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Juerg Feldmann

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 #1 
This thread will try to guide you through a very different idea on looking at assessments and performance..
 It is our personal view  , whcih got  developped over the last 30 plus years. With the integration of new technology and the open discussion on many of the classical models  , we see a great opportunity to open a new chapter for the coach on the road and the athlete to be able to add to the existing ideas some very new and different ideas.
 No posting on here either, as it will work as a kind of a handout for people getting into this ideas of assessment and testing.
Juerg Feldmann

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 #2 
A very different look, or the  difference between test and assessment.
In a test like VO2 max , or max HR, or Wingate and so on, we load the client up with different protocol ls with as it seem the idea to find out his optimal or perhaps maximal performance.
 This means that we take the client and see, where and how  he ends up  during the test.
 In an assessment we look at the development of the performance by  assessing the different systems and their contribution to the overall pe4rformance.
 Let's try to explain it with a picture and perhaps somebody can try to make a summary from the picture on how it comes over as an explanation of assessment.
Here we go :
This will create the simple idea of a team, where we have limitation ( limiter) and compensator.
As such we developed the idea of using some very great theories and name it ECGM
 Extended Central governor model.
 We will give you a daily dosage of this idea.
 The original paper is written by Andri Feldmann BSc from UBC Canada, BSc University of Bern and MSc  University of Bern. He is as well the project  coordinator of the  Research study he launched with MOXY
Here the abstract and the table of Content.

Running head: A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR

A comparison of the roles of a respiratory metaboreflex and a cardiac central governor in limiting exercise performance.

Bachelorarbeit

 

 am Institut fuer Sportwissenschaft der Universitaet Bern

Referent: Dr. Karen Zentgraf

Betreuerin: Dr. Karen Zentgraf

vorgelegt von Andri Feldmann Matrikel-Nr.: 10-114-338

Bern, Januar 2011

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 1

Abstract

This purpose of this meta-analysis is to compare the respiratory metaboreflex and the central governor theory in order to recognize similarities between the two. The two independent research groups have identified that performance limitation is not reserved merely to a classical model of peripheral limitations, but rather is mediated by a combination of feedback and feed forward loops that communicates a loss of homeostasis within any given physiological system. Thereby performance is very well limited by a self-protective mechanism that ensures the continued function of life vital systems, such as the respiratory or cardiovascular systems, during strenuous exercise where energy and oxygen delivery becomes compromised. Acknowledging the research of these groups a progression away from the classical physiological model must be made to accommodate the recent findings.

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 2

Table of Contents

Abstract……………………………………………………………………………… 1

1. Introduction………………………………………………………………… 4

2. Theory……………………………………………………………………….. 5

2.1 Archibald Hill and classical exercise physiology……………………….. 5

2.2 Central governor theory…………………………………………………. 6

2.2.1 Central Governor vs. the classical exercise physiology model…….. 7

2.2.2 Effects of the central governor in hypoxia…………………………. 9

2.2.3 Central governor involvement in the central nervous system………. 10

2.3 Respiratory metaboreflex…………………………………………………… 11

2.3.1 Traditional ideology………………………………………………… 11

2.3.2 Modern interpretation; respiratory metabolic reflex………………… 12

2.3.3 Respiratory training………………………………………………….. 14

3. Comparison……………………………………………………………………… 15

3.1 Common function…………………………………………………………… 15

3.2 Myocardial metaboreflex……………………………………………………. 16

4. Discussion……………………………………………………………………….. 17

4.1 Current dialogue…………………………………………………………….. 17

4.2 Maintaining homeostasis……………………………………………………. 19

4.3 Extended central governor………………………………………………….. 21

4.4 Relevancy of VO2max……………………………………………………… 23

5. Conclusion………………………………………………………………….. 24

A


Juerg Feldmann

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 #3 
here our first part of the  theory

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 4

University of Bern: Bachelors Thesis Disposition   ( Andri Feldmann )

A comparison of the roles of a respiratory metaboreflex and a cardiac central governor in limiting exercise performance.

1. Introduction

The purpose of this paper is to compare two independent physiological phenomenons, the central governor theory and actions of a respiratory metaboreflex, in an attempt to realize their individual and comparative nature and how they affect and or limit exercise performance. In doing so the position of both phenomenons becomes reinforced and a possible new direction for exercise physiology can be prepared. This literary investigation will compare previously published works that represent the given phenomenon to allow a reader to identify commonalities between them. The first phenomenon, the central governor theory, is the work of Professor Noakes and colleagues. The summation of Noakes‟ research and complementary studies present a strong argument against a classical peripheral limitations model of exercise physiology. Noakes and colleagues indicate that exercise is limited by the central nervous system‟s recruitment of motor units (2001). The second phenomenon, the respiratory metaboreflex, is the finding of Dempsey, Sheel, and colleagues. Dempsey and colleagues present a similar argument involving exercise limitation as a result of a respiratory metaboreflex (2002); an argument which is seconded by an alternate research group from ETH Zuerich, Boutellier and colleagues. . Both Noakes and Dempsey realize that exercise limitation transcends mere peripheral restrictions and entails all systems involved in creating and maintaining exercise. Examining the two phenomenons, maximum exercise performance becomes limited by the body‟s ability to maintain homeostasis. The loss of homeostasis at any given time indicates the point of limitation in exercise performance.

