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juergfeldmann

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 #1 
The classical believe  and the idea  that we  should not change current  books on  energy supply   needs perhaps  some reviews . The interesting part is ,that it is not  new  but now  with  Magnetic resonance  and  NIRS and otehr tools we can see, that  the ideas  have changed  due to  new  information.
 The discussion is  getting more heated  on " anaerobic " and aerobic "
 Here a  fun  section  from 1985

ppl Physiol (1985).

Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise.

Bogdanis GC1, Nevill ME, Boobis LH, Lakomy HK.

Author information

Abstract

This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10- and 30-s sprints. At the end of sprint 1, PCr was 16.9 +/- 1.4% of the resting value, and muscle pH dropped to 6.69 +/- 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 +/- 0.03), but PCr was resynthesized to 78.7 +/- 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 +/- 9 mmol/kg dry muscle during the first sprint but was decreased to 139 +/- 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a approximately 45% decrease in glycolysis. Despite this approximately 41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only approximately 18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 +/- 0.10 vs. 3.17 +/- 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01).

These data suggest that aerobic metabolism provides a significant part (approximately 49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.

 

 
ryinc

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 #2 
Thanks for sharing Jeurg. I am currently going through the presentations from the 2016 Moxy seminar through the Moxy Academy and Andri's presentation also touched on this. I would recommend the seminar to Moxy Forum readers - it was quite reasonably priced.
CraigMahony

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 #3 
Most high level track and field sprinters take very long breaks, as much as 1 minute per 10m run. So a 30 sec run at 95 - 100% might have a 10 - 20 minute recovery. This would probably reduce the aerobic metabolism contribution compared to the abstract in the repeated sprints. Now, to my knowledge, this is done for neuromuscular reasons not energetic reasons.
juergfeldmann

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 #4 
Craig  yes  and it  is done  with  SEMG  reactions. Your   feedback  shows  how  the  timing of  rest in between  has a direct impact  on what we  may  or may not stimulate. Now intramuscular  coordination  and NIRS  recovery  go often hand in hand  and that's  again where we  take NIRS  as a   nice live feedback. It is  the  usual  question, what is the limiter if  we do short  rests in between  and what is the limiter  when we  do long breaks in between.  ? The answer to this  question will guide  you to the   solution of whether a  sprint  workout  or  any  workout  will stimulate  more  Cr.P  or  more O2  utilization.
CraigMahony

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 #5 
Now intramuscular  coordination  and NIRS  recovery  go often hand in hand  and that's  again where we  take NIRS  as a   nice live feedback.

Can you explain this a bit more please Juerg? Are you saying that if we have full NIRS, ie SmO2, recovery the intramuscular coordination will have recovered?
juergfeldmann

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 #6 
No  Smo2  will tell you minimal   in this case. SmO2  is a nice  but not  always great feedback  as a trend in Cr.P as  shown in some  magnetic resonance   studded.  in  any first s print or  hard  activity  we see SmO2  dropping  often  lower  than at the end of  an all out  step test.
 Main reason may be the   delivery limitation  due  to low CO  and VE than we  will have  after  the  first sprint  so  for the second sprint.

The  recovery  often goes as  well with SmO2 trend. So  SmO2  alone  a soften mentioned  has some limitation. As  soon we  combine it  with tHb  it  can give much more feedback.
 tHb  is  very close  connected  with SEMG  activities. I know  that when we look at NIRS  studies the  focus  is on metabolic  answers  and questions. BUT  tHb  can give nice feedback on muscle contraction quality.  So  to your  questions  yes I look at NIRS feedback  but at  tHb  first  and than a little bit on SmO2 trend as  activity is  connected  with energy use but  first and  foremost  I look on  thB  reaction  created by muscular  contraction pressure. I am just putting together  a PP  for a client  where this is one  focus  of  the   discussion. will see, whether i can use  one or  the other  picture  to explain this closer   in the next  few days.
CraigMahony

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 #7 
Thanks Juerg. I look forward to anything else you can give on this.
juergfeldmann

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 #8 
Craig
 here some  promised insight  view in a   possibly  very different direction  we  try  to move in  short  term activities, which could be  sprints  or  at least  training  for  short or  middle distance runner. But  for sure in  teams sports  like  ice hockey  or  soccer but as well as  sports like tennis or  badminton.
In  other words  sports  whee either the   sport  itself  leads  to very hard  short  loads  with  relative,  but not always controlled  rests in between.
 So  similar like when we  do perhaps an interval.
 This leads us  far back on this  forum  to a  section I started  long  ago  with  little feedback  and most likely due  to lack  of  explanations    from my  side  for a  discussion.

