neural restitution

[incognito]

Efter en BB-style træningssession (split-dage, forced reps, negativer osv) har jeg DOMS i 3-4 dage. Hvor lang tid går der før mit nervesystem er oppe og køre igen efter en sådan træning? Nogen der har links til et godt paper eller pubmed på emnet? Jeg går nemlig og skumler med noget HIT-træning (hvis ikke den nuværende omgang HST sparker røv), så alle inputs er velkomne.

Edited January 25, 2003 by incognito

[Henning]

Vid ikke med dit nervesystem...

men mit er tilsyneladende længe om det, måneder måske, ellers havde jeg vel nået mine 100 kg. i bæmkpres.

Henning

[incognito]

hehe.... ja, jeg kender det godt.

jeg har jo trænet med BB'ernes infamøse 4-6 split og masser af negativer og forced reps, iøvrigt med relativ stor fremgang i perioder. Men jeg vil prøve det her HIT ting og der skal man jo bare helst vide, hvor lang tid der går før man kan fyre den af igen. Og med at fyre den af mener jeg ikke nødvendigvis forced reps og negativer, men mere end 2-4 sæt til den/de aktuelle kropsdel(e) (hvilket iøvrigt osse er nok til at give mig DOMS i 3-4 dage) per dag som i HST (ovs - det blev en mærkelig sætning, håber den virker).

Så jeg håber at MZ, TJ eller en anden kigger forbi, siger noget klogt og kaster et par pubmed links af sig.

[incognito]

Nu behøver det ikke være pub med links. Men så mange af de programmer, som de omtales herinde er baseret på en idé om, at nervesystemet skal restituere. Nu tror jeg ikke at idéen er opstået fordi en eller psykopatløfter har sagt "hrm... det kan sgu ikke være mine muskler det stopper mig. Så må det være nerverne!", men fordi der foreligger et velfunderet arbejde. Jeg vil bare gerne se det - så er der nogen, der kan fortælle mig om nogle papers, hvor der findes noget om det?

[Thomas J]

Incog> jeg tror du vil få svar på en masse spørgsmål ved at læse nedenstående.....

"Exercise Physiology 552 (1997) Brief Review:

Is Fatigue a Necessary Requirement for Adaptation to a Strength Training Program?

by Tom Chickonoski

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Background Knowledge

Fatigue is viewed by sports scientists and professionals as the main restrictive element of human performance (Bompa, 1990). Researchers have attempted to simplify a complex phenomena with many unknown factors resulting in fatigue and performance failure narrowing the sites to neuro-muscular and metabolic (Bompa, 1990). Fatigue can be viewed as the adaptations that muscles and motor neurons exhibit (McComas, 1996). Fatigue can be seen as the adaptations involving motor neuron firing, sodium and potassium pumping (McComas, 1996). The loss of muscle force which characterises fatigue can be viewed as an adaptation as without it serious muscle damage can occur (McComas, 1996). Fatigue consists of central and peripheral nervous system components in addition to biochemical changes in muscle fibers (McComas, 1996). Fatigue is the consequence of physical work and as a result reduces the capacity of the metabolic and neuro-muscular systems to continue physical activity (Bompa, 1990).

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Learning Objectives

This assignment will discuss the various components that are cited as sources of fatigue, in particular, central fatigue, peripheral fatigue and the biochemical changes that may contribute to fatigue. The importance of recovery and its relationship to fatigue will be discussed. Finally, the clinical implications of fatigue and our responsibilities as sports physiotherapists in organising training programs will be discussed.

Ý

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New Knowledge

Fatigue is defined as the decline in muscle tension capacity with repeated stimulation (McArdle et al, 1996). Fatigue can be generally defined as any reduction in physical or mental performance (McComas, 1996). A more specific definition of muscle fatigue is the failure to maintain a required or expected force (McComas, 1996). The definition can be broadened to include an inability to sustain rapidly executed movements and it is probable that the most important component may be the reduction in the intensity of the commands developed in the central nervous system (McComas, 1996). The rate of fatigue depends on the muscles recruited and whether or not the contractions are intermittent or continuous (McComas, 1996). To fully understand muscle fatigue, the site of fatigue and the cellular factors involved must be determined (McComas, 1996).

