Motor Unit Recruitment
Questioner said:
"But realize you didn't address *failure* itself as a physiological event. Failure as a *physical* (as opposed to physiological) event results from the coincidence of two factors, constant resistance and decreasing momentary strength (which level is determined by fatigue). When these two match, movement stops. This is failure -- a physical event, a matter of simple mechanical physics, and in my opinion something not to be confused with fatigue. But what I'm asking is, does anything "special", from a physiological point of view, occur at the moment of failure and/or during continued exertion after the point of failure, as with deep inroad technique?"
I understand what you are saying. However, as far as most strength training protocols are concerned, “failure” occurs because of muscle fatigue and will not occur without muscle fatigue. Hence, in order to understand what happens when we reach failure, we need to study what occurs when a muscle fatigues. Muscle fatigue is defined as a decline in a muscle's ability to exert force. This is even occurs in isolated muscle fiber studies.
As I previously stated, the majority of the data I have seen suggest that muscle fatigue is due to an inability of the sarcoplasmic reticulum to release calcium. This is influenced by a build-up of metabolic byproducts / osmolytes, the strongest correlator being inorganic phosphate. This generally happens when the rate of ATP utilization outpaces the rate of ATP production (due to a reduction in CTP). During a set of fatiguing strength training contractions (within 1-2 minutes for example), as we approach failure, the larger glycolytic fibers will fatigue and produce less force. As the larger, higher force producing glycolytic fibers begin to decline, the ability of the muscle, as a whole, to produce force is reduced. When the muscle's force production capability is reduced to the resistive force of the load, movement stops. We reach failure.
I prefer to use the term fatigue, because it is more descriptive of a physiological event. We fail in an exercise because we fatigue. Hence, the term “fatigue” is more indicative of what is actually going on inside the muscle.
"As I understand, when we do a set of an exercise with a certain load, to exert the appropriate amount of force, muscle fibers are progressively recruited, according with need, in order of their sizes/type, from SO to FO to FG. Here's a quote from Dr. Mcguff from his article 'Grist for the mill":"If all three types of motor units are fatigued quickly enough (before the slow twitch fibers can recover) then failure under that load will ensue. By the time you are about 85% of the way to failure, you have probably recruited 100% of the motor units that you are capable of recruiting.'"
Yes, motor units are recruited according to the size principle. Although, depending on the muscle(s) being trained, during a maximal or near maximal contraction (especially in well-trained subjects), all motor units available for a particular movement will be recruited simultaneously or at least very early in the set. Depending upon the muscle trained, some studies no new motor unit recruitment with as little as 40% of an MVC (maximal voluntary contraction) – some less, some more. See the following:
Eur J Appl Physiol Occup Physiol 1993;67(4):335-41
Motor unit recruitment during prolonged isometric contractions.
Fallentin N, Jorgensen K, Simonsen EB.
“In contrast to the 10% MVC experiment, there was no indication of de novo recruitment in the 40% MVC experiment.”
Brain Res 219:1, 45-55 (1981)
Comparison of the recruitment and discharge properties of motor units in human brachial biceps and adductor pollicis during isometric contractions.
Kukulka, CG and Clamann, HP
In biceps brachii, recruitment was observed from 0 to 88% maximum voluntary contraction (MVC). In adductor pollicis, no motor unit was observed to be recruited at forces greater than 50% MVC, with the majority of recruitment occurring below 30% MVC.
Electromyogr Clin Neurophysiol 30:8, 483-9 (1990)
The behaviour of the mean power frequency of the surface electromyogram in biceps brachii with increasing force and during fatigue. With special regard to the electrode distance.
Gerdle, B, Eriksson, NE and Brundin, L
The mean power frequency increased upto 60% MVC. Above 60% MVC no change in mean power frequency occurred.
Electromyogr Clin Neurophysiol 37:1, 3-12 (1997)
Motor unit recruitment strategy of antagonist muscle pair during linearly increasing contraction.