Ipahr and ipahd end.jpg 

This  questions   was  asked  far bake from Harre  et all  in the former  DDR.
 It is  or  was a  very intriguing  questions  and is getting traction again  with new  technology.

 Studies  like the one  form Gibala  et all and more  on the  interesting fact  that HIIT  or Tabata  like workouts  seem to have a  surprising  good effect on aerobic development  despite  the  fact  that  some may still argue  they are anaerobic.  Now  integration of NIRS  opens  this  interesting    section  again but  with a very  very different view  due to changes in  bio energetic  assessments.
So here a  start off  where we  started out  with   sprints  and  how we go into a sprint 


2  sprints in a  row.jpg


N
ow  this brings  us  back  to  the 1960  and HIIT  and you  can see why  I often refer  to , when we  not look   at they pats we may or may not repeat  some mistakes   because we can learn  from there, look what changed  and use the same studies  with the new information we have to  review conclusions  based on  theories  and now perhaps more of  facts  and   real information. Below  a  fun study from 1960  30 min  total  work if  possible  with different load  and rest periods. As you can see  the    shorter  the load  and  10 secnds   an  20 sec  rest  the lower the lactate  accumulation.
  . The idea  than was  due to  the  equipment used  and the lag time of the result in blood sampling and VO2  collection, that  the  work here was  " anaerobic "  and alacticid..Today  we know  the loads  were very  highly  O2  involved  at least  from the second  load on  and  there  was a lot  of lactate produced. But  the  short  duration  never  depleted  the  O2  critically and  the load  allowed  a full resaturation as well as  the O2  was  used  of  refueling.. of  Cr.P

Hollmannn Intervall ith different rests.jpg

What we know  as well is, that  ATP  never  dropped or is  allowed  to  drop below a  certain level. This  critical  " survival " level  is  protected  and  before we  try to  create more ATP    when it is not possible  we rather    do 

ATP reactions  may be controlled over CG ( central governor)

Connett says feedback inhibition of energy or regulatory system achieves its set point - a match between ATP supply and demand – by decreasing ATP consumption rather than increasing ATP production....body is slowed down via CG. 

atp crp.jpg 



Now  this leads  to thee question on how  this great  research  can be used practically   for a  coach?  Below  is  some own  case studies  where we look how  to  use  this information
The  top graph  is a  close   view  of  a high intensity  load  where you see  SmO2  and  SEMG  activity in black
 You can easy see that  the  drop in SmO2  and   lowest level  surprisingly  fits  the SEMG increase  and top  of  the SEMG  activity. Than we  can see a  flat  SmO2 
 where we  could argue  if  only  SmO2  would be there, that we now  mkove into  perhaps an " anaerobic " intensity   as we can not  further use  O2.
 OR
 as  we  use  the feedback of  the SEMG.  The  CG  to protect  ATP   levels  simply reduces   motor unit recruitment  as much as needed   so  activity stays  really balanced  aerob  ( supply  and demand  match  and  SmO2  flat


semg  and  thb hiit.jpg 

Now  below  is the tHb trace  and the SEMG  trace  and  the fun part is that you can see that the initial  drop in SmO2  was  so intense , that this athlete created a outflow restriction with a subsequent  Blood pooling  due to the  outflow  restriction. One we ht  it a  critical low  SmO2 level (  and  with this possibly a low Cr.P  level ,) we where not able to maintain  performance  and  we ha d to  find a  way  over CG  to reduce ATP  demand  to a level , where we had   sufficient O2    to   maintain ATP level   and possible  try  to refuel  some Cr. P    storage. The reduction in motor units recruitment   reduced  the  muscular compression  and therefor  the pooling   got  reduce  with a  trend in tHb  drop.  Now  there are different  situation  and here the three most common.
 a)  single muscle protection  and  H + is one of the protection ( in sport  we look at it as  " bad:  but  for survival it may be crucial  as it stops ATP  splitting ( possibly  some additional  factors like CA++  and  Pi  and more)