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 5

Thereby an argument can be made for a function within the central nervous system that controls homeostasis within the entire body and thereby actively limits exercise performance. Future training planning must then be controlled through the identification of homeostatic limitations and how to minimize these limitations through specific training.

Juerg Feldmann

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 #4 

2. Theory

2.1 Archibald Hill and classical exercise physiology

Identifying exercise physiology as a relatively new scientific field it is not at all an exaggerated statement when saying that one clear notion has dominated the exercise physiology field from its conception to the present day. This notion is that exercise is limited by the body‟s ability to intake and transport oxygen to the working muscle. As oxygen supply to working muscles dwindles, a possible result of numerous factors ranging from respiratory, cardiovascular, or metabolic enzyme activity, exercise intensity becomes limited and eventually ceases. Nobel Laureate Archibald Hill identified oxygen uptake and utilization as a limiting factor to maximum exercise performance in his work early in the 20

 

in century (1924). Since Hill‟s work a classical model of fatigue and performance has been established which dominates the exercise physiology field; exercise and peripheral work is limited by oxygen uptake and utilization. The domination of this idea can be witnessed not only in instructional or scientific literature or the establishment of training protocols, but perhaps more importantly in the method with which research is completed. The vast majority of exercise physiology literature, as well as other literature, that deals with exercise limitations utilize VO2max as a starting point and reference point for exercise
performance.
Juerg Feldmann

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 #5 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 6

2.2 Central governor theory

In numerous papers Professor Timothy Noakes and colleagues argue against the classical model and point out obvious flaws involved in a periphery limited performance model. By doing this Noakes identifies an independent model for exercise performance called the central governor theory. Noakes‟ theory originates from Hill‟s work as well and thereby Noakes points out the hypocrisy of self profiting choices that modern exercise physiologists have made to support personal theories while ignoring the rest of Hill‟s work. In his work Hill mentions that "lactic acid" accumulation and insufficient O2 supply are contributors to fatigue in skeletal muscle as the classical model propagates however, he also saw the possibility of exercise limitation resulting not from skeletal muscular fatigue but rather from a danger to cardiac or cerebral function through hypoxia or increased H+ concentration (Hill, Long & Lupton, 1924). Hill proposed the presence of a "governor" that would prevent cardiac and cerebral damage and thereby acting to control exercise intensity (1924). Thereby reading Hill‟s work it is clear where Noakes‟ theory originates, as well as the title of a central governor. Noakes picks up Hill‟s governor theory and expands his work through meta-analysis‟ of recent research and studies of his own.

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 7

Figure 1: The identification and reconstruction of the basic physiological models as seen by Noakes and colleagues. Model 1 is a representation of the classical peripheral limitation model and model 2 is a representation of Noakes modern central governor model

(Noakes, Calbet, Boushel, Sondergaard, Radegran, Wagner & Saltin, 2004, p. 997).

2.2.1 Central governor theory vs. the classical exercise physiology model

Noakes‟ central governor theory differentiates from the classical model in that it recognizes exercise limitation beyond peripheral performance and oxygen utilization. Noakes propagates that exercise limitation includes and is dominated by limitation to physiological systems that maintain life (Noakes, Peltonen & Rusko, 2001). In this Noakes states that the myocardium and or cardiovascular system limit exercise performance prior to reaching a maximal value of their own. This limitation acts as a defensive mechanism to prevent de-saturation of the myocardium and any damage associated with extended periods of high intensity exercise (Noakes et al., 2001). The intensity at which peripheral musculature performs is controlled by the central governor, which is, theorized to be located within the CNS. The central governor regulates exercise intensity through direct control of motor unit recruitment in the working

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 8

muscle (Noakes et al., 2001). With an increase in exercise intensity the demand for energy and the removal of metabolites increases. At some point the uptake and distribution of needed resources is compromised and a choice must be made where resources are sent. The central governor theory argues that at this point the choice is always made to supply the cardiac system at the cost of peripheral exercise output (Noakes et al., 2001). Thereby exercise performance becomes limited by cardiac function rather than the maximum ability to supply peripheral muscles with energy or oxygen as the classical model states. Noakes argues his point in numerous papers (Noakes et al, 2001, 2003, 2005). The logic of this kind of control is easily understood. Systems such as the cardiac system are vital to life; whereas peripheral musculature is not, and therefore, when considering life, keeping the cardiac system active is of greater importance than keeping the periphery active. Noakes goes on by investigating flaws in the classical model and how the central governor modal adequately explains these missteps.

Figure 2: Graphic representation of Noakes’ central governor theory

(Noakes et al., 2001, p. 3232). A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 9

The att. pic is a simple summary of  the CGM and the metaboreflex as we see it as the ECGM ( extended central governor model )


Juerg Feldmann

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 #6 
Intermezzo
 Here a short intermezzo to show you that Andri's  work  has some major back up from sources who where very long sceptically on the idea of Central governor and ECGM
 Here to enjoy
Look at carefully at the end of the  abstract. This  was presented  in London19-21 March 2012 London, UK pts

 

 


A life-time contribution to our understanding of the elite athlete

B. Saltin

CMRC, University of Copenhagen, Copenhagen, Denmark

Sports today are closely linked with sport science; a research field with roots in many early Nobel Prize winners’ work in physiology or

biochemistry with Hill being a key pioneer. The primary goal at the time was to understand basic functions of the human body during

exercise, and not the least providing answers to which organs or functions of the body that set a limit for human performance. Three

examples will be presented, hopefully demonstrating that it is worthwhile and challenging to study the basic mechanisms for human

performance and that the inclusion of elite athletes in this research adds crucial insights.