Central Fatigue

Reduced motor unit recruitment and/or impaired firing rate modulation present during fatiguing exercise is referred to as central fatigue (Miller et al, 1995). Any negative changes in muscular activation which is proximal to the point of stimulation of the motor nerve is viewed as central (Miller et al, 1995). The Central Nervous System (CNS) is involved to a large extent in the limitation of performance and the production of fatigue (Bompa, 1990). Excitation and inhibition are the two main processes of the CNS (Bompa, 1990). Excitation is the favourable and stimulating process required for physical activity, while inhibition is the restraining process (Bompa, 1990).

A constant alternation of excitation and inhibition occurs throughout training (Bompa, 1990). To stimulate, the CNS will send a nerve impulse to the working muscle resulting in muscle contraction and work performance (Bompa, 1990). The frequency, speed and power of the nerve impulse depends directly on the state of the CNS (Bompa, 1990). When controlled excitation prevails the nerve impulses are the most effective as exhibited through a good performance (Bompa, 1990). As a result of fatigue, the nerve cell is in a state of inhibition, as evidenced through a muscle contraction which is slower and weaker (Bompa, 1990). The force of contraction, therefore, is directly related to the electrical activation sent by the CNS and dependable on the number of motor units recruited (Bompa, 1990).

The working capacity of a nerve cell cannot be maintained for a extended period of time (Bompa, 1990). The working capacity decreases under the strain of training and/or competitive demand (Bompa, 1990). If high intensity is maintained, as a result of fatigue, the nerve cell assumes a state of inhibition to protect itself from external stimuli (Bompa, 1990). This effect is the basis for the alternation of high and low intensity training days otherwise the constant intensive stimuli results in exhaustion placing the nerve cell in a state of 'inhibition of protection' (Bompa, 1990). This state of 'inhibition of protection' nerve stimulation is not responding with the same activation and the resulting performance is well below normal (Bompa, 1990). Emotional factors are associated with similar behaviour of the CNS (Bompa, 1990). The continuation of training beyond this level results in overtraining and the athlete may become completely out of shape (Bompa, 1990).

Elements within the CNS produce the psychological factors and emotions responsible for the sense of effort and motivation that can result in fatigue (McComas, 1996). Virtually nothing is known regarding the neurons involved in the desire to move or in the assessment and generation of effort (McComas, 1996).

When analysing the functional capacity of the CNS during fatigue, consideration needs to be made of the athlete's perceived fatigue and past physical capacity achieved in training was above the level of fatigue experienced in testing or competition, it enhances their motivation and can effect the capacity to overcome fatigue (Bompa, 1990). An athlete's level of motivation has to be related to their past experiences (Bompa, 1990).

Impaired central activation of muscle during fatiguing exercise can be determined by examining maximal voluntary contraction and tetanic tension (Miller et al, 1995). When fatigue is central, a greater decline in maximal voluntary contraction as compared with the decline in tetanic tension is present (Miller et al, 1995). Peripheral fatigue is present when the decline in maximal voluntary contraction and tetanic tension are identical (Miller et al, 1995).

Peripheral Fatigue

In highly motivated individuals the major contribution to fatigue are the elements in the periphery of the motor system which include impulse conduction in the motor axons and their terminals, neuromuscular transmission, conduction of impulses in the muscle fibers, excitation-contraction coupling and muscle contraction (McComas, 1996).

Impulse conduction can fail at the branch points and/or the motor nerve terminal when the motor nerve is stimulated repetitively (McComas, 1996). The liberation of acetylcholine from the motor nerve terminal is significantly reduced with repetitive stimulation (McComas, 1996).

It has been identified that when muscle is maximally activated, fatigue can result in the presence of failure of a cellular mechanism following the muscle fiber action potential involving the excitation-contraction coupling or the contraction apparatus (McComas, 1996).

Skeletal muscle produces force by progressively activating its motor units and regulating their firing frequency (Bompa, 1990). This process is progressively increased in order to enhance force output (Bompa, 1990). Fatigue, which inhibits muscular activity, may be neutralised to some degree by a modulating strategy whereby responding to fatigue through the ability of the motor units to alter their firing frequency (Bompa, 1990). This ability can result in the muscle maintaining force more effectively under a certain state of fatigue (Bompa, 1990). If the duration of sustained maximum contraction increases, however, the frequency of motor units firing decreases indicating that inhibition will become more prominent (Bigland-Ritchie et al, 1983).

In a 30 second maximum voluntary contraction, the end firing frequency decreased by 80% (Marsden et al, 197). As the duration of the contraction increased, activation of large motor units decreased, lowering the firing rate below the threshold level (Bompa, 1990). Continuation of contraction beyond this level was possible through short burst or phasic firing which is not appropriate for constant performance (Bompa, 1990).