b )  systemic  protection due to limitation of  CO  and  " steeling " O2  from vital systems If this is the case we  simply see a  loss of   performance like we shown in some rowing  assessments  where  the athlete  did not  had feedback on performance and kept  rowing    hard , but hard  was feeling  and reality  was loss of wattage  same picture  than in all main  leg muscles  and in  rowing  even in  upper body muscles  depending on the athlete.

c )  reaching a critical  ability in one   main muscles  but  having the ability  to integrate  ( inter muscular  coordination.) another muscle  group  to maintain the  demanded performance.


smo2   vl  bi  all.jpg



A
bove  an example  from a cyclist  VL  and Biceps  femoirs, where the VL  reached  its optimal  ability  to   add to the performance but than needed  help and due to a  good intermuscular coordination    this athlete was able to add  some more   help  from his  Biceps  femoris  to the  performance. This is  for me  one reason  why I would not  take  VL  in good  cyclist  as a   key muscle as  we often have a problem  to see trend.
Below a  closer look   so  VL   showed a SEMG  reaction a s above and  Bi  showed a  steady  increase in SEMG

closer look  ddelay  vl   bi.jpg 
Now  this  will lead to one practical   option.
  If  we  can balance  H +  situation we  can sustain longer a   certain performance and we  can  recover  faster  for the next load.

 This will lead perhaps  to the next discussion on how we  do this. To  start this  here some feedback  to  have  to understand  the  idea.

COMPONENTS OF CELLULAR PROTON PRODUCTION, BUFFERING, AND REMOVAL

The cause of metabolic acidosis is not merely proton release, but an imbalance between the rate of proton release and the rate of proton buffering and removal. As previously shown from fundamental biochemistry, proton release occurs from glycolysis and ATP hydrolysis. However, there is not an immediate decrease in cellular pH due to the capacity and multiple components of cell proton buffering and removal (Table 5). The intracellular buffering system, which includes amino acids, proteins, Pi, HCO3−, creatine phosphate (CrP) hydrolysis, and lactate production, binds or consumes H+ to protect the cell against intracellular proton accumulation. Protons are also removed from the cytosol via mitochondrial transport, sarcolemmal transport (lactate−/H+ symporters, Na+/H+ exchangers), and a bicarbonate-dependent exchanger (HCO3−/Cl−) (Fig. 13). Such membrane exchange systems are crucial for the influence of the strong ion difference approach at understanding acid-base regulation during metabolic acidosis (5, 26). However, when the rate of H+ production exceeds the rate or the capacity to buffer or remove protons from skeletal muscle, metabolic acidosis ensues. It is important to note that lactate production acts as both a buffering system, by consuming H+, and a proton remover, by transporting H+ across the sarcolemma, to protect the cell against metabolic acidosis.

Once it is in the blood we  have one  great ability  to  get rid  of H + .

buffer H =.jpg 

Respiration/Expiration


h + balance.jpg 

More depending  where we  go  with this.


CraigMahony

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 #9 
Thanks Juerg. This is all interesting. I believe I have seen the tHb pattern you showed in the graph with tHb compared to SMEG in the longer sprints I have my middle distance athletes do for speed work.

What I was hoping to establish was if it is possible to determine when a 100m track sprinter has recovered after say a 60m hard repetition or even a 150m repetition. SmO2 indicates when we may have recovered energetically. Your tHb/SMEG graphs demonstrate that the subject became neuromuscularly fatigued during the sprint. Is it possible to use SmO2/tHb to determine when the athlete has recovered from their neuromuscular fatigue? Or is it only possible to determine when during the sprint the athlete became fatigued?
juergfeldmann

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 #10 
Craig .
You hit an incredible great  point .
 Your tHb/SMEG graphs demonstrate that the subject became neuromuscularly fatigued during the sprint.

