Sign up Latest Topics
 
 
 


Reply
  Author   Comment   Page 5 of 5     «   Prev   2   3   4   5
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #61 
Wow  Daniele  ,
 thanks  I hope you got may  mail  and it is  there what you just  explain short and  simple  with some additional option.  The studies you referred  on blood flow are really great and would confirm this . Check  may  internal  ideas  and  see, whether  it makes  sense  and where it is confusing still. We  can see two other options  why we may see the  shift of  blood in leg muscles in low intensities  as  blood goes  where it is needed . So if in low intensities  the CO is not  fully  activated  we  have a  big  area, which can be flooded  but a low pressure  to  do this. So BP   protection will create a  vasoconstriction to maintain blood pressure level. We  did  some case studies  , where we  changed  bike technique in low intensities  and  had  NIRS  and SEMG  on the same muscle  and could see drop in tHB  when  SEMG  as well dropped. In the first moment it looked  strange as with less muscle contraction you would  see an increase in tHb as  compression eases  off and normally  this  happens. But in low  not challenging  intensities  when CO  was too low the  VSM  seem to  still stay active  to protect  BP  despite a reduction in SEMG.  Here  an example   from the cardiac  view



paiv 2.jpg


Look at  bottom  right  607. This is the systemic  vascular resistance  during a  step test  followed  by  a lactate balance point    review.  You can see  old old  as we used  heavily  lactate  there as well. This case  shows  that immediately  at the start the  vascular resistance  is reduced  and drops   as a sign of metabolic vasodilatation and shear  force  dilatation  and CO  overrule of  muscle compression. Now  at the end of the step test we can imagine a  high CO  as we can see. In this case  little drop in SV  as w reduce  load   and CO  drops  mainly  due to  drop in HR. We  have  wide open blood  vessels  and  as  such  we have the risk  as he is fatigued  to  drop BP. So you can see that  now  despite  an  again increase in load  we  do not  have a  drop in SVR  but  initially an increase  to maintain Blood pressure  doe  to limited  ability  of his CO  to   keep  every body happy.

  Now look below   another case.

eva G.jpg


Initial overshoot  and   to protect BP  she   started  out  with an increase in SVR and in the  second section  has a very nice  BP  correction reaction. This client  suffers  from " Black outs' during  workouts  when changing  fast positions as well when  changing   to different body parts like   upper body  load  followed by lower body  load  for example in a circuit.
 In this case  we  did  some simple   correction during her  circuit  workout  over some  respiratory   corrections  and it worked  immediately. 
For  completion.  left  light blue  is EF %  information.
 Dark blue middle is LVET  ( left ventricular  contraction time) Now this is interesting for later  as  LVET  x  HR  will give some interesting information on the person  and his cardiac  ability. We name it CCT  or cardiac contraction time. As  crazy as it sounds, but this has some effect on the way  thee tHB  shape    can be.  to  end up here  Danieles  overlap  from his  3 min 7  steps  test  starting  with 150  plus  30 watts  up  and the  4  step  step test  before his  workout  where he  started  120   so I got rid of  120  and overlapped  same loads  form both step test 150 180 210.

First   overlap of SmO2  by the same  wattage levels.
vl 1  1560 strat  andd VL2  120  strat  2mo2  but  bith  150 load compa 3 steps.jpg 

Short question. Why in the dark  SmO2   do we have this  clear  drop in SmO2  reaction but  we do not have it in the lighter green ?

Now  below overlap same loads tHB trends.

vl 1  1560 strat  andd VL2  120  strat  thb2  but  bith  150 load compa 3 steps thb.jpg 

Now  for  fun I  overlapped them  really here the result.

overlapp really PP thb  absolute  ideantical.jpg

Isn't  that amazing  how  nature ( physiology  works ) but as well a  thumb  up  to Roger the genius  behind  MOXY  technology.

 To complete the  idea  below   same overlap idea  with SmO2  with the open questions to the reader of the  difference  at the beginning of SmO2.

overlapp really PP thb  absolute  ideantical  smo2.jpg

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #62 
Daniele  writes :
 and he may be bang on. Remember Kroghs  and new ideas  and where  currently  a lot of  exercise [physiology guys  stay. ? 


Below just some "crazy" personal speculations:
At rest vessels and capillaries are quite full of blood and RBC. The flow cannot be high, low HR and low BP, but tHB is high


Muscle microcirculatory O(2) exchange in health and disease.

Poole DC, Musch TI.

Source

Departments of Anatomy, Physiology and Kinesiology, Kansas State University, Manhattan, Kansas 66506, USA. poole@vet.ksu.edu

Abstract

Much of our understanding of blood-muscle O(2) and substrate exchange is predicated on the presumption that, in resting muscle, a substantial proportion of the capillary bed does not sustain red blood cell (RBC) or plasma flux. According to this notion, with contractions, more capillaries are "recruited" (i.e., begin flowing) and increased metabolic demands are supported by blood-myocyte O(2) and substrate flux in these newly recruited capillaries. This scenario is attractive because additional exchange vessels are added, and radial intercapillary diffusion distances reduced, as demands increase - but is it correct?

 The compelling weight of evidence gathered over the last 3 decades using intravital microscopy, phosphorescence quenching and near infrared spectroscopy (NIRS) techniques challenges conventional "wisdom" and indicates that the majority of capillaries support RBC flux at rest. Thus, at the onset of contractions blood-myocyte O(2) and substrate flux must increase in vessels that were already flowing at rest. This concept forces a radical revision of the control of blood-myocyte O(2) and substrate flux. This revision is essential if we are to understand the control of microcirculatory O(2) and substrate flux in health and resolve the mechanistic bases by which these processes are compromised in diseases such as chronic heart failure.