Human skeletal muscle plasticity. The potential for a marked elevation in mitochondrial capacity is similar in type 1 and 2 fibres of human

skeletal muscle. Usage of the two major motor units during the training is the critical factor. The triceps brachii muscle having the

highest relative percentage of type 2 fibres may reach as high a mitochondrial capacity as a muscle with a dominance of type 1 fibres,

as demonstrated in world class cc skiers. Thus, there is a clear dissociation between phenotype expressions of the contractile proteins as

compared with the proteins regulating energy metabolism. Humans may be quite different from other species where there is a closer link

between contractile and metabolic characteristics of the specific fibre types.

Muscle glycogen and fatigue. The link between the need for a large intake of carbohydrates to maintain large stores of glycogen in the

human body for good endurance performance has a long history. Only recently have these studies reached the subcellular level. Glycogen

granula are stored at different locations in a muscle fibre with two main sites around the mitochondria and close to the transverse tubuli

(TT) and the sarcoplasmic reticulum (SR). Both stores are crucial, but the one close to the TT and SR systems appears to be essential

not only to secure proper propagation of the action potential but also for the maintenance of the SR kinetics. With too low amounts of

glycogen, the reuptake of Ca2+ from the cytosol by the SR system is retarded and peak tension development reduced; a mechanistic

link, which is the same in both the main fibre types. It is worth highlighting that experimental evidence for the intake of ample amounts

of CHO playing a role for endurance has been available since the late 1800. However, it has taken more than a century to explain why

glycogen plays this crucial role.

Was Hill right or wrong? In 1923 Hill and Lupton wrote: “The volume of oxygen actually used by the heart is almost equal to that required

(but not obtained) by voluntary muscle during very violent exercise. The muscle has to stop, owing to oxygen want“.

A view heavily debated through the years up to our time without reaching a consensus. Our data demonstrate that Hill was right. When

elite cc skiers work either with their legs (roller skies on a treadmill), with their upper bodies (double pooling), or by using the ordinary

diagonal style (whole body exercise) it was demonstrated that in the latter exercise muscle blood flow and O2-delivery were markedly

reduced from peak levels, giving support to the notion once proposed by Hill that the heart was unable to deliver the blood flow that the

muscles were asking for.

What is the value of the above given findings? Primarily they serve as tools in the understanding of regulations and limitations of basic

human functions. They may also be of some interest to the “curious” athlete or coach, but they are hardly of any “help” in the athlete’s

preparations to reach Olympic level performance.

Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #7 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 9

2.2.2 Effects of the central governor in hypoxia

In order to examine the central governor theory and the flaws of the classical model closer Noakes looks at extreme situations to see how the body reacts. Studies in modified oxygen partial pressure identify that cardiac output and VO2max measured in hypoxic conditions is always submaximal when compared to normoxic values. Sutton, Reeves, and colleagues recorded a steady decrease in cardiac output with increasing hypoxia in extreme altitude simulation (1988) and in accordance to the central governor theory they indentify that "one might speculate that under extremes of hypoxia, muscle may become less competitive in its demand for blood flow than other hypoxic tissues" ( 1988, p. 1319). The decrease in cardiac output with increasing hypoxia does not support the classical model of peripheral limitation. "If the heart is merely a slave to the skeletal muscle, the [max cardiac output] should be the same during maximal exercise in both hypoxia and normoxia since the heart‟s sole function is to maximize oxygen delivery to the hypoxic skeletal muscles" (Noakes et al., 2001, p. 3227). Because of the oxygen de-saturation with increasing hypoxia the central governor limits the muscular performance to maintain PO2 values. Therefore reduced cardiac output is the result of rather than the cause of reduced VO2max seen in hypoxia. The fall in cardiac output seen in hypoxic conditions is a paradoxical situation when considering the classical modal. Even during chronic hypoxic exposure, which involves specific anemic adaptations that increase pulmonary and muscular oxygen diffusive capabilities and transportation, max cardiac output remains sub-maximal when comparing to normoxic values (Noakes et al., 2001). This furthers the paradoxical nature of the classical model which would dictate a maximal cardiac output to maximize peripheral output. However, the sub-maximal cardiac output in hypoxia is only paradoxical in accordance to the classical modal. The central governor theory would indicate that the decrease in cardiac output is a regulatory function of the central governor to

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 10

maintain function; "parallel upward adjustments in both pulmonary and muscle 02 diffusive transport conductance, at very high cardiac output would cause substantial arterial de-saturation and also impair muscle 02 extraction… the reduced cardiac output max during acute hypoxia would be physiologically beneficial" (Noakes et al., 2001, p. 3229).