In light of these findings, the theory that strength can be improved only by performing each set to exhaustion, as practised by footballers and body builders, is incorrect. The fact is that as contraction progresses the firing frequency decreases, discredits this often followed belief (Bompa, 1990).

Additionally, as a contraction progresses, fuel reserves are depleted, resulting in longer motor unit relaxation time with the resulting muscle contraction conducted at a lower frequency (Bompa, 1990). This neuro-muscular behaviour is attributed to fatigue and indicates that short rest intervals between two sets of maximum contraction is not sufficient to relax and regenerate the neuro-muscular system in order to achieve high activation in the following sets (Bompa, 1990).

Biochemical Changes in Muscle Fibers

Recovery rates from fatigue suggest three contributing components (Miller et al, 1995). First, changes in the muscle action potential occur due to a rapidly recovering alternation of muscle membrane excitation and impulse propagation (Miller et al, 1995). Second, there is a slower recovering rhythm in the metabolic state of the muscle (Miller et al, 1995). Third, impaired neuromuscular efficiency and reduced muscle twitch tension suggest a long duration failure or low-frequency fatigue of excitation-contraction coupling (Miller et al, 1995).

The contractile mechanisms of a fatigued muscle fiber generates tetanic tension slower than normal and prolongs the relaxation phase following twitch and tetanic contractions in addition to producing less force (McComas, 1996). There also significant changes in the chemical composition of the muscle fiber cytoplasm including the following: An accumulation of hydrogen ions and lactate from the breakdown of muscle glycogen, a rise in ADP and inorganic phosphate from the splitting of ATP myosin and membrane ATPases, an increase in inorganic phosphate from the production of lactic acid by the bicarbohydrate/phosphate system, a fall in phosphocreatine, a rise in calcium concentration due to impaired pumping of calcium through the sacroplasmic reticulum, and a gain of water (McComas, 1996).

Muscle fatigue may be associated with the mechanism of calcium flux in skeletal muscle (Bompa, 1990, McComas, 1996). The complex process of muscle contraction is initiated by the nerve action potential which depolarises the surface membrane of the muscle cell, is then conducted into the muscle fibre (Bompa, 1990). This process leads to calcium binding with actin and myosin filaments producing contractile tension (Bompa, 1990, McComas, 1996).

It has been hypothesised that the functional site of fatigue is linked to the excitation-contraction, resulting in either reducing the intensity of excitation-contraction or in decreasing the sensitivity to activation (Bompa, 1990, McComas, 1996, Miller et al, 1995). In testing high-frequency short duration exercise, fatigue could be attributed to metabolic changes in hydrogen ion and inorganic phosphate concentrations (McComas, 1996, Miller et al, 1995). In low-frequency long duration exercise excitation-contraction coupling appeared to be significantly impaired immediately after exercise which increased during the recovery phase (Miller et al, 1995).

The elevation of lactic acid level in blood and muscle has been identified to negatively affect the performance of medium and longer duration, which suggests a relationship between local muscle fatigue and lactic acid accumulation (Bompa, 1990).

The biochemical processes during muscle contraction produce the liberation of hydrogen ions and inorganic phosphates resulting in acidosis also called lactate fatigue which seems to determine the point of exhaustion (Bompa, 1990, Miller et al, 1995). A highly active muscle produces a greater hydrogen ion and inorganic phosphate concentration, increasing blood acidosis which is a state in which hemoglobin has less affinity for oxygen (Bompa, 1990, Miller et al, 1995). To counteract the low level of oxygen at the muscle cell level that will eventuate in acidosis, the hemoglobin will release larger amounts of oxygen during its transport through the capillaries (Bompa, 1990). There appears to be a strong relationship between the presence of inorganic phosphate and fatigue, although hydrogen ion concentration and acidosis play an important role (Miller et al, 1995).

Increasing acidosis inhibits the binding capacity of calcium through inactivation of troponin (Bompa, 1990, McComas, 1996). As troponin is an essential protein for muscle contraction to occur, its inactivation may explain the connection between fatigue and exercise (Bompa, 1990). Low-frequency fatigue may result from decreased calcium released during each action potential also affecting the inactivation of troponin (Clarkson and Newham, 1995, McComas, 1996).

A high state of acidosis affects physical performance through an inhibitory effect on various enzymes resulting in slow glycolysis which produces a limitation in the energy derived from glycolysis (Bompa, 1990). Acidosis produces a sense of discomfort which may influence psychological fatigue (Bompa, 1990).