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #63 
Here some additional food  for thoughts.
Discussion point :

At onset  of  activity  we will  increase blood flow immediately  to try  to cover the demand of  energy needs.
  Based on the discussion one trigger of  increase in blood flow  is the  metabolic  reaction of energy demand as a vasodilatation. There are  other vasodilatation option like adrenaline  for example.
 Now  two  simple  scenario.
a)   health person  with a  poor  cycling  coordination and a healthy but small vascular  bed .
b) experienced  cyclist  with a  great's   pedal technique  so  high intramuscular coordination skills  and a big  so  cycling specific vascular bed.

As both start out  both will increase the vascular  volume  as they vasodilatate.
 
a)  will just use  down push   so   some quadriceps  activity nut minimal hip extension activity and up pull.
b)on the other side will activate  a huge number of  cycling  involved muscle activity.

a)  will  increase as b  cardiac  output  with some delay  but  will stay most likely  higher as it is more  stress   and unknown  for him. The  vascular bed  may  double  due to the vasodilatation effect.

 b) will react the same  with CO  but his  vascular bed  due to the stimulation  and metabolic   vasodilatation will increase  4 fold  as all the muscles  are involved,

So the blood flow  measured in the femoral  blood vessels will increase  in both cases as  more  energy is needed  and more   load is applied.

The difference is, that the CO in a)  is  far sufficient  to  maintain the  BP  in the  new  bigger vascular  bed 

 in b )  as the  CO is not yet sufficient  high  the  vascular bed is  too   big  to maintain BP  and he will have to   get  help  from VSM so vasoconstriction to maintain the needed  BP.

 Now  at rest we  have a  resting flow  and thB  may be relative high.
 As we now open up  and " distribute " the  more blood into an even bigger vascular bed  we may in fact  see a  drop in blood volume   in a low intensity at the area  whether MOXY  assesses. In other areas  we may  see no   effect on this  distribution  as less high  vascularisation  may the there. So we have a higher  blood flow  towards  all  leg muscles  but  we may see in  some muscles a  drop in the blood volume  due to the above reason.
 The main reason  for a  drop in blood flow   and a  good vasoconstriction is again the fight between metabolic demand  and  BP   control.

 This sounds  crazy  so   we had  to search for some support as usual before   start a discussion on a public  space..

So  when they where looking  at  blood flwo in  big  vessels like in  the  great studies  we showed  by Holmberg  and Calving  they  could see a  clear increase in blood flow with increase in  load  and therefore demand.
 In lower intensity , where we  still may have as  explained  a big   amount  of muscles involved, the  delivered  blood volume  may be too small to maintain BP  and   volume , so  vasoconstriction  can occur   to maintain BP  and  limited blood flow to  some of the involved muscles The once who can afford this  due to big vascular bed  and therefor  shorter  exchange distance  for O2 .

 Here  form the same group  who  shows  a  blood flow increase the  interesting  section that in the different muscles  we may  still see a blood flow reduction or better limitation

.

Acta Physiol Scand. 1998 Mar;162(3):421-36.

Skeletal muscle blood flow in humans and its regulation during exercise.

Saltin B1, Rådegran G, Koskolou MD, Roach RC.

Author information

  • 1The Copenhagen Muscle Research Centre, Rigshospitalet, Tagensvei, Denmark.

Abstract

Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is approximately 0.3 L min(-1) at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6-10 L min[-1] (Q= 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2-3 L kg(-1) min(-1), i.e. approximately 100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T 1/2 of 2-10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within approximately 10-150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L-NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group IIl-IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown.

However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.

Now in highly   dense   areas  for blood vessels like in  trained  cyclists  the VL  has  a much higher vascular bed  , than  for example  calf  or hamstrings. So we may see the U SHAPE  reaction in VL  due to this but not in a less vascularisation  hamstrings muscle. And it has to be in a low enough activity. As  soon CO increase the  pressure is  increasing , so less need  for  VSM  and  once the pressure as  reached 120 mmHg +- , the  VSM will give up  and vasodilatation will occure.  except,  if CO  can not maintain it, than   BP  has again to be protected.

Here some  I additional ideas of  O2   delivery  and vascularisation situation between good and not  as good  trained. Easy  to imagine   when more blood vessels  are  around  and more  cells.

diffusion distance.jpg 


juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #64 
Here a  ice  small insight in a great  study  group on the discussion we have  to add some more thoughts.
 It   shows  the great idea  and thoughts  form Daniele  as well. The   paper  was  sent to my  buy Ruud.

Reduced Heterogeneity of Muscle

Deoxygenation during Heavy Bicycle

Exercise

RYOTARO KIME1,2, JOOHEE IM1, DANIEL MOSER3, YUANQING LIN1, SHOKO NIOKA1,

TOSHIHITO KATSUMURA2, and BRITTON CHANCE1

1Department of Biochemistry and Biophysics, University of Pennsylvania, Philadelphia, PA; 2Department of Preventive

Medicine & Public Health, Tokyo Medical University, Tokyo, JAPAN; and 3Graduate Hospital Human Performance &

Sports Medicine Center, Wayne, PA

ABSTRACT

KIME, R., J. IM, D. MOSER, Y. LIN, S. NIOKA, T. KATSUMURA, and B. CHANCE. Reduced Heterogeneity of Muscle

Deoxygenation during Heavy Bicycle Exercise. Med. Sci. Sports Exerc., Vol. 37, No. 3, pp. 412–417, 2005. Purpose: This study

evaluated heterogeneity of muscle O2 dynamics in a single muscle during bicycle exercise using an eight-channel near-infrared

continuous wave spectroscopy (NIRcws) mapping system. Methods: Nine healthy subjects performed bicycle exercise at fixed

workloads of 20, 40, 60, 80, and 100% maximal workload for 5 min at each level. Muscle oxygenation in the vastus lateralis (VL) during

and after each exercise was monitored using the NIRcws mapping system. Pulmonary O2 uptake and heart rate were monitored

continuously during the experiment. Blood samples were taken to measure blood lactate concentration at 30 s after each exercise stage.