Bernardi, M, Solomonow, M and Baratta, RV
When quadriceps and hamstrings acted as agonist, most of the motor units were recruited in a linear manner up to 60% of maximal voluntary contraction (MVC).
There are many other studies demonstrating similar results. These are also corroborated with studies showing type IIb fiber fatigue (not just recruiment) with dynamic movements with as little 60% 1 RM (non-fatiguing protocol). See the following:
J. Strength and Cond. Res. 12(2):67-73. 1998.
Skeletal muscle glycogen loss evoked by resistance exercise.
Tesch, P.A., LL. Ploutz-Snyder, L. Ystrom, M.J. Castro, and G.A. Dudley.
Because type IIab + IIb fibers showed glycogen loss at loads of 60% of maximum, it is suggested that fast-twitch subtypes are used at lower loads than generally appreciated.
Given the above data, with heavy loads (80% of 1RM for example) it is likely that maximal motor unit recruitment is occurring in the beginning of the set (or at least very early in the set). Thus, an increase rate coding (firing frequency) is probably responsible for most of the force production until fatigue (and not new motor unit recruitment).
It goes without saying that I think Doug McGuff is a brilliant individual. But, I'm fairly certain he is not correct on this one. Failure in an exercise does not occur due to the simultaneous fatigue of all three motor unit types. Movement in an exercise stops when the total force output capacity of the muscle is reduced to the resistive force of the load. This is due to the larger FG fiber fatigue, not because all fibers fatigue. It is unlikely during high intensity, short duration resistance training that we will be able to significantly fatigue the SO fibers, due to their metabolic profile. ST motor units / SO fibers have less force potential, but can exert that force for a longer period of time. Most of the research I've seen regarding muscle fatigue involves FG fibers due to their fatigability. See the following:
J Electromyogr Kinesiol 14:5, 531-8 (2004)
Selective fatigue of fast motor units after electrically elicited muscle contractions.
Hamada, T, Kimura, T and Moritani, T
Results indicated that mean MU spike amplitude, particularly those MUs with relatively large amplitude, was significantly reduced while those MUs with small spike amplitude increased their firing rate during the 40% MVC test contraction after the ES.
“Summation is what happens. The involved motor units are fired at a faster rate, sort of like revving an engine to get the pistons to fire faster. What happens at failure and during deep inroad? Tetany is what happens. Tetany means that the motor units are receiving nerve impulses so quickly that there is no opportunity for a relaxation phase∑all the motor units are essentially stuck in the "on" position."
Tetanic contractions are most likely occurring when we approach failure in an exercise and probably even before reaching failure in some fibers. However, this is not necessarily a bad thing. In fact, in isolated muscle fiber studies, tetanic contractions on FG fibers are the preferred method for studying fatigue. For a good review of this see the following:
Journal of Physiology (2001), 536.3, pp. 657-665
Role of phosphate and calcium stores in muscle fatigue
D. G. Allen and H. Westerblad
“Investigations on mechanism (i) started with the classic work of Eberstein & Sandow (1963). They fatigued intact muscles with repeated tetani until force was greatly reduced and then increased the level of activation by increasing extracellular K+ or application of caffeine. Both these manoeuvres increased force substantially in the fatigued muscle suggesting that a reversible failure of activation was an important contributor to fatigue.”
See also:
LÄNNERGREN, J. & WESTERBLAD, H. (1991). Force decline due to fatigue and intracellular acidification in isolated fibres from mouse skeletal muscle. Journal of Physiology 434, 307-322
"If tetany occurs for a long enough period, all of the acetylcholine (the neurotransmitter at the junction between the nerve and the motor unit) will be exhausted.(...) Such a practice, if done infrequently is a great mechanism for improving strength in a given movement. By recruiting as many motor units as possible, and forcing them to fire as rapidly as you can you are "beating a neuromotor dog-trail" that will result in better performance in that movement over time. By exhausting neurotransmitter, I think you might produce a situation where the motor end-plate would act by upregulating its acetylcholine receptors.With more receptors, each motor unit could be recruited more efficiently.(...) If this theory were correct, there would necessarily be a dark side to all of this. The million dollar question is this∑.How long does it take to recover a functional level of neurotransmitter in the fast twitch units? My guess is that in the fast twitch motor units, it may be several days of even weeks. If this is true, that is long enough for those particular motor units to suffering from what I call "functional dennervation".
