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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
Studies are spares ????
Not at all there  are many hundreds of studies in that directions  but many of them are  from Europe or Australia. So very often we see a trend, that what is not coming from our own country is often simply of non existence.
 What is spares is the  fact, that respiratory  training and reactions are looked upon a different way , than just  observing changes in VO2 max and lactate threshold.
 The critical question here is :
  ' What if, there is  no such thing like a lactate threshold. What if  lactate is not what it " used " to be  and it may in fact be a great metabolic marker  for other ideas  than  actually values of performance and or fatigue. ?
 What if we  actually can't use VO2  max as an absolute value., as we may have a problem to actually  test for VO2 max. Perhaps we test a maximal VO2 value at a give  day with a given protocol but even if we change the protocol slightly by increasing or decreasing step length we may have different VO2  max values.
 Or what happens when we change  altitude  and  look at VO2 Max  and so on. Once you have  a MOXY and you open up for some different options you will see, how respiration can change the bioavailablity of the oxygen (  influence of the O2 Diss. curve due to change in CO2 values.)
 You will very early on see, that you can change the SmO2 trends   with respiration, but only if the respiratory system is not working on a close to  its own limitation. As long you can " Play " with respiration you can play with Oxygenation. We showed  already many examples of this on this forum here  and in other discussions.
 Here some thoughts.
 a) If your physiological limitation is the ability to   create ATP with an optimal O2 supply ( mitochondria density ) than the ability to  supply more O2   with a great cardiac  or respiratory system is of little value, as the limitation was not the supply of O2 but rather the ability to use the supplied O2.
 B) on the other side if the respiratory system is  working on its limitation , than the  possibility of a  metaboreflex ( over CG )  will start to influence  not the use of O2  but rather the supply of O2.
 Wi5th MOXY we now have a tool, when proper . combine with other  bio marker to actually see, what may be limiting performance and what may try to compensate for performance.
  A influence of the metaboreflex or cardiac reflex is a reduce blood flow in the extremity muscles  and as such we will see a drop in tHb  at the moment   the limiter will kick in.
 The second reaction we can observe is the bioavailability  of O2  due to change in the CO2 situation ( O2 Diss curve shift).
 For MOXY users with Spiro tiger access you will see incredible nice reactions when using Spiro Tiger under load  to increase Pa  and PA and EtCO2  ( shift of the curve to the right and as an immediate result a drop in  The puls oxynmetrie SpO2 ( Don't' drop below 90 % )
 As such  the goal of respiratory training can't be to look at VO2 max change but rather on the  change in O2 use due to the ability to  have a much wider range of respiratory reactions.
 In the cardiac system we have CO = HR x SV  and we look at trends in HR or SV.
 In the respiratory assessment we have VE = RF x TV  where as RF  is like HR and TV is like SV.

Effects of respiratory fatigue on intercostal and on the forearm muscle oxygenation in CHF patients are attenuated with respiratory training

AC Nobrega et al performed the present study that tested the hypothesis that inspiratory muscle training (IMT) could attenuate the reduced intercostal and forearm muscles oxygenation during respiratory fatigue in pacientes with chronic heart failure (CHF) and inspiratory muscle weakness.

Study population consisted of 26 patients (10 women; mean age of 61 ± 14 yrs) with clinical stable heart failure (left ventricle ejection fraction: 36 ± 6%) and respiratory weakness, who were randomly assigned to either;
  • Inspiratory muscle training group (n=13, 5 women) or control (no training; n=13, 5 women).
All the enrollees underwent a respiratory muscles fatigue protocol (4-min step increase in inspiratory resistance up to fatigue), before and after respiratory training or control period. subsequently, researchers recorded the perceived exertion (0-10 scale), blood pressure, heart rate, cardiac output, capillary lactate concentration, minute volume, respiratory rate, arterial oxigen saturation (pulse oximetry) and end-tidal pCO2. In addition, muscle microvascular blood volume and oxygenation were continuously monitored by near infra red spectroscopy (NIRS) at the left 7th intercostal space and at the left forearm.

The resulting finding showed a 77% increase in the respiratory training upon peak inspiratory pressure (table 1, p<0.05).