Results: Half time reoxygenation, the time taken to reach a value of half-maximal recovery, was significantly delayed in distal sites

compared with proximal sites of VL. Conversely, muscle deoxygenation for all measurement sites increased incrementally with higher

exercise workloads, and no significant difference of deoxygenation level showed within each channel. However, relative dispersion of

muscle deoxygenation during exercise significantly decreased when the workload increased. Moreover, relative dispersion of muscle

deoxygenation between the subjects also decreased with an increase in the workload. Conclusion: Muscle deoxygenation in a single

muscle was more heterogeneous at lower exercise workloads, and variations of the muscle deoxygenation heterogeneity between

subjects were greater at lower exercise workloads. Key Words: MUSCLE O2 DYNAMICS, NEAR INFRARED SPECTROSCOPY,

PULMONARY O2 UPTAKE, LACTATE

Muscle perfusion is a key parameter of aerobic metabolism under various conditions and has been a popular research subject for many years. It is clear that muscle oxygen consumption (muscle V˙ O2) increases linearly in relation to muscle perfusion (14,27). Moreover, it has been also shown that muscle perfusion and muscle V˙ O2 are affected by differences in muscle fiber composition, microvascular structure, and motor unit recruitment pattern (21,24). Recently, heterogeneity of muscle perfusion and muscle V˙ O2 during exercise in humans has been evaluated using positron emission tomography (PET)

(11,15). However, the device is expensive and only produces low time resolution. In addition, the PET device cannot obtain information during dynamic exercise because of movement artifacts. Therefore, it is essentially impossible to monitor heterogeneity of muscle perfusion and muscle V˙ O2 during dynamic whole body exercise such as bicycle exercise using PET.

Near infrared continuous wave spectroscopy (NIRcws) was first applied to the study of exercising skeletal muscle in humans in 1992 (1). Since then, NIRcws technology has continually been updated and widely applied to the evaluation of muscle tissue oxygenation during bicycle exercise (2,4,13,25).

 Muscle oxygenation observed using NIRcws reflects the balance between muscle V˙ O2 and O2 supply in localized muscle as demonstrated by its gradual decrease during incremental exercise, and by its dramatic increase after whole body exercise (1,13). More recently, a NIRcws mapping system has been developed to monitor the functional imaging of muscle tissue oxygenation during exercise (17,22,26). However, most of the NIRcws mapping studies were conducted during static exercise due to reduced signal to noise ratio during dynamic exercise. We developed a NIRcws mapping system that enables monitoring of muscle deoxygenation during bicycle exercise, and detailed information of the mapping system has already been published (17). The purpose of this study was to evaluate heterogeneity of muscle deoxygenation and reoxygenation in a single muscle during and after bicycle exercise at specific intensities using an eight-channel NIRcws system.

Now  you  can see what Daniele  did in a  small portion  when we looked  not on the same muscle but on the same leg in different muscle groups.
 We did this  with 5  MOXYs on  one screen . 2  on quadriceps  VL  and VM
  two on  hip extensor  Glut  and Hamstrings biceps  section  and one on calf. Than we played live to see, how we  where able  with change in  bike position  to change SmO2  and tHb levels  and what  causes  what trend. To be able to do this you  have to bike in a  lower intensity   and the intensity is   in what we  stupidly call ARI.
 We  could better call the  two  sections we see. MOXY  one or MOXY  2  for PR reason but smarter  would be  SmO2  1  and SmO2  .2.
 SmO2  1 is where the SmO2   is steady increasing till it reaches a current plateau. SmO2 2 is where SmO2  starts  dropping or in other words.  First  SmO2 1  is  where supply  is higher than utilisation. SmO2  2  is where utilisation is higher than  supply.



juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #65 
I liketo show  a fun information  from Daniele's step test  .

You can see the now  very familiar  SmO2  trace  in green  and his HR  in this data collection.