First, Doug admits he is guessing or postulating a hypothesis. I guess we all do this at some point. Yes, enhancements in neural activation occur with strength training – lots of evidence on this. Some animal research even points to greater adaptations of the neuromuscular junction with higher intensity protocols. See the following:
J Neurocytol 1993 Aug;22(8):603-15
The effects of exercise training of different intensities on neuromuscular junction morphology.
Deschenes MR, Maresh CM, Crivello JF, Armstrong LE, Kraemer WJ, Covault J.
Results indicate that training did induce hypertrophy of the neuromuscular junction that was independent of muscle hypertrophy. Although the HIT and LIT groups exhibited similar hypertrophic responses of the neuromuscular junction, the HIT group displayed more dispersed synapses than the LIT group. Neither exercise training program, however, resulted in altered densities of acetylcholine vesicles or receptors, nor did training significantly change synaptic coupling. Nerve terminal branching was also affected by exercise training. Neuromuscular junctions from the HIT group demonstrated a greater total length of branching, average length per branch, and number of finer, or secondary, branches than those of the LIT group.
However, what Doug seems to be suggesting is that damage to the neuromuscular junction (at least in the larger FG units) may be responsible for an extended recovery requirement. In order for this to occur, one would expect that the neuromuscular junction is the site of fatigue. This is not supported in the scientific literature. Almost all of the exercise physiology / muscle physiology text reference the early work of Merton (1954).
I'm quoting from Brooks et al. (2000). Exercise Physiology, Third Edition: Human Bioenergetics and Its Applications.
“In a now classic series of experiments, Merton (1954) determined that the site of fatigue in the adductor pollicis muscle was peripheral to the neuromuscular junction (i.e., it was within the muscle itself and not the neuromuscular junction)… When the voluntary tension developed by the adductor pollicis decreased to indicate significant fatigue, Merton applied electrical shocks to the ulnar nerve to increase stimulation of the muscle. As indicated, muscle action potentials indicated clear conduction of the signal from the nerve to muscle, but there was no tension response in the fatigued muscle.”
We've discussed this before on the other list. Here is a quote from a previous email I sent regarding this:
“This is in agreement with other references I've seen, suggesting short duration fatigue is peripherally mediated. In "Skeletal Muscle Structure and Function: Implication for Rehabilitation and Sports Medicine", Lieber (1992) cites the early work by Merton (1954) wrt muscle fatigue involving an electrical stimulus superimposed onto an MVC with no increase in force production, suggesting that "CNS fatigue was not the cause for muscle fatigue." Further, "This type of experiment has been confirmed by others, and it is generally agreed that muscle fatigue in highly motivated subjects is not due to CNS fatigue." He also cites work by Bigland-Ritchie (1982) "performed to determine whether fatigue of the neuromuscular junction or sarcolemma occurs during muscle fatigue." He notes that her and "her colleagues demonstrated that almost no change in M-wave occurred in spite of the force decrease", suggesting that "the weak link in fatigue was also not the neuromuscular junction or muscle sarcolemma."
In "Skeletal Muscle Form and Function", McComas (1996) cites evidence suggesting that "impaired E-C coupling is likely to be the most important of the peripheral factors", regarding muscle fatigue. However, the impairment is not a neural event, but due mostly to an interference of the sarcoplasmic reticulum to release CA2+. This is influenced by metabolic by-products, largely the accumulation of the various forms of Pi.”