Fatigue, from an energy systems aspect, occurs when creative phosphate is depleted in the working muscle, or when muscle glycogen is depleted, or when the carbohydrate store is exhausted (Bompa, 1990). Fatigue results in decreased work performed by the muscle possibly due to the fact that in a glycogen depleted muscle, ATP is produced at a lower rate than it is consumed (Bompa, 1990). Carbohydrates are essential for a muscle to maintain high levels of force (Bompa, 1990). Endurance capabilities during prolonged moderate to heavy physical activity is directly related to the amount of muscle glycogen in the muscle prior to exercise (Bompa, 1990). This strongly indicates that fatigue occurs as a result of muscle glycogen depletion (Bompa, 1990). Resistance exercise can significantly decrease muscle glycogen which may result in strength loss and fatigue (Conley and Stone, 1996). Carbohydrate ingestion is essential in maintaining glycogen stores in the muscle and liver (Conley and Stone, 1996).

For very high intensity, short duration activities the source of energy for muscular contraction are ATP and CP (Bompa, 1990). Complete consumption of these energy systems in the muscle significantly limits the ability of the muscle to contract (Bompa, 1990).

Free fatty acids and glucose are the fuels required to provide energy for prolong, submaximal work (Bompa, 1990). Glucose is supplied in large amounts from the liver. The inhibition of free fatty acids increases the rate of glycogen degradation thereby affecting performance (Bompa, 1990).

The power of oxidation is dependent on the availability of oxygen (Bompa, 1990). When oxygen is in limited supply, carbohydrates oxidize instead of free fatty acids (Bompa, 1990). Maximal free fatty acids oxidation is determined by the inflow of the fatty acids to the working muscle and by the aerobic training of the athlete since aerobic training increases both the availability of oxygen and the power of free fatty acids oxidation (Bompa, 1990).

Recovery

Natural means of recovery includes kinotherapy, sleep and lifestyle (Bompa, 1990). The process of recovery is multi-dimensional, however, for the purposes of this paper fatigue and its effects on recovery will be discussed. The recovery of biological parameters and substances occurs in a sequential fashion (Bompa, 1990). Heart rate and blood pressure can recover in 20-60 minutes following the completion of work (Bompa, 1990). The restoration of glucides takes 4-6 hours, proteins take 12-24 hours while fats, vitamins and enzymes take over 24 hours (Bompa, 1990).

Kinotherapy is defined as the therapy through movement or active rest and is a significant factor in recovery and regeneration (Bompa, 1990). It has been demonstrated that a fatigued muscle can increase its rate of recovery and working capacity if while resting the antagonist muscle group performs work instead of being inactive (Bompa, 1990). This principle is illustrated utilising the compensatory effects of the CNS (Bompa, 1990). By transferring the emphasis of excitation to another centre, the recovery of the previously over excited neurons is enhanced (Bompa, 1990). Recovery has been shown to occur faster and more effectively than through total rest (Bompa, 1990). Kinotherapy is applied during emotional fatigue and during the transitional phase of training (Bompa, 1990). This principle is utilised as part of recovery to prevent acquiring high levels of fatigue in strength training by alternating the muscle groups worked (Bompa, 1990). For example, if two training sessions are employed in one day, to facilitate recovery, one session can be dedicated to the upper body and the second to the lower extremity (Bompa, 1990).

Overtraining is the pathological state of training and occurs when the work-recovery ratio is repeatedly exceeded, exposing the athlete to high intensity stimuli when they are in a state of fatigue (Bompa, 1990, Zachazewski et al, 1996). High intensity stimuli, as compared to submaximal or moderate, requires longer recovery periods (Bompa, 1990, Zachazewski et al, 1996). Therefore, if a fatigue athlete does not recover, overcompensation will not occur and the athlete will reach a state of exhaustion (Bompa, 1990, Zachazewski et al, 1996). Overtraining results if extreme fatigued and exhaustion is ignored as high level training continues (Bompa, 1990, Zachazewski et al, 1996).

Recovery of central fatigue must be considered. The regeneration of a neuron is seven times slower than a muscle fiber, therefore, neuro-psychological recovery is significant (Bompa, 1990, Zachazewski et al, 1996). When the CNS is fully recovered, the athlete can concentrate better, perform skills more correctly, react faster and more powerfully to external and internal stimuli, in turn maximise their working capacity (Bompa, 1990, Zachazewski et al, 1996). The treatment of fatigue through psychological means must consider the foundation of motivation, understanding fatigue as part of a normal training outcome, coping with stress and frustration, model training to adapt to various competitive stresses and the importance of a strong team atmosphere (Bompa, 1990, Zachazewski et al, 1996).