Juerg Feldmann

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 #8 

.2.3 Central governor involvement in the central nervous system

Noakes‟ central governor functions within the central nervous system to control motor unit recruitment in working muscles. Through this the central nervous system can directly influence performance in order to ensure exercise does not exceed dangerous levels. This premise is a defining characteristic in Noakes‟ theory. Noakes argues that if the periphery limit exercise performance as the classical model says it does, max performance should be represented by 100% motor unit recruitment in the given muscle or muscle groups (Noakes, Gibson & Lambert, 2005). The fact that motor recruitment in working muscles never reaches 100% indicates another paradox in the classical modal and favors Noakes‟ central governor theory. The inability of reaching 100% motor unit recruitment indicates that some other system is limiting potential motor unit recruitment before a maximum is reached (Noakes et al., 2005). The classical modal gives no reasonable explanation for this. Similar findings are presented during exercise in hypoxic conditions (Noakes et al. 2005). Finally, according to the classical model, lowered exercise performance in hypoxic conditions must come from a decreased ability in the periphery to generate force. However, Kayser and colleagues (1994) and Peltonen and colleagues (1997) identify that the typical sign for neuromuscular fatigue, an increase in integrated electromyogram data, is no presented during hypoxia. Therefore an increased neuromuscular output must be hindered by an alternate source.

Juerg Feldmann

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 #9 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 11

2.3 Respiratory Metaboreflex

2.3.1 Traditional ideology

Respiratory limitation during exercise has long been considered non-existent. Research data has shown that this notion must be re-evaluated as for the arguments that assume respiration to be a non-limiting factor. The two key points used to argue respiration as a non-limiting factor are:

1) Ventilation at a maximal workload never reaches maximum voluntary ventilation; and 2) even untrained subjects are able to hyperventilate while performing exercise at intensities above the anaerobic threshold. (Boutellier, 1997, p. 1169).

Identifying these two arguments Boutellier goes on to discuss their unconvincing positions and therefore a need to re-evaluate the entire premise. The first point is not applicable to real world exercise. Exercise bouts are never restricted to mere ventilatory work, nor are they restricted to short time frame as dictated by a maximum voluntary ventilation test (MVV). If a MVV test was extended in duration the given ventilation would decrease with duration as well (Boutellier, 1997). The second point, as proclaimed by Boutellier, "is more valid and more difficult to oppose" (Boutellier, 1997, p. 1169). However, as in the indicated paper and in numerous continued works by Boutellier and colleagues, which identify the exercise limiting potential of the respiratory system, the argumentative value of the second point is limited by its complexity to analyze rather than scientific premise.

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 12

2.3.2 Modern interpretation; respiratory metabolic reflex

The exercise limiting potential of the respiratory is broken down by Dempsey and colleagues, who identify the cause and effect of fatiguing respiratory muscles. During strenuous prolonged exercise respiratory muscle fatigue which, as a result of metabolite accumulation (Sheel, Derchak, Morgan, Pegelow, Jacques & Dempsey, 2001), triggers a respiratory metaboreflex which causes re-distribution of blood flow by the sympathetic nervous system using vasoconstrictor neurons (Sheel, 2001). This forced re-distribution of blood flow through respiratory fatigue is a relevant limiting factor in maximal exercise performance and is investigated to a great extend by Dempsey and colleagues. A self protective mechanism is a plausible explanation for these actions. A respiratory metaboreflex would ensure oxygen and energy delivery to the respiratory muscles, which in turn maintains proper pulmonary ventilation vital for continued life. Work by Dempsey and colleagues investigate the function and origin of the metaboreflex in numerous published papers clearly identifying its impact on the working body; "It appears that limb muscles in both exercising humans and dogs are susceptible to sympathetically mediated vasoconstriction from a metaboreflex originating in respiratory muscle" (Sheel, Iellamo, Raven & Wurster, 2006, p. 371). Interesting is the temporal nature of the response. No change in muscle sympathetic nerve activity is recorded in the initial 2 minutes of the fatiguing exercise. Rather a progression could be recorded as the duration of the exercised increased (Sheel, 2001). This indicates that the metaboreflex does actual function as a result of metabolite accumulation or progression (chemoreflexors). Thereby a theoretical flow chart can be constructed on the basis of Dempsey‟s work (Figure 3). During prolonged strenuous exercise the respiratory muscles fatigue and metabolites accumulate which trigger the metaboreflex resulting in group III/IV phrenic afferent discharge (Dempsey, Sheel, St. Croix & Morgan, 2001). Through the central nervous system

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 13

a sympathetic efferent discharge responds to the situation in the respiratory system which activates the peripheral vasoconstrictors reducing blood flow to the working muscle (Dempsey, 2001). This changes the distribution of blood flow to favor the respiratory system ensuring that during strenuous exercise, which creates excessive metabolite accumulation, oxygen and energy delivery to the respiratory system is maintained (Dempsey, 2001). Having stated this, it is clear that through this process the respiratory system becomes a legitimate limiting factor to maximum performance as it actively re-distributes blood flow away from working muscles to the respiratory system. In this maximum peripheral performance is limited by the respiratory system‟s ability to maintain itself and thereby, as discussed above, is a paradoxical reaction to the classical peripheral limitation model."