"Perhaps this mechanism that Dr. Mcguff describes can explain, as he himself suggests, what for instance Drew and other people (including myself) have experienced with certain applications of SS, with regard to size gains (or lack thereof). In my opinion Dr. Mcguff's article is much less an argument for rest/pause at failure as it is an argument against the use of the deep inroad technique. Since the strongest correlation with hypertrophy is, as I understand, mechanical stress and not neurotransmitter exhaustion, if what Dr. Mcguff suggests is correct, deep inroad technique may perhaps be the best possible protocol for performance gains in absence of size increases, but of course also the worst for hypertrophy. In pushing beyond failure, with all available fast twitch fibers already recruited and fatiguing at an accelerated rate, especially if in a state of tetany, we get a situation where there is a disproportionate amount of neural activity for very little mechanical stress, since deep inroad technique is performed primarily as an isometric action. This may overstimulate the neural component of strength gains and at the same time understimulate, or more likely, as Dr. Mcguff suggests, short-circuit the structural adaptations (hypertrophy) because of "functional dennervation" of the motor units. This of course is complete speculation on my part, but I think it's possible that the extent of the exhaustion of neurotransmitters in a single set taken to failure and beyond, with deep inroad technique, may equal that of multiple sets not taken to failure. As Drew has pointed out in his website, the total TUL of a SS workout, with sometimes over 120 seconds of uninterrupted loading in every set, may easily exceed the total TUL of a multiple set workout. But with a good percentage of the that TUL spent under deep inroad technique, with increased rate of neurotransmitter release, the toll on some components of the nervous system may be even greater."
Again, failure / fatigue of the neuromuscular junction regarding muscle fatigue is not supported in the scientific literature. Although I have a great deal of respect for Doug, his theory regarding “functional denervation” is based on a guess. The experimental evidence shows this not to be the case. Even in sustained tetanic isometric contractions, the latest evidence suggests that reduced force output (fatigue) is due metabolic factors. On the site's file section, I will post two very good reviews on this.
Journal of Physiology (2001), 536.3, pp. 657-665
Role of phosphate and calcium stores in muscle fatigue
D. G. Allen and H. Westerblad
Conclusion:
Failure of SR Ca2+ release has been shown to be a major contributor to muscle fatigue. Increasing evidence supports the hypothesis that precipitation of CaPi in the SR contributes to the failure of SR Ca2+ release. We suggest that this mechanism may be important in high intensity activities which lead to fatigue in > 1-2 min but other mechanisms are probably more important in lower intensity activities which cause fatigue in > 1 h.
News Physiol Sci 17: 17-21, 2002
Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause?
Håkan Westerblad, David G. Allen and Jan Lännergren
"But look at the example of (drug free) powerlifters, Olympic weightlifters, gymnasts, etc. They rarely if ever train to failure, load intermittently and use very high volume. And despite all that there's no denying that they're able to achieve great physiques and very impressive strength levels. If we are to explain why SS is productive, this model must also explain why these people also get such good results in spite of using improper training methods by our standards. And genetics can't explain everything..."
We will have to agree to disagree on this. The more I see regarding myostatin deletion and the genetic over-expression of local muscle IGF-1, the more I'm convinced that genetics explain most of this. If you have not seen the latest article concerning myostatin deletion in the New England Journal of Medicine, I suggest you take a look. These genetic mutations are being identified in infants and children, as well as their families. It's quite amazing.
"The mechanism that Dr. Mcguff describes in "Grist for the mill" appears to be something along those lines, only the component of the nervous system that "burns out" would be peripheral."
Again, not supported in the scientific literature.
"Yes, but you seem to use fatigue and failure interchangeably. In my opinion they're entirely different animals and cannot be confused: -Fatigue is the physiological process you described that explains the decrease in maximal force output (strength) secondary to continued high intensity exertion. -Failure is the physical consequence of trying to continue moving a constant weight despite the strength decrease caused by fatigue. But where I'm trying to get at is, that one thing is fatigue with submaximal loading (before failure) and another quite different may be fatigue with maximal loading (after failure)."
Fatigue and failure are not entirely different. I use them interchangeably because one (failure) is caused by the other (fatigue), at least in most strength training protocols. Sure, failure is the inability to lift a given load. But this happens because of muscle fatigue. We fail because we fatigue, not the other way around.