Short-term fatigue resulting from the depletion of substrates, fuels, accumulation of metabolites, dehydration and/or heat stress will limit the bodyís ability to work at optimal intensities or durations (Zachazewski et al, 1996). To maximize training stimulus and adaptation, recovery from fatigue should be accomplished with proper dietary, rehydration, and active and passive recovery strategies (Zachazewski et al, 1996).

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Clinical Implications

Peaking is the natural goal of a well-organised and systematically conducted training program (Bompa, 1990). The training demand should meet or slightly surpass the athlete's working capacity and in turn the athlete experiences improvement in various training factors (Bompa, 1990). The result of surpassing the demands as a form of training stimuli, the athlete will acquire fatigue and if allowed to recover, physical fatigue can recuperate within 24 hours (Bompa, 1990).

Eccentric exercise, as compared to isometric an/or concentric muscle activity, causes significant changes including force fatigue (Clarkson and Newham, 1995). Eccentric exercise has demonstrated the largest and longest sustained changes in the total electrical activity and mean power frequency (Clarkson and Newham, 1995). Eccentric exercise conducted in a lengthen muscular state causes greater pain and fatigue than when carried out in shorter length positions (Clarkson and Newham, 1995). Eccentric exercise results in greater fatigue during both low-frequency fatigue and maximal force generation (Clarkson and Newham, 1995).

As a sports physiotherapist and/or coach you need to understand that learning is more effective when neurons are still rested, therefore, technical and tactical elements should be included in the initial part of a training session (Bompa, 1990). If it is imperative that learning or perfecting a technical element be performed following speed, strength or endurance exercises, then retention of the element will be hindered due to fatigue (Bompa, 1990).

As part of a strength training program, drills will be conducted at the end of a training session at a certain level of fatigue or under conditions of residual fatigue as a training effect to reproduce specific game conditions (Bompa, 1990). As long as full recovery is allowed over the following days adaptation will occur resulting in fatigue occurring at higher levels of threshold (Bompa, 1990).

In organising a strength training program for an athlete the various components of fatigue must be considered to optimise the training effect and avoid overtraining. The training program should teach new techniques and perfect current drills in the initial portion of the training session. High level stimuli should be applied to specific regions of the body with submaximal training utilised on other portions of the body to enhance recover of the heavily worked body parts. Heavy training sessions should be alternated with submaximal training sessions as part of a weekly regimen. A highly motivated team approach should be employed to prevent or deter psychological fatigue. Kinotherapy should be applied 24 hours before and after competitions to allow for optimal recover of all body systems and top performance during competition.

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Summary

In summary, fatigue consists of central, peripheral and biochemical components which can in isolation on in combination determine the level of performance of any athlete. Fatigue is a necessary requirement for a strength training program to produce over compensation and raise the threshold for the effects of fatigue during competition. Recovery is an essential component to prevent adverse effects of fatigue and to avoid the pathological conditions of overtraining"

Thomas

[Morten Z]

Det er jo en spændende diskussion som vi ikke er færdige med. Ovenstående tekst beskriver rimeligt bredt forskellige aspekter ved træthed, men har et par punkter hvor jeg må løfte pegefingeren. Der angives referencer i teksten, men det er næsten alle blot referencer til bøger som andre har skrevet - ikke til videnskabelige artikler. Ikke at det gør teksten forkert, men den efterlader herved læseren med det indtryk at længerevarende træthed i CNS er et dokumenteret fænomen. Det er det ikke!

Sætningen:

The regeneration of a neuron is seven times slower than a muscle fiber, therefore, neuro-psychological recovery is significant (Bompa, 1990, Zachazewski et al, 1996).

betragter jeg fortsat som nonsens.

Min forklaring er fortsat at hæmningen i det output som CNS er i stand til at yde er et resultat af hæmmende input til CNS fra resten af kroppen som helhed. Hæmmende input foranlediget at ufuldstændig restitution mange forskellige steder fra - herunder potentielt ALLE dele af bevægeapparatet.

Selv om CNS optræder som hæmmet, så er hæmningen er ikke i selve CNS, men et resultat af CNS's tolkning af hvordan resten af kropepn har det. Dette kan synes som et spørgsmål om ord, men det har afgørende betydning for vores forståelse for hvorledes vi skal træne for at reducere denne form for restitutionskrav.