The pic below  shows the flow chart on the left side and adds the information we can find, when looking at NIRS trends in tHb combined with respiratory and cardiac information  to understand drop in tHb during a load.
3: Theoretical flowchart of the functioning respiratory metaboreflex

 

 

 

 

Attached Images
Click image for larger version - Name: NIRS_AND_METABO.jpg, Views: 70, Size: 37.22 KB 

Juerg Feldmann

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 #10 

2.3.3 Respiratory training

At peak rates the metabolic cost of the respiratory system is estimated at 16% of total cardiac output (Harms, Wetter, St. McClarn, Pegelow, Nickele, Nelson, Hanson & Dempsey, 1998) and with progressive respiratory unloading an increase in endurance performance can we see up to 15% (Harms, Wetter, St. Croix, Pegelow & Dempsey, 2000). Similar results were also made by Boutellier and colleagues. Boutellier, Spengler, and colleagues identified, to a greater extent than Dempsey and colleagues, the performance enhancing effect of respiratory training. As Dempsey, Boutellier identifies a redistribution of blood flow as the responsible factor for the deteriorating effect of fatigued respiratory muscles. In numerous papers Boutellier and colleagues go on to identify the beneficial effects of isolated respiratory training on exercise performance for both untrained and trained individuals (1992, 1997). Dempsey and colleagues also says that unloading or "relieving much of the inspiratory and expiratory muscle work during heavy, whole body exercise… will cause vasodilatation and increased blood flow to the working limb, even in the face of a reduced cardiac output and unchanged arterial blood pressure" (Derchak, 2002, p. 1551). The positive effects of isolated respiratory training can be attributed to numerous physiological changes, with obvious super compensating effects that take place in the respiratory muscles as seen in any other skeletal musculature (Derchak, 2002). However, both Dempsey and Boutellier, recognize that the most beneficial change that is associated with respiratory training is a postponement or de-sensitization of the respiratory metaboreflex. If the activation of the metaboreflex can be delayed because of the respiratory muscles own enhanced performance, the re-distribution of blood away from the working muscles can be delayed allowing an extended or increased performance output (Seals, n.d.). Considering this information and the idea of enhanced athletic performance, the potential of respiratory training revolves to a greater extent around A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 15

delaying a metaboreflex during exercise than the actual increase in ventilatory capacity, in a hope of maintaining blood flow to the working muscle.

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #11 
Here  our take since many years of now more and more accepted ideas. See our old picture of ECGM

And here a great abstract from one of the big names in exercise physiology . Read and compare to the picture.

"

A life-time contribution to our understanding of the elite athlete

B. Saltin

CMRC, University of Copenhagen, Copenhagen, Denmark

Sports today are closely linked with sport science; a research field with roots in many early Nobel Prize winners’ work in physiology or

biochemistry with Hill being a key pioneer. The primary goal at the time was to understand basic functions of the human body during

exercise, and not the least providing answers to which organs or functions of the body that set a limit for human performance. Three

examples will be presented, hopefully demonstrating that it is worthwhile and challenging to study the basic mechanisms for human

performance and that the inclusion of elite athletes in this research adds crucial insights.

Human skeletal muscle plasticity. The potential for a marked elevation in mitochondrial capacity is similar in type 1 and 2 fibres of human

skeletal muscle. Usage of the two major motor units during the training is the critical factor. The triceps brachii muscle having the

highest relative percentage of type 2 fibres may reach as high a mitochondrial capacity as a muscle with a dominance of type 1 fibres,

as demonstrated in world class cc skiers. Thus, there is a clear dissociation between phenotype expressions of the contractile proteins as

compared with the proteins regulating energy metabolism. Humans may be quite different from other species where there is a closer link

between contractile and metabolic characteristics of the specific fibre types.

Muscle glycogen and fatigue. The link between the need for a large intake of carbohydrates to maintain large stores of glycogen in the

human body for good endurance performance has a long history. Only recently have these studies reached the subcellular level. Glycogen

granula are stored at different locations in a muscle fibre with two main sites around the mitochondria and close to the transverse tubuli

(TT) and the sarcoplasmic reticulum (SR). Both stores are crucial, but the one close to the TT and SR systems appears to be essential

not only to secure proper propagation of the action potential but also for the maintenance of the SR kinetics. With too low amounts of

glycogen, the reuptake of Ca2+ from the cytosol by the SR system is retarded and peak tension development reduced; a mechanistic

link, which is the same in both the main fibre types. It is worth highlighting that experimental evidence for the intake of ample amounts

of CHO playing a role for endurance has been available since the late 1800. However, it has taken more than a century to explain why

glycogen plays this crucial role.

Was Hill right or wrong? In 1923 Hill and Lupton wrote: “The volume of oxygen actually used by the heart is almost equal to that required

(but not obtained) by voluntary muscle during very violent exercise. The muscle has to stop, owing to oxygen want“.

A view heavily debated through the years up to our time without reaching a consensus. Our data demonstrate that Hill was right. When

elite cc skiers work either with their legs (roller skies on a treadmill), with their upper bodies (double pooling), or by using the ordinary

diagonal style (whole body exercise) it was demonstrated that in the latter exercise muscle blood flow and O2-delivery were markedly

reduced from peak levels, giving support to the notion once proposed by Hill that the heart was unable to deliver the blood flow that the

muscles were asking for.

What is the value of the above given findings? Primarily they serve as tools in the understanding of regulations and limitations of basic

human functions. They may also be of some interest to the “curious” athlete or coach, but they are hardly of any “help” in the athlete’s

preparations to reach Olympic level performance.

Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements.


