link.
 1. RQ  = RER ?  so  what is the  RER  or RQ  difference  in this 2  groups  at the end  of the  all out  load ?
 Is there a  difference.
 If  one group    uses  30 %  more  Fat ?
2.
  Higher  VO2  means as well higher VE.
 What  can limit the ability  to move  more VE ?

3.  Carbs  burn   and  Fat  burn .
 What creates  more  " exhaust "  of  CO2  ?
4.  What happens  when  CO2  is increasing  and we  can not get rid  of  it ? How  would  tHb  and SmO2  react accordingly .
5.  How  or  what  is the fastest  way to try to balance  CO2  levels ?
6. What is the single    biggest difference between the top performance  physiological in Pro  cyclists  to amateur  cyclist. ( Remember the Rabobank  study  from Maastrich. ( NL)
Etiennebest

Development Team Member
Registered:
Posts: 34
 #11 
I know nothing about physiology, so these are just guesses based on what I have been reading/looking at the last couple of days, so excuse me if I get something totally wrong.

1. Not sure what the difference would be, but I expect the RT runners would have produced less CO2 "overall".
2. VE can be limited by lung capacity, development/fitness of intercostals and diaphragm (influences RF?)? Perfusion Zone changes during exercise? Others?
3. Glucose + Oxygen = Carbon dioxide +water +Energy...so I would guess more glucose and oxygen is burnt? But then why are the WT runners creating more CO2? Is their fire "bigger" or just using  more of a different "fuel"?
4. Higher CO2 = possible Hypercapnia->Hypoxemia? Disscurve to right? tHb will increase, and SmO2 recovery will slow down because O2 cannot bind?
5. Decrease work load, depends on limiter?
6. I can't find this study - would like to read it, but my guess would be the amount of training and sponsorship [tongue].

Ruud_G

Development Team Member
Registered:
Posts: 279
 #12 
From the Maastricht study: "
Despite its general use, VO2max has not been shown to be reliable in predicting endurance performance, as witnessed by the lack of difference between professional and amateur cyclists. Rather, other parameters seem to be highly beneficial in assessing and predicting cycling endurance performance. The most important parameters are power output (W), breathing pattern (minute ventilation, VE; breathing frequency; tidal volume, Vt), ventilatory equivalent (eqVO2), delta VO2 versus delta workload ratio (dVO2/dW), blood lactate levels, gross efficiency (GE), delta efficiency (DE), cycling economy (CE), and the intensity where the highest absolute fat oxidation occurs (Fatmax). Furthermore, two relatively new parameters have been presented recently, which have been rarely studied. These are the minimal power output that elicits VO2max (wVO2max) and the response in oxygen consumption in reaction to changes in exercise intensity (dVO2)

Research has shown that VO2, %VO2max and power output at these VT’s also seem to be good predictors of cycling performance.

Furthermore, previous research has shown that, in general, professional cyclists perform better at all above mentioned parameters compared to amateur cyclists, with an exception for VO2max. The major explanation for this finding is that the history of professional cyclists includes a higher cycling mileage. This higher mileage results in a higher percentage type 1 muscle fibres, and consequently, a higher aerobic capacity. "
Ruud_G

Development Team Member
Registered:
Posts: 279
 #13 
And you can find the "Maastricht" study from point 6 here:

http://www.in2motion.eu/attachments/article/48/Physiological%20parameters%20in%20professional%20and%20elite%20road%20cyclists,%20Rabobank%20Cycling%20Team.pdf
Previous Topic | Next Topic
Print
Reply

Quick Navigation:

Easily create a Forum Website with Website Toolbox.

HTML hit counter - Quick-counter.net