Spørgsmålet er bestemt ikke endelig afklaret, men er nok af en karakter hvor vi kun kommer videre ved at hente skyts direkte i Medline.

[incognito]

Sætningen:

The regeneration of a neuron is seven times slower than a muscle fiber, therefore, neuro-psychological recovery is significant (Bompa, 1990, Zachazewski et al, 1996).

betragter jeg fortsat som nonsens.

Endelig!!! HAHAE

Det var en af de ting jeg overvejede meget, da jeg startede tråden. Jeg syntes ikke det kunne passe at skroget gør ondt i 4 dage og kabelføringen er smadret i en måned.

Takker.

Iøvrigt TJ, har du en litteratur liste du kan copy-paste med fra teksten du postede. Så jeg ikke skal sidde og lede blandt alle artikler som hver af personerne har lavet det pågældende år.

[Thomas J]

Morten> jeg ved godt vi har haft diskussionen et utal af gange. Og jeg er også enig i at der ikke eksisterer en endegyldig forklaring (hvad jeg ved af). Men jeg er dog sikker på at nervesystemet spiller en væsentlig rolle i plateaudannnelse. Hvordan det skal forklares, er så det store spørgsmål ??

Og selvom det virker som nonsens at påstå at en neuron har en restitutionsrate som er 7 gange så lang som en muskelcelle, så tror jeg sagtens at restitutionen imellem muskler og nervesystem kan være af forskellig karakter (omend ikke så udtalt som det gøres til i artiklen). Laver man f.eks 15 tunge singles med 95 % af ens 1RM, så kan jeg kun forestille mig at muskelprotein degradationen er minimal, mens stresset på nervesystemet er overordentligt stort.

Thomas

[Thomas J]

Her er referencerne.....

Bigland-Ritchie B, Johansson R, Lippold OCJ and Woods JJ (1983): Contractile speed and EMG changes during fatigue of sustained maximal voluntary contractions. Journal of Neurophysiology 50: 313-324.

Bompa TO (1990): Theory and methodology of training: The key to athletic performance. (2nd ed.) Dubuque: Kendall/Hunt Publishing Company.

Clarkson PM and Newham DJ (1995): Associations between muscle soreness, damage, and fatigue. In Gandevia SC, Enoka RM, McComas AJ, Stuart DG, Thomas CK and Pierce PA (Eds): Fatigue: Neural and muscular mechanisms. New York: Plenum Press, pp. 457-469.

Conley MS and Stone MH (1996): Carbohydrate ingestion/supplementation for resistance exercise and training. Sports Medicine 21: 7-17.

Marsden CD, Meadows JC and Merton PA (1971): Isolated single motor units in human muscle and their rate of discharge during maximal voluntary effort. Journal of Physiology (London) 217: 12-13.

McArdle WD, Katch FI and Katch VL (1996): Exercise physiology: Energy, nutrition and human performance. (4th ed.) Baltimore: Williams & Wilkins.

McComas AJ (1996): Skeletal muscle: Form and function. Champaigne, IL: Human Kinetics.

Miller RG, Kent-Braun JA, Sharma KR and Weiner MW (1995): Mechanisms of human muscle fatigue: Quantitating the contribution of metabolic factors and activation impairment. In Gandevia SC, Enoka RM, McComas AJ, Stuart DG, Thomas CK and Pierce PA (Eds): Fatigue: Neural and muscular mechanisms. New York: Plenum Press, pp. 195-210.

Zachazewski JE, Magee DJ and Quillen WS (1996): Athletic injuries and rehabilitation. Philadelphia: W.B. Saunders.

[Morten Z]

Jeg har ikke læst de nævnte referencer specifikt, men jeg kender alle forfatternes arbejde generelt. Bortset fra Bompa og Zachewski er der ikke nogen der drister sig til at snakke om længerevarende CNS-træthed og de to forfattere har som nævnt ikke støtte i tilgængelig videnskabelig litteratur.

Det neurale output er ikke altid optimalt - det er jo også derfor at det kan trænes. Hos utrænede kan man måle graden af "activation failure" ved at give suprafysilogiske elektriske stimulationer til musklen og sammenligne kraftudviklingen med den der kan etableres frivilligt. En metode jeg selv har anvendt i adskillige studier (forsøgspersonerne skreg af smerte - he-he-he).