During the same meeting in London this great summary on the second "TEAM MEMBER:
  "

 

 

 

Pulmonary system limitations to endurance exercise performance in humans

 

 

 

M. Amann

 

 

Internal Medicine, University of Utah, Salt Lake City, UT, USA

 

 

 

Accumulating evidence over the past 25 years depicts the healthy pulmonary system as a limiting factor of whole body endurance

 

 

exercise performance. This brief overview emphasizes three respiratory system-related mechanisms which impair O2 transport to the

 

locomotor musculature [arterial O2 content (CaO2) x leg blood flow (QL)], i.e. the key determinant of an individual’s aerobic capacity and

 

 

 

ability to resist fatigue. First, the respiratory system often fails to prevent arterial desaturation substantially below resting values and

 

 

thus compromises CaO2. Especially susceptible to this threat to convective O2 transport are well-trained endurance athletes characterized

 

 

 

by high metabolic and ventilatory demands and, likely due to anatomical and morphologic gender differences, active females. Second,

 

fatiguing respiratory muscle work (Wresp) associated with strenuous exercise elicits sympathetically-mediated vasoconstriction in limbmuscle

 

 

vasculature which compromises QL. This impact on limb O2 transport is independent of fitness level and affects all individuals,

 

 

 

however, only during sustained, high-intensity endurance exercise performed above ~85% VO2max. And third, excessive fluctuations in

 

intrathoracic pressures accompanying Wresp can limit cardiac output and therefore QL. Exposure to altitude exacerbates the respiratory

 

 

system limitations observed at sea level and further reduces CaO2 and substantially increases exercise-induced Wresp. Taken together,

 

the intact pulmonary system of healthy endurance athletes impairs locomotor muscle O2 transport during strenuous exercise by failing

 

 

 

to ensure optimal arterial oxygenation and compromising QL. This respiratory system-related impact exacerbates the exercise-induced

 

development of fatigue and compromises endurance performance.

 

 

Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements.


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #12 
Now there are different opinions on this ideas and I do not like to keep them out of here.
   here a short inside view :
 
LUNG TRAINING DEVICES Quote | Reply

Does anyone have any experience with using these devices? I have been using a Powerlung(r) for a few weeks, and have been able to increase the resistance level 2 or 3 times so far. But, I haven't been keeping sufficient records to analyze any improvements in my swim/bike/run times. What do you think? Am I wasting my time and money?

nosmo king

Apr 16, 03 13:19

Post #2 of 9 (2360 views)
Re: LUNG TRAINING DEVICES [tri_bri2] [In reply to] Quote | Reply

Since everyone on this site seems to be pretty opinionated, am I safe to assume I am the only one using one of these things?

Kevin in MD

Apr 17, 03 7:24

Post #3 of 9 (2307 views)
Re: LUNG TRAINING DEVICES [tri_bri2] [In reply to] Quote | Reply

We have studied these where I work.

We've found that resisted breathing makes you more comfortable and effective at resisted breathing.

We haven't found any gains in performance in from training with them. Real honest to goodness papers, but not available to the public.

It is the opinion of the physiologist here that the diaphragm isn't a limiter in athletic performance.

I suspect that the powerling folks disagree with the opinion.

Ed Reid

Apr 17, 03 8:19

Post #4 of 9 (2285 views)
Re: LUNG TRAINING DEVICES [tri_bri2] [In reply to] Quote | Reply

I've not tried these devices, but my 2 cents is that using aerobic training (speed work) to increase hemocrit levels would be a lot more beneficial.

The blood can only absorb a limited amount of oxygen. Most of the oxygen that you breathe in is not used and is breathed out. This is why you can give someone mouth–to-mouth resuscitation. For the same reason, giving athletes pure oxygen at a football game is mostly a nice gesture. They can breathe easier, but significantly more oxygen is not being absorbed. Most of the benefit is psychological, not physiological.

Philbert

Apr 17, 03 9:13

Post #5 of 9 (2260 views)
Re: LUNG TRAINING DEVICES [tri_bri2] [In reply to] Quote | Reply

Lung training devices are a sham, pure and simple. The diaphragm (and the smaller muscles that can assist when you are REALLY breathing hard, i.e. in the middle of an asthma attack) are in no way, shape or form a limiter to respiration in a normal human being. Stop by the library and pick up a phys book...it will explain that when your circulatory system is maxed out, as is the transport of O2 across the lungs and into the blood, there is still plenty more 02 hanging around in your lungs that is going unused.

Frank Day, who is an anesthesiologist as well as PC guy, could probably give you an in depth explanation off the top of his head, which I can't at the moment. I'd return the damn thing and ask for your money back, because those clowns are preying on people's poor understanding of respiratory physiology.

For what it is worth, in rehabilitation medicine we often do "pulmonary rehab" for people with extensive lung disease. These people constantly feel that they cannot breathe due to lifelong smoking, etc ad nauseum. While treatment reduces their subjective FEELING of being out of breath, rehab has NEVER been shown to improve anyone's actual function (i.e. the measurable numbers).

Sorry if I rained on anyones parade,

Philbert.
Dr. Philip Skiba
PhysFarm Training Systems
Coaching, Consulting and Technology for World Champions, and You.
Dr. Phil's Books available here

Frank Day

Apr 17, 03 10:43

Post #6 of 9 (2244 views)
Re: LUNG TRAINING DEVICES [Philbert] [In reply to] Quote | Reply

these devices go to peoples observations that upon close scruitiny make absolutely no sense. A person gets out of breath and it makes sense that improving the breathing muscles will make a difference. Nice thought but it will NEVER happen. We get out of breath when we start developing lactate at the exercising muscles. Lactate is buffered by the bicaarbonate system in the blood, the biy product of this buffering is CO2, lots of it per ATP produced. This huge amount of CO2 "production" overwhelms the lungs ability to expel it and a little bit of breathing muscle improvement will not change anything. Further, even if one were able to do this to these muscles, improvement would be limited by the development of turbulent flow in the upper respiratory tract.

