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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
I got over the last few month  regular the question, whether with MOXY only we may be able  to find  out , whether  respiration is a limitation in an athlete.

 The answer is  yes.
  The easier  way to be very sure is, if you already have a VO2  equipment to  combine MOXY  and your VO2  equipment as you have additional feed backs on VE 9 RF x TV)  as well as  indirect VO2   in  comparison  with  RF  and TV  as well as CO2  ) EtCO2 )  in comparison  with RF  and TV.
 There are some tricky situations  , where  with MOXY alone you may run into some  open questions.
  We  compared  over   many years VO2  reaction with NIRS   , originally with using Portamon and now  with   MOXY  and we use MOXY   than on an involved  one on a  noninvolved  and  one MOXY intercostal .
 This  gives us   answers  to two common questions.
 1. Is the athlete in a situation, where the  muscles   simply  try to  " steel " too much O2  from the  delivery systems, and they have to  cut the delivery down  to maintain their own pO2  needs.
 If this is the case we  talk  about   Dempsey  suggested   metaboreflex. or  The interesting group around  Spengler  and Boutellier.
2. If the athlete  simply has a weak  respiratory muscle system but no  risk of  " steeling " blood due to a relative weak muscular system  with  not  too many  capillarsiations and mitochondria density . So simple weak  developed muscles like any muscle can be.

 So this will create some fundamentally different situations in the body.
  The number one  will show up in some clear tHb reactions  the number 2  will show up   as well with tHb reactions but nicely    as well with the SmO2  reactions.

 Below is a nice summary of the metaboreflex  and  despite that   many  coaches  still believe  respiration is never a limitation, reality and proper assessment show that is is  very often a  limitation.
It is not always a question of O2 intake  but   very often a question of  immediate  support  for a H +  balance  and as  such  the  VE  we can improve   will be a direct help in H + balance.
, but   only if the respiration  has a certain ability.
 We have  t  ice hockey players on specific   training ideas    with Brian Kozak  .
 Here simple number   info.
 A  top    NHL  player  not  train in respiration will blow  about  130 - 180 L / min VE. That's' it . A proper   respiratory train NHL  player  can blow  somewhere between 250 - 350 liter. We have some kids using a 6 L  bag in Spiro tiger workouts  and  can blow a  RF  of  40- 50 . So you can calculate the VE needed  so The Spiro Tiger  does not shut    down.
 So here the challenge. How  would we see in a  5/1/5  , whether it is a metaboreflex  or a simple  weakness of the respiratory muscles.
. How  can a VO2 max  tell you that or a FTP   assessment or a  lactate threshold test. ??

J Physiol. Nov 15, 2001; 537(Pt 1): 2.
PMCID: PMC2278934

Robin Hood for the lungs? A respiratory metaboreflex that ‘steals’ blood flow from locomotor muscles

 
 

In this issue of The Journal of Physiology, Dempsey and colleagues (Sheel et al. 2001) contribute another key chapter in their ongoing series of elegant investigations on novel interactions involving the respiratory muscles, autonomic nervous system and cardiovascular regulation in humans. Earlier, they demonstrated that manipulation of the work of breathing during maximal exercise resulted in marked changes in locomotor muscle blood flow, cardiac output and both whole-body and active limb oxygen uptake (Harms et al. 1997, 1998). They also established the remarkable metabolic costs of supporting respiratory muscle function during maximal exercise, requiring up to 16 % of the cardiac output (Harms et al. 1998). Importantly, the reduced locomotor muscle blood flow and vascular conductance in the elevated work of breathing condition was associated with augmented noradrenaline (norepinephrine) spillover from the active limbs, suggesting enhanced sympathetic vasoconstriction (Harms et al. 1997). These physiological effects of the work of breathing have important functional consequences, as demonstrated by an ~15 % improvement in endurance performance with respiratory muscle unloading (Harms et al. 2000).