Det er også påvist at der kan opstå en kortvarig træthed i nervesystemet. Se f.eks. dette forskningsreferat..

Jeg kan ikke se noget belæg for at trætheden 4 dage eller mere efter et tungt træningspas skal kunne lokaliseres til CNS. Jeg kan derimod finde på adskillige ligeså plausible årsager andre steder i systemet.

Jeg forstår at subkjektive observationer ifm. træning får folk til at mene at CNS-træthed er en god forklaring, men det er ikke tilstækkelig argumentation.

Jeg farer til pennen fordi jeg efterhånden ser mange - også på udenlandske boards - der skråsikkert forklarer at hvis man træner sådan her .... så tømmer man sine glykogendepoter og hvis man træner sådan her ... så udtrætter man CNS.

Og jeg finder virkelig ikke at der (for nuværende) er belæg for udtalelsen.

[Jørgen L]

Hos utrænede kan man måle graden af "activation failure" ved at give suprafysilogiske elektriske stimulationer til musklen og sammenligne kraftudviklingen med den der kan etableres frivilligt. En metode jeg selv har anvendt i adskillige studier

(forsøgspersonerne skreg af smerte - he-he-he).

Har selv arbejdet med FES (Er det dét du har brugt?)

Lavede du intramuskulær stimulering?

Hvor kraftig kontraktion forsøgte du at opnå? Vel ikke max - det må have krævet en uhyggelig høj strømstyrke.. (Har selv set patienter spjætte allerede ved ca. 20mA)

[incognito]

er der lavet nogle molekylærbiologiske undersøgelser om, hvad denne neurale fatigue består i? Sker det i motor cortex eller i motorneuronets synapser, f. eks.

[incognito]

Lige en anden ting... Hvad skulle grunden være til, at forced reps og negativer skulle inducere en højere neural fatigue?

Og TJ, du nævner i en anden tråd at den reelle kraftudvikling ved 65-85%1RM belastning i en eksplosiv bevægelse er omtrent den samme som ved 1RM, og som jeg har forstået det er det maksimal kraftudvikling, der tærer, så skulle eksplosiv træning ved 65% være ligeså tærende som træning meget tættere på max.

(ahh pis, jeg lærer det jo nok engang)

[Thomas J]

Og TJ, du nævner i en anden tråd at den reelle kraftudvikling ved 65-85%1RM belastning i en eksplosiv bevægelse er omtrent den samme som ved 1RM

Faktisk er det power output man kan måle, STØRRE ved 65-85 %, end det power output man kan måle ved en 1RM præstation. Det kræver selvfølgelig at man løfter med maksimal acceleration.

så skulle eksplosiv træning ved 65% være ligeså tærende som træning meget tættere på max.

Selvom nervesystemsaktiviteten er voldsomt stor ved eksplosiv træning, så sker den samme udbrænding og plateaudannelse ikke ved den slags træning. Det sker typisk kun ved træningstyper, hvor man ligger og bevæger sig på grænsen af ens formåen, som ved failure træning, forced reps, hyppig 1RM træning osv.

Iøvrigt så smed jeg lige et spørgsmål om central fatique over på HST forummet. Jeg ved Bryan Haycock snakker meget om central fatique, så jeg tænkte at måtte vide noget om specifikke undersøgelser. Hans lille HST-hjælper Blade smed følgende undersøgelser:

Pichot V, Busso T, Roche F, Garet M, Costes F, Duverney D, Lacour JR, Barthelemy JC. Autonomic adaptations to intensive and overload training periods: a laboratory study. Med Sci Sports Exerc. 2002 Oct;34(10):1660-6.

Busso T, Benoit H, Bonnefoy R, Feasson L, Lacour JR. Effects of training frequency on the dynamics of performance response to a single training bout. J Appl Physiol. 2002 Feb;92(2):572-80.

Busso T, Denis C, Bonnefoy R, Geyssant A, Lacour JR. Modeling of adaptations to physical training by using a recursive least squares algorithm. J Appl Physiol. 1997 May;82(5):1685-93.

Jeg kunne finde 2 af dem på PubMed, og umiddelbart synes jeg ikke de giver noget tilfredsstillende svar. Han nævnte også at der efter sigende skulle være mange relevante referencer i Supertraining, så jeg må igang med at lede. The search continues.....

Thomas

[Kra Kra Kra]

jeg har læst noget om at man kan forkorte CNS restitutionstiden ved at spise flere simple kulhydrater ! er det rigtigt ?