So, while it makes sense on the surface to the uninformed, it is unlikely to have ANY effect in practice.

Frank
--------------
Frank,
An original Ironman and the Inventor of PowerCranks


(This post was edited by Frank Day on Apr 17, 03 11:53)


Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #13 
I like this first section of the explanation .

Don't feel stupid. None of us can have knowledge of everything. Even "experts" can differ in recommendations derived from the same data.  Frank Day.


So here some of a small section on the discussion on respiratory ideas..
 Based on the above  forum discussion   we may have a lot of "stupid"   ????? Researchers below

 

 

Effects of different respiratory muscle training regimes on fatigue-related

variables during volitional hyperpnoea

Samuel Verges, Andrea S. Renggli, Dominic A. Notter, Christina M. Spengler

Exercise Physiology, Institute for Human Movement Sciences, ETH Zurich, and Institute of Physiology and Center for Integrative Human Physiology (ZIHP),

University of Zurich, Zurich, Switzerland

a r t i c l e i n f o

Article history:

Accepted 7 September 2009

Keywords:

Respiratory muscle endurance training

Hyperpnoea

Respiratory muscle fatigue

Respiratory sensations

a b s t r a c t

We compared the effects of the most commonly used respiratory muscle (RM) training regimes: RM

endurance training (RMET; normocapnic hyperpnoea) and inspiratory resistive training (IMT), on RM

performance. Twenty-six healthy men were randomized into 3 groups performing 4 weeks of RMET, IMT

or sham-training. Lung function, RM strength and endurance were tested before and after training. RM

fatigue during intermittent hyperpnoea was assessed by twitch oesophageal (Poes,tw) and gastric pressures

with cervical and thoracic magnetic stimulation. Respiratory sensations (visual analogue scale, 0–10) and

blood lactate concentrations ([La]) were assessed during hyperpnoea.RMETincreased maximal voluntary

ventilation while IMT increased maximal inspiratory pressure. Both RMET and IMT increased vital capacity

and RM endurance, but only RMET improved the development of inspiratory muscle fatigue (from

31% to 21% Poes,tw), perception of respiratory exertion (4.2±0.1 to 2.3±2.3 points) and [La] (1.8±0.4

to 1.3±0.3mmoll1) during hyperpnoea. Whether these specific RMET-induced adaptations observed

during hyperpnoea would translate into greater improvements in exercise performance compared to IMT

remains to be investigated.

© 2009 Elsevier B.V. All rights reserved

 

The Biomedical Basis of Elite Performance

19-21 March 2012

London, UK

Pulmonary system limitations to endurance exercise performance in humans

M. Amann

Internal Medicine, University of Utah, Salt Lake City, UT, USA

Accumulating evidence over the past 25 years depicts the healthy pulmonary system as a limiting factor of whole body endurance

exercise performance. This brief overview emphasizes three respiratory system-related mechanisms which impair O2 transport to the

locomotor musculature [arterial O2 content (CaO2) x leg blood flow (QL)], i.e. the key determinant of an individual’s aerobic capacity and

ability to resist fatigue. First, the respiratory system often fails to prevent arterial desaturation substantially below resting values and

thus compromises CaO2. Especially susceptible to this threat to convective O2 transport are well-trained endurance athletes characterized

by high metabolic and ventilatory demands and, likely due to anatomical and morphologic gender differences, active females. Second,

fatiguing respiratory muscle work (Wresp) associated with strenuous exercise elicits sympathetically-mediated vasoconstriction in limbmuscle

vasculature which compromises QL. This impact on limb O2 transport is independent of fitness level and affects all individuals,

however, only during sustained, high-intensity endurance exercise performed above ~85% VO2max. And third, excessive fluctuations in

intrathoracic pressures accompanying Wresp can limit cardiac output and therefore QL. Exposure to altitude exacerbates the respiratory

system limitations observed at sea level and further reduces CaO2 and substantially increases exercise-induced Wresp. Taken together,

the intact pulmonary system of healthy endurance athletes impairs locomotor muscle O2 transport during strenuous exercise by failing

to ensure optimal arterial oxygenation and compromising QL. This respiratory system-related impact exacerbates the exercise-induced

development of fatigue and compromises endurance performance.

Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements.

Fatiguing inspiratory muscle work causes reflex reduction

in resting leg blood flow in humans

A. William Sheel, P. Alexander Derchak, Barbara J. Morgan *,

David F. Pegelow, Anthony J. Jacques and Jerome A. Dempsey

Department of Population Health Sciences, John Rankin Laboratory of Pulmonary

Medicine and * Department of Surgery, University of Wisconsin-Madison, Madison,

WI, USA

(Received 20 April 2001; accepted after revision 12 July 2001)

1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a

time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al.

2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow

also accompany inspiratory muscle fatigue.