What is  neuromuscular fatigue  an on going discussion with possibly no  end.

It started  far far  back  and  confused  some of the great brains  like noble price winner  A. Hill
And  we  are not  much further really , we have the  2  main  directions.
 a)  centrally regulated  due  to survival  reasons.
 b) local  failure  due to biochemical reactions?

One  of  Hills  first  hints is .

cgm.jpg 


Your tHb/SMEG graphs demonstrate that the subject became neuromuscularly fatigued during the sprint.

Now I am less sure, whether the tHb /SEMG  graphs demonstrate a neuromuscular  fatigue. I  would rather say  that  somewhere in this load   something   triggered a  drop in muscular recruitment (SEMG ) drop  and as  such a  chnage from a  compression to the blood vessels which created in this case a venous  outflow restriction and now  due to reduction of  motor unit recruitment  allowed  a pooling outflow. 

 Some  would argue  with the below idea and as hinted  by  Hill's.

ecgm pic.jpg






Now here a  short  info on  how  neuromuscular fatigue is  defined in exercise physiology.

•In Exercise Physiology, neuromuscular fatigue can be defined as a transient decrease in muscular performance usually seen as a failure to maintain or develop a certain expected force or power.


You  can see how  "close " or how  apart  this definition  is going .

So  we will  later perhaps come back on this if  we have  some feedback.
 I like to move a little bit further in  the direction of  repeat  short  term loads  like sprints  or other  ideas.

We had  the interesting reaction between a  first load  and a  second  load . And we have the idea in our assessments  to start    " cold "  to see the bodies  reaction, when we know we have a delivery limitation. So  in a first sprint   we have less  help  from delivery than we  have in a  second  repeat sprint.
 So  if we look just  at one single sprint  all out , due we have the same intriguing  increase in VO2  reactions as we have in repeat  sprints.

Here  a  fun study  .

Eur J Appl Physiol. 2016 Aug;116(8):1511-7. doi: 10.1007/s00421-016-3409-8. Epub 2016 Jun 6.

Exercise training comprising of single 20-s cycle sprints does not provide a sufficient stimulus for improving maximal aerobic capacity in sedentary individuals.

Songsorn P1, Lambeth-Mansell A2, Mair JL3, Haggett M1, Fitzpatrick BL3, Ruffino J1, Holliday A2, Metcalfe RS3, Vollaard NB4.

Author information

  • 1Department for Health, University of Bath, Bath, BA2 7AY, UK.
  • 2Institute of Sport and Exercise Science, University of Worcester, Worcester, WR2 6AJ, UK.
  • 3School of Sport, Ulster University, Derry, Londonderry, BT48 7JL, UK.
  • 4Department for Health, University of Bath, Bath, BA2 7AY, UK. n.vollaard@bath.ac.uk.

Abstract

PURPOSE:

Sprint interval training (SIT) provides a potent stimulus for improving maximal aerobic capacity .VO2, which is among the strongest markers for future cardiovascular health and premature mortality. Cycling-based SIT protocols involving six or more 'all-out' 30-s Wingate sprints per training session improve VO2, but we have recently demonstrated that similar improvements in  VO2 can be achieved with as few as two 20-s sprints. This suggests that the volume of sprint exercise has limited influence on subsequent training adaptations. Therefore, the aim of the present study was to examine whether a single 20-s cycle sprint per training session can provide a sufficient stimulus for improving VO2.

METHODS:

Thirty sedentary or recreationally active participants (10 men/20 women; mean ± SD age: 24 ± 6 years, BMI: 22.6 ± 4.0 kg m(-2),: 33 ± 7 mL kg(-1) min(-1)) were randomised to a training group or a no-intervention control group. Training involved three exercise sessions per week for 4 weeks, consisting of a single 20-s Wingate sprint (no warm-up or cool-down).  was determined prior to training and 3 days following the final training session.

RESULTS:

Mean VO2 did not significantly change in the training group (2.15 ± 0.62 vs. 2.22 ± 0.64 L min(-1)) or the control group (2.07 ± 0.69 vs. 2.08 ± 0.68 L min(-1); effect of time: P = 0.17; group × time interaction effect: P = 0.26).

