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.
- 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.
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
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.
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.
An old old discussion now just much more fun to follow as we now have new tools.
Here flash back
john hunter stated that â€œblood goes where it is neededâ€ (1794).1 John Hunter's intuition was often superb; he must have wondered how a system â€œknewâ€ 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?