"I insist, there's the general physiological process (fatigue) that explains the decrease in momentary strength. But then there's failure itself, which in my view, is simple newtonian physics: net force equals momentary strength plus opposing resistance. When momentary strength drops below the opposing resistance, the net force applied to the weight becomes negative, and movement slows down to a stop. This is the moment of failure and it is, in my opinion, pure physics."
Yes. I agree with the above.
"However, at a physiological level, this represents a turning point -- from a state of submaximal loading to a state of maximal loading. This may have, as Dr. Mcguff suggests, repercussions in terms of neurotransmitter release rate, which may lead to eventual neurotransmitter exhaustion. Or am I getting it all wrong?"
No. “Neurotramitter exhaustion” is not supported in the literature (as per the previous references), at least not in the references I've seen. Again, even during maximal tetanic isometric contractions this has not been shown to be the case.
I hope this answer some of your questions.
Ryan A. Hall
"But realize you didn't address *failure* itself as a physiological event. Failure as a *physical* (as opposed to physiological) event results from the coincidence of two factors, constant resistance and decreasing momentary strength (which level is determined by fatigue). When these two match, movement stops. This is failure -- a physical event, a matter of simple mechanical physics, and in my opinion something not to be confused with fatigue. But what I'm asking is, does anything "special", from a physiological point of view, occur at the moment of failure and/or during continued exertion after the point of failure, as with deep inroad technique?"
I understand what you are saying. However, as far as most strength training protocols are concerned, “failure” occurs because of muscle fatigue and will not occur without muscle fatigue. Hence, in order to understand what happens when we reach failure, we need to study what occurs when a muscle fatigues. Muscle fatigue is defined as a decline in a muscle's ability to exert force. This is even occurs in isolated muscle fiber studies.
As I previously stated, the majority of the data I have seen suggest that muscle fatigue is due to an inability of the sarcoplasmic reticulum to release calcium. This is influenced by a build-up of metabolic byproducts / osmolytes, the strongest correlator being inorganic phosphate. This generally happens when the rate of ATP utilization outpaces the rate of ATP production (due to a reduction in CTP). During a set of fatiguing strength training contractions (within 1-2 minutes for example), as we approach failure, the larger glycolytic fibers will fatigue and produce less force. As the larger, higher force producing glycolytic fibers begin to decline, the ability of the muscle, as a whole, to produce force is reduced. When the muscle's force production capability is reduced to the resistive force of the load, movement stops. We reach failure.
I prefer to use the term fatigue, because it is more descriptive of a physiological event. We fail in an exercise because we fatigue. Hence, the term “fatigue” is more indicative of what is actually going on inside the muscle.
"As I understand, when we do a set of an exercise with a certain load, to exert the appropriate amount of force, muscle fibers are progressively recruited, according with need, in order of their sizes/type, from SO to FO to FG. Here's a quote from Dr. Mcguff from his article 'Grist for the mill":"If all three types of motor units are fatigued quickly enough (before the slow twitch fibers can recover) then failure under that load will ensue. By the time you are about 85% of the way to failure, you have probably recruited 100% of the motor units that you are capable of recruiting.'"
Yes, motor units are recruited according to the size principle. Although, depending on the muscle(s) being trained, during a maximal or near maximal contraction (especially in well-trained subjects), all motor units available for a particular movement will be recruited simultaneously or at least very early in the set. Depending upon the muscle trained, some studies no new motor unit recruitment with as little as 40% of an MVC (maximal voluntary contraction) – some less, some more. See the following:
Eur J Appl Physiol Occup Physiol 1993;67(4):335-41
Motor unit recruitment during prolonged isometric contractions.
Fallentin N, Jorgensen K, Simonsen EB.
“In contrast to the 10% MVC experiment, there was no indication of de novo recruitment in the 40% MVC experiment.”
Brain Res 219:1, 45-55 (1981)
Comparison of the recruitment and discharge properties of motor units in human brachial biceps and adductor pollicis during isometric contractions.