CONCLUSION:

Although we have previously demonstrated that regularly performing two repeated 20-s 'all-out' cycle sprints provides a sufficient training stimulus for a robust increase in vo2, our present study suggests that this is not the case when training sessions are limited to a single sprint.

 Question  from our side.
 In a  single sprint  what may be the limiter. In a repeated  sprint  what may be the limiter

Now  the interesting  part is , that  the  single   heavy load not only  has a different reaction on   energy release and utilization but as well on hormonal reactions.

GH hprmon and intervall.jpg 



Now  repeated  loads lie  sprints or other loads  create  as we see a  certain specif  energy demand  and with this we  need a  good  " delivery " system  to sustain  the repeated loads  due to metabolic reactions.

 One of  the often discussed  reasons  of   loss of performance is  the  O2   and ATP  protective level  but as well the  substances, which   avoid ( to protect   further ATP  splitting like H +

Now  what we see  is, when we improve  the  bodies ability to rleaese  H +  (CO2 ) better we  can sustain   performance level longer.

The goal  is : Now  watch  again the time of the study and yo can see  why we  are sometimes  wondering  .

J Clin Invest. 1988 Apr;81(4):1190-6.

31P nuclear magnetic resonance studies of high energy phosphates and pH in human muscle fatigue. Comparison of aerobic and anaerobic exercise.

Miller RG1, Boska MD, Moussavi RS, Carson PJ, Weiner MW.

Author information

  • 1Neuromuscular Research, Children's Hospital, San Francisco, California 94119.

Abstract

The goal of these experiments was to investigate the relationship of ATP, phosphocreatine (PCr), inorganic phosphate (Pi), monobasic phosphate (H2PO4-), and pH to human muscle fatigue. Phosphates and pH were measured in adductor pollicis using 31P nuclear magnetic resonance at 2.0 Tesla. The force of muscle contraction was simultaneously measured with a force transducer. The effects of aerobic and anaerobic exercise were compared using two exercise protocols: 4 min sustained maximal voluntary contraction (MVC) and 40 min of repeated intermittent contractions (75% MVC). The sustained maximal contraction produced a rapid decline of MVC and PCr, and was accompanied by a rapid rise of Pi, H+, and H2PO4-. Intermittent exercise produced steady state changes of MVC, pH, and phosphates. No significant changes of ATP were found in either protocol. During fatiguing exercise, PCr and Pi had a nonlinear relationship with MVC. H+ showed a more linear correlation, while H2PO4- showed the best correlation with MVC. Furthermore, the correlations between MVC and H2PO4- were similar in sustained (r = 0.70) and intermittent (r = 0.73) exercise.

The highly significant linear relationship between increases of H+ and H2PO4- and the decline of MVC strongly suggests that both H+ and H2PO4- are important determinants of human muscle fatigue.

Which moves us in the  direction.
  If   repeated sprints  trigger the need of a  better  gas exchange  CO2  out  due to the   need  to balance  H +  than we  should see  that this  is the  case in some studies.

J Physiol. 1997 Jun 15;501 ( Pt 3):703-16.

Enhanced pulmonary and active skeletal muscle gas exchange during intense exercise after sprint training in men.

McKenna MJ1Heigenhauser GJMcKelvie RSObminski GMacDougall JDJones NL.