Table 1:

Respiratory training

Blood lactate during fatigue


Stable Heart Failure Patients

controls

Before peak inspiratory pressure

60 cmH2O

41 ± 8%

40 ± 9%

After peak inspiratory pressure

106 cmH2O

34 ± 8%

41 ± 11%

P values

<0.05

<0.05

>0.05


Notably, either before or after respiratory training, the minute volume, respiratory rate, arterial oxygen saturation and end-tidal pCO2 remained unchanged during fatigue. Concomitantly, there was a less increase in the blood lactate during fatigue after training (table 1 above).

Regarding the NIRS data, intercostal muscle oxygen saturation decreased lesser during respiratory fatigue post-training while it remained unchanged in controls (table 2).

Table 1:

Intercostal Muscle Oxygen Saturation


Stable Heart Failure Patients

controls

Before peak inspiratory pressure

-15 ± 2%

-15 ± 3%

After peak inspiratory pressure

-4 ± 2%

-14 ± 2%

P values

<0.05

>0.05


A similar effect was observed in the forearm muscle (table 3). Deoxy-hemoglobin concentration in intercostal muscle increased less during respiratory fatigue after respiratory training (table 3). On the forearm, the same pattern was observed.

Table 3:

Forearm Muscle

Deoxy-hemoglobin concentration in intercostal muscle

 

Stable Heart Failure Patients

controls

Stable Heart Failure Patients

controls

Before peak inspiratory pressure

-4 ± 1%

-4 ± 1%

53 ± 8%

51 ± 9%

After peak inspiratory pressure

-0.3 ± 1%

-4 ± 1%

27 ± 3%

52 ± 15%

P values

<0.05

>0.05

<0.05

 

However, the heart rate, blood pressure, and cardiac output responses to fatigue remained unchanged by respiratory training.

In conclusion, these findings demonstrated the attenuated effects of respiratory fatigue on intercostal and also on forearm muscle oxygenation, reflexly, by respiratory training in CHF that was suggestive at a less intense stimulus for the activation of the respiratory metaboreflex.
 


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Are there medical publications  for respiration and training.
 Yes   here a  short list of some:
 http://www.idiag.ch/fileadmin/documents/stmedical/studien/Studienliste_STM_Page.pdf


and here  a list of publications including the metanalyses from UBC.
 http://www.idiag.ch/fileadmin/documents/spirotiger_sport/studien/2013-0516_ST_STM_Studienliste.pdf
Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
And here a question which may go with our other topic.
 The question being :
 Could it be, that  different physiological system  may interact with each other and support each other in case of limitation ?
 
Appl Physiol Nutr Metab. 2008 Jun;33(3):434-40. doi: 10.1139/H07-196.

Assessment of exercise capacity and respiratory muscle oxygenation in healthy children and children with congenital heart diseases.

Source

Faculte des sciences du sport, Universite de Picardie, Amiens, France. wassim.moalla@gmail.com

Abstract

Muscular and cardiorespiratory dysfunction contributes to exercise intolerance. Therefore, the aim of the present study was to characterize the cardiopulmonary response andrespiratory muscle oxygenation of children with congenital heart diseases (CHD) when compared with those of healthy children. Twelve children with CHD in New York Heart Association (NYHA) class II or III, and 14 healthy children participated in the study. All subjects performed conventional spirographic measurements and a cardiopulmonary exercise test on a cycle ergometer. Oxygen uptake (VO(2)), carbon dioxide production (VCO(2)), minute ventilation (VE), heart rate (HR), and power output were measured. Oxygenation of respiratory muscles was assessed by near-infrared spectroscopy (NIRS) during exercise and recovery. Pulmonary function was normal and no significant difference was found between groups. At rest, CHD patients had cardiorespiratory variables comparable with those of the healthy group. At submaximal intensity (ventilatory threshold) and at peak exercise, power output, HR, VO(2), VCO(2), and VE were significantly reduced (p < 0.01) in CHD patients. Respiratory muscles deoxygenated during exercise in both groups. However, deoxygenation was more pronounced in the CHD group than in the healthy children from an intensity of 40% up to exhaustion. Likewise, children with CHD showed a slower recovery of oxygenation than healthy children (113.4 +/- 17.5 vs. 74.6 +/- 13.0 s; p < 0.001). Compared with healthy children, these results demonstrated that children with CHD have reduced performance and present a defected exercise capacity. Children with CHD showed a more pronounced decrease of respiratory muscle oxygenation and slower recovery of oxygen kinetics.

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