hr  smo2  3 min  first  step test 7  steps.jpg

You can see   a lot out of this graph. The most impressive one is the 1080 time line. You can see that the Cardiac system now really starts  to get pushed  and I the   balancing out  as  every body is happy  with the  delivery of O2  is over  CO  has to go up  all the time ( as usual  exception  as theoretically SV  could drop  . ) you as well can  see that  at the start the HR  even was able to drop  after an initial overshoot  and  this  can be   out of different reason. One often seen is that  SV picks  up  so to  keep the need CO  HR  can drop as SV  with a  small lag time can pick up.  SV  picks  up  due to  return  of blood so  often higher EDV  so  higher preload  which increase EF %  and SV  goes up. This in turn  creates  a higher  BP  and a such  the VSM  can back of    in case BP  reaches  120 +-  levels
You can see the  HR  reactions  level out  till point in step 4. Now  till there the  need for a  very strong help  by the cardiac system is  not  there  so  the lower  cardiac  work  will take longer till he  reaches a  decent  BP level so VSM  can let go  and he can afford  to move into vasodilatation. ( if  the CO  can support it. If this is the case, than we  have the first step a  " lazy "  bad  word   cardiac system , which  does not support BP  well so VSM  has to  stick  in there  for a while  and  tHb will drop  locally  ( not systemically in VL )   once  the cardiac  system has to  jump in to compensate  and  deliver  step  4  plus than we  will have  as well in VL a sufficient BP  and  tHb  can increase.
thb polyn  curve  and SmO2 first 3 min  7  steps.jpg 
Another  info you can see  is  that in step  5  the cardiac system is  successful at least  for the three minutes we see to maintain  SmO2  levels  after that it is  despite  an increase in HR  and most likely CO not enough delivery capacity  and it is a  time question now how long he  can turn  O2  to  energy  with  an insufficient  delivery ability. Si o when we look metabolically by 240 / 270 he reaches a critical intensity , where the battle   between  delivery and utilization starts   out. The cardiac system  pushes  hard  but  can not   keep  up  so we  may see  an accumulation of CO2  and as  such a  compensatory   try  from the respiratory system. Now  classic a school.
 a) the increase in glucose  higher  energy usage  will increase CO2  but as well may start to create more H +/ This means we have to try to balance H + in the  cell and can do this by  using buffer abilities  and lactate is one of them . Once the H + is in the blood we can sue  respiration.
 So here the connection  between lactate increase ( but  we  could as well take blood sugar as it will increase as well [wink]  and the increase in VT    so  VThreshold.
 Now  that's where LT  and VT  seems to be equal  . BUT as usual . If respiration  can compensate than wee have  a VT  but no  LT  as  we balance  H +  and e we can increase lactate  in the blood as it has no effect on  stopping the performance in fact we  can go longer because of it  but only if  respiration  can  balance the H+  to avoid this   level to go out of balance. (Is  discussed as well )  At the end it is all about  O2  balance  and in the past we needed indirect feed backs  like   respiration info  or   blood lactate info's  to  find   this  out of balance  intensity.  Now  as we  can see that live  we  hesitate  to take IT AND MOVE BACK TO THE INDIRECT  DELAYED INFO  OF LACTATE  AND vo2 .

 Isn''t' that  weird ??

 Nobody seems to ask critical  questions  , once something is  established but than once we found  what we  tried to find  over all this years  indirectly   we  to no  appreciate this   direct information but rather abuse the technology  and push it back into a blood less lactate analyzer.
 Is that   strange or is it a  PR  stunt  as many  simply love the threshold idea  and mystical blood values. 
 It is  even more strange, when we have   incredible smart  exercise physiologist out there who told  the limitation of  anaerobic threshold   soon  20 years ago.


ANAEROBIC THRESHOLD - A RELATIVELY USELESS CONCEPT FOR COACHING

Billat, L. V. (1996). Use of blood lactate measurements for prediction of exercise performance and for control of training: Recommendations for long-distance running. Sports Medicine, 22, 157-175.

 

This article contains a very concise summary of the concept of anaerobic threshold and how it is depicted in the literature. The implications of each individual statement are particularly important given the pre-occupation of many coaches with this concept. The major points of the article are discussed below. Further features are introduced in the "Implications" section.

The concept of anaerobic threshold itself is not universally consistent. Long dynamic exercise that is predominantly aerobic ranges between two extremes of physiological dynamics resulting in very different blood lactate levels.

  • At the lowest level, an exercise can be sustained for a very long time. After 2-5 min a state of overall oxidative energy supply is established where lactate production is balanced by lactate elimination at a low level. Fat (lipid) metabolism is the primary source of fuel. Exercise limits are mainly associated with eventual increases in internal temperature. Potential dehydration can be prevented by supplementation of water and substrate (carbohydrate and electrolytes) during performance. (p. 158)
  • At the highest extreme, the workload requires an additional formation and accumulation of lactate  to maintain power output. Exhaustion results through the disturbance of the internal biochemical environment of the working muscles and whole body caused by a high or maximal acidosis. Generally, accumulation of  H + limits performance to periods from 30 sec to 15 min. For example, the average time to exhaustion at the minimal velocity which elicits VO2max is 6:30 and is not correlated with the blood lactate level developed during the task. (p. 159)

Between these two extremes are transition stages, several of which are labelled similarly as "anaerobic threshold" or "lactate threshold." Thus, the same label is used for different concepts and their assessment protocols that lead to different values and training implications. Billat displays the various implications of this confusing situation. According to a variety of "authorities," changes in blood lactate accumulation are termed and defined differently as well as being associated with different levels and characteristics of accumulated lactate. H+ They are also differentiated by the protocols used to measure them. Some examples are listed below.

  • "Onset of plasma lactate accumulation" is established as being exercise induced levels which are 1 mM/l above baseline lactate values. [Farrel, P. E., Wilmore, J. H., Coyle, E. F., et al. (1979). Plasma lactate accumulation and distance running performance. Medicine and Science in Sports and Exercise, 11, 338-344.]
  • "Maximal steady-state" is displayed when oxygen, heart rate, and/or treadmill velocity produce a lactate level which is 2.2 mM/l. [Londeree, B. R., & Ames, A. (1975). Maximal steady state versus state of conditioning. European Journal of Applied Physiology, 34, 269-278.]
  • "Onset of blood lactate accumulation" (OBLA) occurs when continuous incremental exercise produces a lactate level of 4 mM/l. [Sjodin, B., & Jacobs, I. (1981). Onset of blood lactate accumulation and marathon running performance. International Journal of Sports Medicine, 2, 23-26.]
  • "Individual anaerobic threshold" is the state where the increase of blood lactate is maximal and equal to the rate of diffusion of lactate from the exercising muscle. Values range from 2-7 mM/l. [Stegemann. H., & Kindermann, W. (1982). Comparison of prolonged exercise tests at the individual anaerobic threshold and the fixed anaerobic threshold of 4 mM/l. International Journal of Sports Medicine, 3, 105-110.]
  • "Lactate threshold" is the starting point of an accelerated lactate accumulation and is usually around 4 mM/l and is expressed as % VO2max. [Aunola, S., & Rusko, H. (1984). Reproducibility of aerobic and anaerobic thresholds in 20-25 year old men. European Journal of Applied Physiology, 69, 196-202.
  • "Maximal steady-state of blood lactate level" is the exercise intensity that produces the maximal steady-state of blood lactate level and ranges from 2.2-6.8 mM/l. [Billat, V., Dalmay, F., Antonini, M. T., et al. (1994). A method for determining the maximal steady state of blood lactate concentration from two levels of submaximal exercise. European Journal of Applied Physiology, 69, 196-202.