Author information

Abstract

  1. This study investigated the effects of 7 weeks of sprint training on gas exchange across the lungs and active skeletal muscle during and following maximal cycling exercise in eight healthy males. 2. Pulmonary oxygen uptake (VO2) and carbon dioxide output (VCO2) were measured before and after training during incremental exercise (n = 8) and during and in recovery from a maximal 30 s sprint exercise bout by breath-by-breath analysis (n = 6). To determine gas exchange by the exercising leg muscles, brachial arterial and femoral venous blood O2 and CO2 contents and lactate concentration were measured at rest, during the final 10 s of exercise and during 10 min of recovery. 3. Training increased (P < 0.05) the maximal incremental exercise values of ventilation (VE, by 15.7 +/- 7.1%), VCO2 (by 9.3 +/- 2.1%) and VO2 (by 15.0 +/- 4.2%). Sprint exercise peak power (3.9 +/- 1.0% increase) and cumulative 30 s work (11.7 +/- 2.8% increase) were increased and fatigue index was reduced (by -9.2 +/- 1.5%) after training (P < 0.05). The highest VE, VCO2 and VO2 values attained during sprint exercise were not significantly changed after training, but a significant (P < 0.05) training effect indicated increased VE (by 19.2 +/- 7.9%), VCO2 (by 9.3 +/- 2.1%) and VO2 (by 12.7 +/- 6.5%), primarily reflecting elevated post-exercise values after training. 4. Arterial O2 and CO2 contents were lower after training, by respective mean differences of 3.4 and 21.9 ml l-1 (P < 0.05), whereas the arteriovenous O2 and CO2 content differences and the respiratory exchange ratio across the leg were unchanged by training. 5. Arterial whole blood lactate concentration and the net lactate release by exercising muscle were unchanged by training. 6.
  2. 2.      The greater peak pulmonary VO2 and VCO2 with sprint exercise, the increased maximal incremental values, unchanged arterial blood lactate concentration and greater sprint performance all point strongly towards enhanced gas exchange across the lungs and in active muscles after sprint training.
  3. 3.      Enhanced aerobic metabolism after sprint training may contribute to reduced fatigability during maximal exercise,
  4.  
  5. whilst greater pulmonary CO2 output may improve acid-base control after training

 This leads  to  what we do in many a cyclic  sports  and teams now  since  many years.
 Improve  the ability  to  get rid  of CO2.

10 reasons.jpg 

 



Fixed  part  of  today's  team sports  training in many countries. Here a   ice hockey  junior  A  team  age  group.

Hockey Spiro.jpg 




CraigMahony

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 #11 
Thanks Juerg. Let me have a think about all of this and I will no doubt have some more questions for you.
juergfeldmann

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 #12 
Craig  for sure  as I have   always  more questions to myself  so yes  great. I had a long phone discussion with a  track  coach  and the   target  was to  show  how a limitation in VE  directly will influence  your  sprint  or  short term  high intensity performance. So we did  some practical  works  on the phone  with him   working with a limited  VE  and he  very fast  understood  the concept.
If we look how hard a  100 m sprinter  is  actually breathing. Not  for O2  in but  for ??????

CraigMahony

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 #13 
I would guess they are breathing to expel the CO2 to allow a reload of O2.
juergfeldmann

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 #14 
The other   bigger  question is  the  H +  balance ??
juergfeldmann

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 #15 

Muscle metabolism during sprint exercise in man: influence of sprint training.

Abstractrkoutsn order to examine the influence of sprint training on metabolism and exercise performance during sprint exercise, 16 recreationally-active, untrained, men (VO2peak= 3.8+/-0.1 l.min(-1)) were randomly assigned to either a training (n= 8) or control group (n= 8). Each subject performed a 30-sec cycle sprint and a test to measure VO2peak before and after eight weeks of sprint training. The training group completed a series of sprints three times per week which progressed from three 30-sec cycle sprints in weeks 1 and 2, to six 30-sec sprints in weeks 7 and 8. Three mins of passive recovery separated each sprint throughout the training period. Muscle samples were obtained at rest and immediately following the pre- and post-training sprints and analysed for high energy phosphagens, glycogen and lactate; the activities of both phosphofructokinase (PFK) and citrate synthase (CS) were also measured and muscle fibre types were quantified. Training resulted in a 7.1% increase in mean power output (p<0.05), an 8% increase in VO2peak (p< 0.001), a 42% increase (p< 0.01) in CS activity and a 17% increase (p< 0.05) in resting intramuscular glycogen content. In contrast, neither PFK activity nor fibre type distribution changed with training. An increase (p< 0.05) in mean power output and attenuated (p< 0.01) ATP degradation were observed during sprint exercise following training. Glycogen degradation during sprint exercise was unaffected by sprint training. These data demonstrate that sprint training may have enhanced muscle oxidative but not glycolytic capacity

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