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Ruud_G

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 #16 
A few quick remarks on your good data collection. In general I see the same in data I have collected for these muscles. Same cadence in the two workouts? Same position in the two workouts? These two factors can (apart from muscle you measure) contribute a lot to the results you see.
ryinc

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 #17 
Hi Ruud - thanks, yes cadence and position was almost identical. 
juergfeldmann

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 #18 
Nice  work and great thoughts. Nice to se  that  readers get  closer to understanding physiological  training ideas. And it all starts  with  interpretation  of the  NIRS info in combination  with  other physiological systems. I had a very long  phone discussion today  with a great  university   and  the  fun part  was, that  at the end  we   agreed , that  the O2  utilization in the  muscles  is not reflected  properly  with a VO2  peak test as  VO2 peak is a  summary of the  total O2   used  and not a feedback on where and  who    has  the O2  used or may need  it. I  am juts going  though a   huge  amount of data's  sent to me from different places, where they now start to combine  VO2  and  Physio flow and blood testing and SEMG as we proposed   far back  and   it is fun to see the many great  questions again coming up we had, when  the classical believes  crashed  with  live feedbacks.  The  data's Ruud and Daniel  sent once  as well now  your data's  suggest  what we proposed   back as well. In  good trained  cyclists the VL is not  an optimal muscle to look for trends. The RF  is much better. Why  to we  are stuck  with VL. Because somebody started  to  use it  with some stdueis  and now we  blindly follow it  with  not a lot of  critical thoughts.
 The RF  has   as a dual joint muscle a much better feedback information on  technique but as well on integration. If  you do  step tests instead of   5/1/5  you will as well see, that the  what some call break point of  NIRS  signal is  at very different  intensities  if  you    fix a  NIRS on a  calf  or  VL  or  RF  or hamstrings. If you  than change bike position  form up right to aero position or you move  forward  or back words on the seat it changes again. We see in world  class cyclists, that they due  that  without  actuallu knowing what happens , they  just feel they can maintain a certain performance  much longer.  I compare it  with a piano player  and  myself  . I  could use  barely  a  few  keys in front  of me, where a   real piano player uses  all the keys.
 Same in  sport. A  top cyclists  has a  huge  ability  to  integrate  a lot of  different muscles  ( intermuscular coordination) into his  ability to  find the most efficient  way.)


For  VO2   equipment user  what you see here in VL  and RF  reaction  is often as well   a reaction you see some  may call  the slow  VO2  component.


Am J Physiol Regul Integr Comp Physiol. 2007 Aug;293(2):R812-20. Epub 2007 Apr 25.

Thigh muscle activation distribution and pulmonary VO2 kinetics during moderate, heavy, and very heavy intensity cycling exercise in humans.

Endo MY1, Kobayakawa M, Kinugasa R, Kuno S, Akima H, Rossiter HB, Miura A, Fukuba Y.

Author information

  • 1Department of Exercise Science and Physiology, School of Health Sciences, Prefectural University of Hiroshima, 1-1-71, Ujina-higashi, Minami-ku, Hiroshima 734-8558, Japan.

Abstract

The mechanisms underlying the oxygen uptake (Vo(2)) slow component during supra-lactate threshold (supra-LT) exercise are poorly understood. Evidence suggests that the Vo(2) slow component may be caused by progressive muscle recruitment during exercise. We therefore examined whether leg muscle activation patterns [from the transverse relaxation time (T2) of magnetic resonance images] were associated with supra-LT Vo(2) kinetic parameters. Eleven subjects performed 6-min cycle ergometry at moderate (80% LT), heavy (70% between LT and critical power; CP), and very heavy (7% above CP) intensities with breath-by-breath pulmonary Vo(2) measurement. T2 in 10 leg muscles was evaluated at rest and after 3 and 6 min of exercise. During moderate exercise, nine muscles achieved a steady-state T2 by 3 min; only in the vastus medialis did T2 increase further after 6 min. During heavy exercise, T2 in the entire vastus group increased between minutes 3 and 6, and additional increases in T2 were seen in adductor magnus and gracilis during this period of very heavy exercise. The Vo(2) slow component increased with increasing exercise intensity (being functionally zero during moderate exercise). The distribution of T2 was more diverse as supra-LT exercise progressed: T2 variance (ms) increased from 3.6 +/- 0.2 to 6.5 +/- 1.7 between 3 and 6 min of heavy exercise and from 5.5 +/- 0.8 to 12.3 +/- 5.4 in very heavy exercise (rest = 3.1 +/- 0.6). The T2 distribution was significantly correlated with the magnitude of the Vo(2) slow component (P < 0.05). These data are consistent with the notion that the Vo(2) slow component is an expression of progressive muscle recruitment during supra-LT exercise

Now  do not  forget, This  can as well be  seen , when a nonpriority muscle  in the upper body start to get integrated into he performance. 

But  only  if  the cardiac  output  is  ready and able  to maintain  the BP  so  an integration of any additional muscels  who now  asks  for O2  supply  and often as well therefor  for  an increase in blood supply  will challenge the ability of the  cardiac system  as a supplier  and  as  the key  system to maintain  BP. If this start to  reach  a limitation we will see   shift of  blood flow  from less priority  to more priority  areas.
 If  the  respiratory system  as  muscular limitation  has  reached its  limitation, than we see a  shift in O2 disscurve  due to the  inability to release sufficient  CO2. We  see a  hypercapnia  increasing  and as such a EIAH  on the SpO2  sensor on the finger

blood pressure.jpg 

Above  out  of Holmberg  /Calbet
 This  reaction   is  something you can se sometimes  in thee thB reaction in  athletes  as a  nice   nearly sinus  wave of   a  15  second  +-  amplitude, when  the athlete is  just boarder online   cardiac limitation. Some may remember this discussion   long time back.

limitation of performance.jpg 

moxy vo2 2.jpg 

sleeping giant blood flow 2.jpg 
And last  equipment we used  to  finally see  that  a lot  can be seen by just looking  at NIRS feedbacks in nonpriority  muscles  and  priority muscles.

vo2  over all.jpg 
  An  old  old  discussion now just  much  more fun to follow as we  now have new  tools.
 Here    flash back
 

john hunter stated that “blood goes where it is needed” (1794).1 John Hunter's intuition was often superb; he must have wondered how a system “knew” where flow was needed and how the right amount got to the right place. He must have suspected that metabolism (need) was involved. Sir William Harvey pointed to the importance of mechanical factors in 1628. Vasomotor nerves were discovered by F. Pourfois du Petit in 1727, and Hunter may have pondered neural vasodilation as well. Experimental glimpses of metabolic, neural, and mechanical control of muscle blood flow (MBF) began late in the 19th century. Enthusiasm for these three ideas waxed and waned cyclically with periodicity depending on satisfaction of each generation with new vs. old answers. These ideas are the backbone of this historical perspective,
as are four related questions.
1) What causes the vasodilation?
2) What is muscle's mechanical contribution to its own blood flow, including its effect on cardiac output?
3) To what extent is neural (vasoconstrictor) control of MBF blunted by muscle's metabolism?
4) What reflexes initiate this neural control?

 


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