Many scientists and coaches use the label "anaerobic threshold" interchangeably with these concepts confusing what is supposed to be a scientific coaching principle. Just because the same label is used does not mean analogous concepts are being discussed. Since there would be different coaching and performance implications from each of the above concepts, the blanket use of this term will foster many erroneous coaching prescriptions and procedures.

Lactate accumulation indicates a shift from solely oxidative to an additional glycolytic energy supply. Lactic acid production is due to the activation of glycolysis which is more rapid than activation of oxidative phosphorylation. This is indicated by a steep non-linear increase of blood lactate in relation to power output and time. That accumulation can be attributed to disparities in the rate of lactate production and removal, even for work intensities under those which elicit VO2max. Lactate production is not related to oxygen deficit but rather to the increase of the glycolysis flux. (p. 159)

Lactate is produced constantly, not just during hard exercise. It may be the most dynamic metabolite produced during exercise since its appearance exceeds that of any other metabolite studied. The constancy of the blood lactate level means that entry into and removal of lactate from the blood are in balance.

The turnover of lactic acid during exercise is several times greater for a given blood lactate level than at rest. For a given blood lactate level, lactate removal is several times greater in trained than in untrained persons.

Several factors are responsible for the lactate inflection point during graded exercise.

  • Contraction stimulates glycogenolysis and lactate production.
  • Hormone recruitment affects both glycogenolysis and glycolysis.
  • Recruitment of glycolytic fast-twitch fibers increases lactate production.
  • Blood-flow redistribution from lactate-removing gluconeogenic tissues to lactate-producing glycolytic tissues causes lactate levels to rise as exercise requires continually increasing power output.

Lactate values differ according to several variables: the activity being performed, the site from where the blood sample is taken, the environment itself (both physical and its effect on the athlete's psychology), and the state of glycogen stores prior to testing. Unless these variables and others, such as day-to-day cycles in general physiology, as well as variations in test administration and athlete performance of each test segment, can be controlled and made consistent between test administrations it is likely that score differences will be unreliable. The practice of attributing any observed lactate-test differences, no matter how small, to training effects or as revealing the trained state is extremely dubious at best.

Practical Implications

When scientists cannot agree upon a concept's definition, let alone the appropriate label to use, as well as the appropriate method/protocol of assessment, then the practical use of the "general implications" of the concept is foundationally prohibited. Until this situation is clarified and discrepancies removed, field testing for "lactate-threshold" should be avoided. There are more profitable and useful activities for athletes and coaches to be engaged in.

Of significance to coaching is the concept itself. The common misunderstanding that the anaerobic threshold is the state where aerobic activity is dominant and maximal and anaerobic activity constant but "insignificant" is very prevalent. There are few competitive activities or events where such a circumstance is desirable.

Most activities do not require all body parts to be involved in an activity at the same intensity level. A cyclist will work the legs extremely hard but, by comparison, the rest of the body will function comfortably in an aerobic zone of metabolic activity. A swimmer pounding out stroke after stroke in a 1500 m race works the arms at an intensity that employs a high level of anaerobic energy supply but the rest of the body is "relaxed" and functioning at quite a basic aerobic level. Even in running, in a marathon the legs work hard while the arms and upper body "save energy." In these activities, lactate is produced by the primary working muscles and resynthesized by the muscles engaged in mild supportive activity. Those muscles cleanse or "sponge" out lactate so that the blood supply to the hard working muscles is quite low in acidity when returned to those muscles. Thus, any lactate measure is a measure of the "general functioning" of the body, not the actual work performed by the primary sporting muscles. Differences in technique most probably would account for a significant portion of many inter-individual differences in lactate assessments than work levels or movement economy.

In many "aerobic" sports the actual prime mover muscle groups work at an anaerobic level rather than aerobically as is inferred from anaerobic threshold testing. The common perception of anaerobic threshold does not give any information or understanding of what actually is happening in important aspects of a performance. Even the slightest improvement in movement economy (technique) in the "anaerobic prime movers" could make a significant difference to performance.

Of all the concepts of anaerobic-type thresholds or measures that are proposed perhaps the maximum lactate steady-state (MLSS) is the one that is most applicable to the field of sports. In cycling events of one hour, athletes have been measured to "tolerate" and demonstrate sustained lactate levels in the region of 7 mM/l. In most events where "effort" is required as part of the competitive strategy, lactate levels will be sustained in a competitive performance in excess of the anaerobic threshold (if one can be demonstrated). There is a much greater proportion of many competitive performances that is more anaerobic than is generally acknowledged. If appropriate and sane anaerobic training is ignored then an athlete will not be trained optimally and a theoretically "best" performance will not be possible.

How can one test for maximum lactate steady state? Simply ask trained, experienced athletes to perform a task equal to the duration of their competitive event and they are likely to produce a performance that is close to demonstrating the MLSS. To be sure of this, if performance intensities, usually velocities, are performed at an increment above and below the first trial, verification should be forthcoming. Repeating many trials usually is not necessary. Is this too simple of a concept for complicated science? In practical circumstances it works. But since this could be a procedure that is implemented by coaches would it be endorsed by scientists which would seemingly remove a coach's dependence on them?

But a central perplexing question still remains: what does one get from measures of lactate and performance? What do they tell more than is already known? If lactate values are specific to the task/testing-protocol/event there can be no inference beyond the observations themselves.