The next generation of experiments attempted to establish the mechanisms underlying these fascinating physiological connections. In a paper recently published in this journal (St Croix et al. 2000), high-resistance, prolonged duty cycle breathing at rest, resulting in respiratory muscle fatigue, evoked an increase in leg muscle sympathetic nerve activity (MSNA) that was independent of central respiratory motor output, indicating a reflex origin. Moreover, the temporal nature of the response (MSNA was unchanged during the initial 1–2 min of the fatiguing task but increased progressively thereafter) was characteristic of a slower-developing muscle metaboreflex (chemoreflex), rather than a mechanoreflex stimulated by force development (which would be expected to evoke sympathoexcitation at the start of contractions).

The present article by Sheel et al. (2001) represents a critical extension of this work by establishing that this presumed respiratory muscle-limb reflex has the ability, at least under resting conditions, to reduce significantly limb blood flow and vascular conductance. Thus, together with previous observations (St Croix et al. 2000), the present contribution provides compelling evidence for the existence of a metaboreflex, with its origin in the respiratory muscles, that can modulate limb perfusion via stimulation of sympathetic nervous system vasoconstrictor neurones (Fig. 1

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Here  some more feedback on a  mail I got after the above forum information. Why would a non involved   muscle or a  intercostal muscle placement add additional information.
 In short. With the non-involved   muscle we  may see a  systemic reaction  and than combined with the   actual involved muscle we can make further conclusion. If we add an intercostal muscle we  get even more  feedback  on  the bodies reaction due to  load  and overload   or as so often  mentioned : The limiter  and the compensator. or the Greece idea of Materialism ." unseen real  und  unreal seen"
 which is a basic principle of research. Is  what we see real  and the reason or is  the real reason not   seen in that information.

 In Prag  a very  far ahead of the classical idea group  with Jiri Dostal and Martin Dvorak  use this idea in depth. Here  the  confirmation , that it may be a very smart move  supported  by another group.


Related trends in locomotor and respiratory muscle oxygenation during exercise.

Legrand R1, Marles A, Prieur F, Lazzari S, Blondel N, Mucci P.

Author information

  • 1Laboratory of Human Movement Studies, Faculty of Sports Sciences and Physical Education, Lille University, Lille, France.

Abstract

PURPOSE:

We investigated the potential effect of respiratory muscle work on leg muscle oxygenation without artificial intervention in non-endurance-trained young subjects and searched for the range of intensity when this effect could occur.

METHODS:

We simultaneously monitored accessory respiratory and leg muscle oxygenation patterns with near-infrared spectroscopy (NIRS) in 15 healthy young men performing maximal incremental exercise on a cycle ergometer. Pulmonary gas exchange was measured. The respiratory compensation point (RCP) was determined. Oxygenation (RMO2) and blood volume (RMBV) of the serratus anterior (accessory respiratory muscle) and of the vastus lateralis (LegO2 and LegBV) were monitored with NIRS. The breakdown point of accessory respiratory muscle oxygenation (BPRMO2) and the accelerated (BP1LegO2) and attenuated fall (BP2LegO2) in leg muscle oxygenation were detected.

RESULTS:

BPRMO2 occurred at approximately 85% .VO2max and was related to RCP (r = 0.88, P < 0.001). BP2LegO2 appeared at approximately 83% .VO2max and was related to RCP (r = 0.57, P < 0.05) and with BPRMO2 (r = 0.64, P = 0.01). From BP2LegO2 to maximal exercise, LegBV was significantly reduced (P < 0.05).

CONCLUSION:

In active subjects exercising at heavy exercise intensities, we observed that the appearance of the accelerated drop in accessory respiratory muscle oxygenation-associated with high ventilatory level-was related with the attenuated fall in leg muscle oxygenation detected with near-infrared spectroscopy. This suggests that the high oxygen requirement of respiratory muscle leads to limited oxygen use by locomotor muscles as demonstrated in endurance-trained subjects. The phenomenon observed was associated with reduced leg blood volume, supporting the occurrence of leg vasoconstriction. These events appeared not only at maximal exercise but onward above the respiratory compensation point.

 

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