2. In six healthy human subjects at rest, we measured leg blood flow («QL) in the femoral artery

with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while

subjects performed two types of fatiguing inspiratory work to the point of task failure

(310 min). Subjects inspired primarily with their diaphragm through a resistor, generating

(i) 60 % maximal inspiratory mouth pressure (PM) and a prolonged duty cycle (TI/TTOT = 0.7);

and (ii) 60 % maximal PM and a TI/TTOT of 0.4. The first type of exercise caused prolonged

ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm

with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of

contraction. End-tidal PCO2 was maintained by increasing the inspired CO2 fraction (FI,CO2) as

needed. Both trials caused a 2540 % reduction in diaphragm force production in response to

bilateral phrenic nerve stimulation.

3. «QL and LVR were unchanged during the first minute of the fatigue trials in most subjects;

however, «QL subsequently decreased (_30 %) and LVR increased (5060 %) relative to control

in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery,

the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +413 mmHg)

and heart rate (+1620 beats min_1) increased during fatiguing diaphragm contractions.

4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by

increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or

inspiratory flow rate (5 w eupnoea), «QL, MAP and LVR were unchanged; although continuing

the high force output trials for 3 min did cause a relatively small but significant increase in

LVR and a reduction in «QL.

5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance,

LVR was reduced and «QL increased significantly; these changes were attributed to the negative

feedback effects on MSNA from augmented tidal volume.

6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect

on «QL and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in «QL

and increases in LVR. We attribute these changes to a metaboreflex originating in the

diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #14 

3. Comparison

3.1 Common function

The two physiological phenomenon investigated above would represent an evolutionary mechanism that ensures the function of life vital systems (respiration and cardiovascular) during strenuous exercise; perhaps with an exception during life threatening circumstances (fight or flight). It is clear that circumstances exist where, due to extraordinary stimuli, a human being would be permitted to act at maximal performance even if this created a dangerous situation for the homeostasis of the being. With the exception of these extraordinary events the physiological nature of both mechanisms are to regulate the supply of oxygen and energy to their corresponding systems by limiting skeletal muscle activity. According to the evidence provided so far and the theories of the given researchers the two mechanisms appear to function slightly different, even though the goal is the same. The respiratory metaboreflex described by Dempsey activates peripheral vasoconstrictors to limit blood flow to working muscle. The central governor, as described by Noakes, (even though Noakes does not state in specifics how the central nervous system would act) functions through the central nervous system and limits motor unit recruitment and thereby limits working muscle performance. However, acknowledging the complexity of human physiology the process by which the body regulates and limits peripheral performance can be attributed to other processes.

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #15 

3.2 Myocardial metaboreflex

As with the respiratory metaboreflex, there are indications that a myocardial metaboreflex may act in a similar way to regulate peripheral work favoring blood flow to the myocardium when energy or oxygen delivery is compromised; as identified by Ansorge and colleagues "coronary vascular response to muscle metaboreflex activation was dependant on whether substantial increase in myocardial O2 demand occurred" (2002, p. 532). Metabolite accumulation trigger metabolic reflexes which release group III/IV phrenic afferent discharge thereby communicating with the central nervous system. A sympathetic efferect discharge then activates peripheral vasoconstrictors re-distributing blood flow away from the working muscle and thereby favoring the myocardium (Ansorge, Augustyniak, Perinot, Hammond, Kim, Sala-Mercado, Rodriguez, Rossi & O‟Leary, 2004). Metabolic reflexes communicate information in feedback/forward loops in any system and therefore what Ansorge is describing as a myocardial metaboreflex is very similar to Dempsey‟s respiratory metaboreflex. Metabolite accumulation in both systems (cardiovascular and respiratory) and in peripheral working muscle communicates with the central nervous system, as if continuously updating metabolic status. Through this the central nervous system can control blood flow and motor unit recruitment in order to optimize performance. Considering Ansorge and colleagues‟ work and comparing it to Noakes‟ central governor theory it is very conceivable that the cardiac system limits exercise performance as Noakes propagates. How the central nervous system directly activates both regulatory metabolic reflexes can be further discussed, nonetheless it appears that both function as a metabolic response which communicates through the central nervous system to alter blood distribution and ultimately change motor unit recruitment in order to prevent an overload in a given system. This would again describe a defensive mechanism. Further evidence for a cardiac metaboreflex as a

 

A COMPARISON OF THE RESPIRATORY METABOREFLEX AND A CARDIAC CENTRAL GOVERNOR 17

defensive mechanism to protect the myocardium is noted in studies performed with patients recovering from chronic heart failure. Patients with chronic heart failure realize a "heightened metaboreflex activation, when confronted causes an exaggerated vasoconstriction during exercise" (Piepoli & Coats, 2007, p. 494). Similar limitations in the myocardium are documented in dogs with induced heart failure. "In dogs with heart failure, cardiac dysfunction likely prevents the normal elevation in cardiac output observed with muscle metaboreflex activation" (Ansorge, 2004, p. 1381). Ansorge and colleagues show that a balance between metaboreflex induced sympathetic nervous system activity to the heart and vasodilator and or vasoconstrictor activation exists (2004). Ansorge‟s work again shows a strong relationship between nervous system activity and performance limitations as Noakes hypothesizes. Ansorge and Noakes present a similar function in the cardiac system. Comparing then Ansorge work directly to Dempsey‟s work a triangular assertion can be made that links all three parties work to strengthen each individual‟s findings. Therefore similarity of the two documented theories, the central governor theory (or a cardiac metaboreflex shown by Ansorge et al.) and respiratory metaboreflex must be noted and, more importantly, together strengthen a modern position that argues against the classical model of exercise performance.

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