When two athletes with the same physiological capacities perform the same activity, one using arms only the other using arms and legs, the performance results are often different, particularly when energy supply is an important aspect of the task demands. In this case, it is not the "anaerobic threshold" that differentiates the two but the movement economies, one using more muscle mass to produce a performance outcome. An attempt to shift the anaerobic threshold by further training of a particular type in an hypothesized metabolic zone with appropriate heart rates is clearly the wrong approach to solving the less-efficient athlete's problem. A skill element change to reduce unnecessary movements would result in greater movement economy and would shift the velocity that supports the MLSS to the right.

It is dubious to attribute shifts in anaerobic threshold values to physical training. Given that so many variables render field tests of this phenomenon practically unreliable, what is attributed to score differences obtained between two tests is more of a guess than an informed judgment.

Sport scientists can produce graphs of swimmers, runners, rowers, etc. showing an "inflection point" that occurs in a region of performance velocity. Equally, other athletes tested with the same protocol do not show any inflection or exhibit measures that cannot be interpreted in terms of a traditional anaerobic threshold. A few selected demonstrations do not prove the existence of a phenomenon that can be applied universally. The trend in field testing is rather one of more people not demonstrating a clear "anaerobic threshold" than doing so. Complicate that further with deciding upon which threshold protocol fits the sport from the existing array of definitions and confusion results rather than a clearly usable training tool.

Anaerobic threshold results must be reliable, that is, capable of replication. When a particular protocol is used for a series of periodic assessments, as is commonly followed in "sport science testing" programs, if that protocol is altered, the previous results cannot be used for comparison purposes. A protocol change will produce unrelated results, often different response phenomena, and above all different implications and interpretations. The definitions and discrepancies listed above all originate from different testing protocols. Thus, results from one protocol to the next, no matter how small the change is explained to be, should not be compared. Essentially, a new data base is developed.

An unavoidable dilemma. Sport scientists are ethically bound to represent the worth of lactate testing and the inferences that are commonly proposed. This is what is known.

  1. Lactate concepts and measures are limited/specific to each testing protocol.
  1. Results from one protocol cannot be used to generalize or infer values to other testing protocols.
  2. If one cannot infer from one lactate testing protocol to another then it is illogical to generalize lactate testing results to a competitive performance.
  3. It is a greater stretch of the imagination to leap conceptually from an inferentially-limited measure under controlled conditions to the dynamic circumstances of a competitive or practice setting.
  4. At most, lactate and lactate threshold measurements reveal changes but have limited to possibly non-existent inferential capacities about future performances (even training performances let alone competitive performances).
  5. Lactate and lactate threshold measurements can reveal that they have changed as a result of training, but, if those changes are unrelated to competitive performances what is their value?
  6. There are no national or international competitive events that reward medals for lactate threshold changes, levels, or testing protocols.

A story. During the spring of 1996, this writer attended the ARCO Training Center in Chula Vista, California. One day a USOC testing group had completed lactate threshold and aerobic parameter testing sessions on the US men's heavyweight rowing eight that was to compete later that year at the Atlanta Olympic Games.

The eight had just completed a European tour and performed worse than at any time in the previous three years. Based on comparative racing performances, it was a boat in trouble.

The head USOC scientist related that the members of the eight were still improving in fitness as the measures that were taken were better than previous test results.

Despite improved "fitness measures" the eight recorded a performance that was worse than any in the previous four Olympic Games, and compared to the boats that it had raced during the recent European tour, it had also degraded in racing capability. The fitness measures indicated that training was progressing satisfactorily. Unfortunately, racing performances were declining. Training improvements in physiological indices were negatively correlated with racing achievements. In 1994, the eight were world champions, in 1995 world bronze medalists, and in 1996, when they had the best testing results, were fifth out of six at the Olympic Games.

Just what is the value of lactate and lactate threshold/MLSS testing for making coaching decisions that relate to competitive performances?

 





juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #66 
This is a great discussion  on here. What many  readers may not know is, that  we  run many different discussion off line  with many different groups. Sometimes  this very helpful for many  but for sure  for us.
 I like to give one summary  on U  shape  from one of this outside discussions. It is a  great example  on hwo we  should look at  many reactions  and how  we often than ( including me ( get lost ion  to  small details  and forget the overall idea of exercise physiology..
 Here   for all an inside view in some of  our daily discussions.
 This is a  input  by Andri Feldmann . He runs   the IK IRS  groups in Europe  and in specific  a  training consulting  company   SWINCO ( Swiss innovative  company ) in Zuerich.

 U  Shape from a  physiological  survival point of view

This is some serious stuff for sure. I am going to give this a go and hope that I do not get in over my head. There is a lot of material here so I will try to address Daniele question/interpretation of the U shape tHb response. I also hope that I do not repeat something that someone has already said (this is usually Juerg), and therefor add something productive to the conversation. 

 

I always tell people that tHb is more complicated to understand than SmO2 and therefore to take things one step at a time. This is because otherwise I would have to explain tHb and I am not sure I really understand what is going on. So the first point I would like to say about this is the label or name for tHb, and I would simply stay with tHb or total hemoglobin, as this is the closest representation of what the measure is. We can explain that this is an indirect measure of blood flow or blood volume, etc. but I do not think giving it a different label helps because we are in my opinion not adding any more understanding or even simplicity by changing the name, but what we are doing is giving it a potentially inaccurate label. 