[Thomas J]

kra kra> det er med 110 % sikkerhed noget sludder.....

Thomas

[Morten Z]

Thomas J -> fint med referencerne, men jeg konkluderer det samme som dig: at de ikke siger noget om mekanismerne bag akkumuleret træthed.

Jørgen L -> jeg har brugt 400 mA eller mere i en enkelt kortvarig serie af impulser, appliceret på henholdsvis en MVC og en afslappet muskel. Se figur.

[jarvig13]

MZ, TJ -> Here we go again! :D

Naaa, driller bare - det er altid spændende at følge med i Jeres diskussioner (i nærmer Jer hinanden en anelse efterhådenden ;) ).

[incognito]

MZ, er der lavet forsøg som dit, hvor man har sammenlignet MVC med den elektrisk inducerede efter længere tid - say 24 timer eller 48 timer?

Det lyder umiddelbart ikke vildt svært at konstruere et forsøg, der kunne vise hvor lang tid, man havde nedsat ydelse som konsekvens af ikke-muskulære årsager (er det lavet?).

Edited January 28, 2003 by incognito

[Jørgen L]

Jørgen L -> jeg har brugt 400 mA eller mere i en enkelt kortvarig serie af impulser, appliceret på henholdsvis en MVC og en afslappet muskel.

400 MILLIAMPERE?????? :dropjaw:

Nu er jeg oprindeligt uddannet elektronikmekaniker, og ved derigennem lidt om strøm, og 400mA lyder edderm.... vildt!!

Du kørte vel bipolært, og undgik derved de værste 3. grads forbrændinger? For en strømstyrke af den størrelse, omend kun kortvarigt introduceret, må give en lettere brændt lugt i labbet :retard: :lol:

[Morten Z]

Det lyder umiddelbart ikke vildt svært at konstruere et forsøg, der kunne vise hvor lang tid, man havde nedsat ydelse som konsekvens af ikke-muskulære årsager (er det lavet?).

Det er nu sværere end det lyder. Den oprindelige diskussion går egentlig heller ikke på om længerevarende træthed har en muskulær årsag eller ej, men om årsagen findes i CNS - og det er utroligt svært at vise.

Hvis nu f.eks. senetenene (sanseceller i senerne) ændrer deres følsomhed på grund af den summerede kraftpåvirkning ved tung træning - og dette fører til et øget hæmmende input til CNS - hvordan skulle man så adskille det fra en træthed lokaliseret i selve CNS?

Ja, man skulle lave et studie hvor man specifikt undersøgte ændringer i følsomheden for senetenene. Hvis dette studie intet viste, kunne man så sige at trætheden var i CNS? - Nej, for hvad nu hvis træningen medfører en ændring af følsomheden for mekanoreceptorer omkring leddene? - Nyt studie! Osv.

Og hvordan er det forøvrigt når man har muskelømhed efter tung træning - hvordan opfører CNS sig så? De ømme muskler giver anledning til smerte når man forsøger at lave maksimale kontraktioner. Smertesignalet har en klar hæmmende effekt på CNS's villighed overfor at give maksimalt output. CNS er dermed hæmmet - men årsagen er et andet sted.

og 400mA lyder edderm.... vildt!!

Jeg sagde jo at de skreg.

Ved at bruge meget store elektroder mindsker man den værste bacon-effekt. Mindre strømstyrker udløser ikke maksimale kontraktioner. Vi lavede en del metodeudvikling på det med alskens kombinationer af frekvens, varighed, impulsbredde etc.

[Jørgen L]

Et spørgsmål til selve forsøget: Hvordan kunne du vide at smerten ikke bare virkede faciliterende på den voluntære kontraktion, og at strømstyrken derved var mindre vigtig?

Jeg ved, når man faciliterer en muskel ved eks. at klappe på den - det kunne være Vastus Med. Obliq., så opnår man mere spænding (muskelspænding altså ;) )

[jarvig13]

så opnår man mere spænding (muskelspænding altså ;) )

:lol: :lol: :lol:

Vigitg detalje. MZ holder sikkert af begge spændinger. :D

[Jørgen L]

Jarvig: Sikkert, men nu mente jeg altså Volt/"tonus" ;)

[Lille Py]

400 mA!!!

Det er jo helt vildt.

Jeg har lige fået lavet en SSEP-undersøgelse, hvor de brugte 15 mA - eller noget i den stil - og det var fandeme ikke særlig rart.

Edited January 29, 2003 by Lille Py