 

Now to the U shape. I follow an evolutionary derived understanding of exercise physiology and therefore try to understand physiological reactions derived from a logical approach of survival and reproduction. This means that trends we see in exercise have to do with environmental needs and efficiency. The body will do everything as efficiently as possible unless the situation demands some kind of maximal effort for survival purposes. The analogy is a car drives most efficiently considering fuel consumption at about 80 km/h, and therefore as long as I can, in order to save gas I will maintain this speed (or 0 speed = rest). But if I need to because the police are coming ( [wink] this if or Roger in the US) I can survive by being very inefficient and driving at 200 km/h. The inefficiency was necessary for survival, and therefore it is ok. What I am trying to get at is a practical approach to the understanding. In the U shape tHb we see a steady drop in tHb at the beginning but an increase in SmO2, this could/should actually imply a decrease in VO2 at the local level. Potentially increased efficiency. Now of course on a systemic level (pulmonary) VO2 increases. Well during exercise not only the skeletal peripheral muscles become more active, so an increase in VO2 is an overall measure of increased activity. If I increase my efficiency during lower performance exercise I can potentially maintain other functions much better. This is where we get the the crux of may point, finally! Vasodilation and constriction (and other factors of course) as a response to metabolic demand and survival during exercise. Obviously in the U shape example during the onset of exercise at low intensity we see a decrease in tHb and we identify this as a decrease in blood flow. This can be caused by muscle compression, or system chemo/mechano receptors and so on. The fact is that it appears to be happening, but the athlete does not seem to ahve a negative response to this and SmO2 does not really seem to mind either. It is not until SmO2 begins to decrease that we see an increase in tHb again, well apparently the system does not like the dropping SmO2 value. As long as we can supply enough resources there is no reason to increase supply, even in the case of supply dropping. No until there is a supply limitation will the body react to increase supply locally. So it is possible that pure muscle compression is the cause of tHb, or a response to a systemic vasodilation that results in vasoconstriction in the local muscle being measured to maintain blood pressure (since supply is good enough anyways this loss of blood flow is irrelevant for the moment). This hold true for the whole system, including non-exercise systems like the stomach and so on. The idea that the stomach stops having blood flow at the onset of exercises not true, neither is it for other systems. Blood flow to the stomach is maintained in sub maximal exercise as is it to other systems. This makes complete sense, why shut down the digestive system if you do not have to. Consider a 8-10 hour hunt, which is what humans excel, chase animals to fatigue. Being able to digest and function apart from just skeletal muscles can be very useful in maintaining performance. It is not until we start exercising towards maximal levels that blood flow starts to be greatly restricted and redistribution from other non exercise based systems. If we consider the U shape pattern, perhaps the increase is the point at which the real distribution of blood starts happening, and the reals vasodilatory responses start to take shape. Important to note here is that animals experiments nicely how blood is distributed during graded exercise, and that training greatly effects the degree and efficiency to which this re-distribution occurs. In other words a well trained organism will maintain blood flow to non exercise based systems longer and have a more radical response afterwards. Consider this after 7 hours of iron-man and you have to force down some power gel.

 

Quickly on the fact that often VL and hamstring do not have the same tHb curve (but often still have the same smo2 curve). If we consider efficiency again during low effort cycling the pressure created by the cycling motion is going to be greater on the VL than the hamstring (unless perhaps if someone is consciously pulling pulling pulling). If both hamstring and VL get a similar response to onset of low level activity it would make sense that due to muscle compression VL will show a drop while hamstring my not. This may just be a response or a non-response because this change in tHb is irrelevant for the physiological performance. It is not until the "real" distribution occurs at higher intensities that we see an increase in tHb in both active muscle groups.  

 

To conclude this rant, the U shape to me is a standard picture of local blood flow in an efficient system responding to need. But for this argument to make sense we need to look at smo2 at the same time. SmO2 and THb most be looked at together as the efficiency argument only holds true if SmO2 supply is sustained. 


cheers

Andri

 
DanieleM

Development Team Member
Registered:
Posts: 264
 #67 
One more step test, this time repeated twice with the same steps to show how prior activity can make a big difference in terms of efficiency (blood flow vs fractional extraction).
1. Step test from min 0 to min 15, start at 160W and increase 30W every 3 minutes.
2. 3 minutes very easy pedalling (40W), from min 15 to 18.
3. Stame step test as point 1 (from min 18 to min 33).
steptest_x2.png 

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #68 
Great  work  Daniele  and you can see, where we had the same question many years back . Fick  is great method  of  systemic  feedback , but than the  controversial  findings initially , that tHb  would  drop despite  higher intensities . It  would made no sens  looking  from a  system  reaction, but it   makes a lot of  sense  looking  from a regional  perspective.
 Ruud will do the  same warm  and not warm up  and he  is doing some other  repeats  we did  as it is  fun to see data independent  and not biased  produced from our side.
Thanks so much  for all the great feedback's. If you have the csv  we can overlap to show it nicer.

 I hope   as well it makes a little bit more sense  after our  ongoing  behind the scene  discussion , why  FICK  and  tHb local  may  work together  but not the way we all thought and got educated on. As you suggested  we will move some of the  behind the scene  discussion back on here.
 will be back later  with some fun   pictures  from Ruuds   2  step test.
DanieleM

Development Team Member
Registered:
Posts: 264
 #69 
Csv file is attached

 
Attached Files
csv steptest10novx2.csv (330.96 KB, 10 views)

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #70 

Here a  first feedback on  Ruuds  great data collection.
 Here the overview pic

thb smo2  all in one.jpg


2   3 min step test in a  row. 180 -1300+-  and than 1440 =- to2880
 . Calibration as usual ( 0 - 180)  than " cold " start .  or in other words  set up a situation, where he  will challenge  delivery from the start Low CO  to start out  and low  VE as well as low  recruitment pattern an so on. Really ,  real  survival  idea  from a hunted  animal   who is getting surprised  and has  to go with no time to warm up.
Than  you can easy see a  break after the first step test followed with a repeat of  the same steps  but  with a very different start situation now
 

Now  as usual,  I like that you  help thinking here , so I  will just show  in these case  , what I am looking at  so I show you  graphs  what graphs I will look at closer  for interpretations. This  graphs than can give us  more feedback  of this athlete's    current ability  and limiter  and compensators. Similar like a 5/1/5  but here in a  comparison of  2  in a row  step test.

Remark. Ruud  actually  as well had a BS X insight  system on the same muscle to compare  trends  and numbers.

So here  some interesting overlap  I was looking  at.

Now let's look  first  at the  HR  overlap  of the two step test.

HR overlap.jpg 
  
.It is  always  amazing  how  physiology  can work  accurately isn't it. Now this overlap  will be a nice picture  for  HR supporters  .

Next up  SmO2 overlap

smo2 1 2  overlap.jpg 
Next up tHb  trend overlap


thb 1 and 2 overlap.jpg 
Now  as  often explained  from a visual  point of  view  I like the biased  picture  so assuming  all starts  by zero  and we look relative changes

bias  1.jpg

and  second  step test biased  below

bias  2.jpg 

Now you can again see how many feedbacks we  can get  from NIRS  equipment  and here  from MOXY. This allows  now the coaches  and or athletes  to make a very nice  decision on how  to train  and what do  to  and than reassess  with the same  individual protocol to see, what changed  and whether we  expected  and therefore planned the changes  or  whether they  surprise us. ?
I will show the same on Daniele's  2  step test  later

juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #71 
Here just  for  fun  and why I like  v bio marker ideas versus  performance. But as well an interesting   discussion. It all started out  with U  shape  and what  can cause a  U  shape.
 One of the goals  we often have is  to use a  specific   shape  for a  prediction or   to create a  categories  of  good bad  and ugly. It seems we all  like this  and we like it very much  when we are in the  categories  good   and less   optimal  when we  end in the  categorize  ugly.  Physiological testing  does  not create this categories.  And that's  why it is  hard  to sell. We all like to   have a  category  so we feel  comfortable.
 We like to have a feedback   from YOU as an individual customer  or client  to work  with YOU  to make the best  out  from what we  can  with what we  have  and take it  from there. There is  always a winner here, as  YOU improve  your personal  best as you go along.
So back to U  shape. It looked as if Danielle  and Ruud  had both a U  shape. We discussed in depth the reason  why  we see that  and Andris  summary   was  the easy  way  to  get rid of all the readings we had.
 Now  here the  question  when we look at closer  at  2  steps test ( there here was a difference  how they did  it  but still  just  for fun lets  look at  the  biased  overall view including  tHb  concentration change.

 First Ruuds  both  step test over all biased  including thB

ruud  bias  plus thb all.jpg 


Now below  Danieles 2  step tests overall

dan bias all plus thb.jpg 



DanieleM

Development Team Member
Registered:
Posts: 264
 #72 
In both cases, the second step test has less fractional extraction (SmO2 is higher) which support the hypothesis of higher delivery.

In my own case I think HR is a bit higher and tHB is increasing.

In Ruud case HR seems to be the same while tHB is quite flat with increase only in the last 2 loads.




juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #73 
Absolutely  and I will show later  some more intriguing differences and how   both systems react different to the demand or  to find the smartest  way  to full fill the task on hand.
juergfeldmann

Development Team Member
Registered:
Posts: 1,501
 #74 
Okay  here  some  hints  where the big difference is between the two step test  sent to us  by Ruud  and Daniele.
  Remember  when we look    at  physiological reactions we have to  areas we can look at. Unfortunately   all the test   we do   or did in the   past  miss one section  to look at it repeatedly.

a). Sections where we know  for sure we  have a delivery limitation.
b)  sections where we know  we  stopped  O2  demand   of the   biggest user the loco motor  muscles. 
b 1) sections  where  we know we  add a big  demand of  O2  again.
  Now in this double step test  we have at least one b  and B 1  complete  and we have one B  and  one
B 1

 So look again  what I mean  and let's see  whether we  look at the same    feedback. Below is  Ruuds  biased feedback including tHb. 


ruud  bias  plus thb all.jpg

Now  below this is  Ruuds  overlap HR  as a part of  CO




HR overlap.jpg


Now  below  Daniele's  biased  including tHb  graph.

dan bias all plus thb.jpg 

and below his  HR overlap




hr  overlap  dan.jpg



Now  important this  to just  look at what we see  so  reality  and not too fast draw any conclusions. I will tell you later  why  and what has to be done before we  can get to any decent   acceptable conclusion.
 You can see  once you think in the physiological terms a  nice difference.
 As well once  we are ready  to accept that  what we  do  with NIRS  is a local information  only  first and  foremost  and to make a general   conclusion  we  use  at least 2 MOXYS   to see, whether the reactions is very locally or is it very systemically.
  Remember  a part of  this discussion.
 Fick  and the calculation of VO2  is a great systemic  feedback  but  may not  hold  true  for  local reactions . Now this is one of the interesting  situations now , where we see  big names   struggling  with NIRS, sent them back  for calibration because   they think   still  systemically  and  not  as well local .
Using  any  blood flow   measuring technique in a  femoral arterial    does not mean that the  flow result  there done with Doppler or what ever great  ideas  reflects the blood flow  reaction in a local muscle. On the other hand a  tHb  reaction in a  local area  does not reflect  the reaction in the system. To use  NIRS to have a  bigger  option to as well look  at systemic reactions  you  have to have a second one  and see  whether we  have the same trends.
 In Daniele's case we had  hamstrings  and Quad  and we had different reactions in some of the tests he  did.

Previous Topic | Next Topic
Print
Reply

Quick Navigation:

Easily create a Forum Website with Website Toolbox.

HTML hit counter - Quick-counter.net