Kukulka, CG and Clamann, HP
In biceps brachii, recruitment was observed from 0 to 88% maximum voluntary contraction (MVC). In adductor pollicis, no motor unit was observed to be recruited at forces greater than 50% MVC, with the majority of recruitment occurring below 30% MVC.
Electromyogr Clin Neurophysiol 30:8, 483-9 (1990)
The behaviour of the mean power frequency of the surface electromyogram in biceps brachii with increasing force and during fatigue. With special regard to the electrode distance.
Gerdle, B, Eriksson, NE and Brundin, L
The mean power frequency increased upto 60% MVC. Above 60% MVC no change in mean power frequency occurred.
Electromyogr Clin Neurophysiol 37:1, 3-12 (1997)
Motor unit recruitment strategy of antagonist muscle pair during linearly increasing contraction.
Bernardi, M, Solomonow, M and Baratta, RV
When quadriceps and hamstrings acted as agonist, most of the motor units were recruited in a linear manner up to 60% of maximal voluntary contraction (MVC).
There are many other studies demonstrating similar results. These are also corroborated with studies showing type IIb fiber fatigue (not just recruiment) with dynamic movements with as little 60% 1 RM (non-fatiguing protocol). See the following:
J. Strength and Cond. Res. 12(2):67-73. 1998.
Skeletal muscle glycogen loss evoked by resistance exercise.
Tesch, P.A., LL. Ploutz-Snyder, L. Ystrom, M.J. Castro, and G.A. Dudley.
Because type IIab + IIb fibers showed glycogen loss at loads of 60% of maximum, it is suggested that fast-twitch subtypes are used at lower loads than generally appreciated.
Given the above data, with heavy loads (80% of 1RM for example) it is likely that maximal motor unit recruitment is occurring in the beginning of the set (or at least very early in the set). Thus, an increase rate coding (firing frequency) is probably responsible for most of the force production until fatigue (and not new motor unit recruitment).
It goes without saying that I think Doug McGuff is a brilliant individual. But, I'm fairly certain he is not correct on this one. Failure in an exercise does not occur due to the simultaneous fatigue of all three motor unit types. Movement in an exercise stops when the total force output capacity of the muscle is reduced to the resistive force of the load. This is due to the larger FG fiber fatigue, not because all fibers fatigue. It is unlikely during high intensity, short duration resistance training that we will be able to significantly fatigue the SO fibers, due to their metabolic profile. ST motor units / SO fibers have less force potential, but can exert that force for a longer period of time. Most of the research I've seen regarding muscle fatigue involves FG fibers due to their fatigability. See the following:
J Electromyogr Kinesiol 14:5, 531-8 (2004)
Selective fatigue of fast motor units after electrically elicited muscle contractions.
Hamada, T, Kimura, T and Moritani, T
Results indicated that mean MU spike amplitude, particularly those MUs with relatively large amplitude, was significantly reduced while those MUs with small spike amplitude increased their firing rate during the 40% MVC test contraction after the ES.
“Summation is what happens. The involved motor units are fired at a faster rate, sort of like revving an engine to get the pistons to fire faster. What happens at failure and during deep inroad? Tetany is what happens. Tetany means that the motor units are receiving nerve impulses so quickly that there is no opportunity for a relaxation phase∑all the motor units are essentially stuck in the "on" position."
Tetanic contractions are most likely occurring when we approach failure in an exercise and probably even before reaching failure in some fibers. However, this is not necessarily a bad thing. In fact, in isolated muscle fiber studies, tetanic contractions on FG fibers are the preferred method for studying fatigue. For a good review of this see the following:
Journal of Physiology (2001), 536.3, pp. 657-665
Role of phosphate and calcium stores in muscle fatigue
D. G. Allen and H. Westerblad
“Investigations on mechanism (i) started with the classic work of Eberstein & Sandow (1963). They fatigued intact muscles with repeated tetani until force was greatly reduced and then increased the level of activation by increasing extracellular K+ or application of caffeine. Both these manoeuvres increased force substantially in the fatigued muscle suggesting that a reversible failure of activation was an important contributor to fatigue.”
See also:
LÄNNERGREN, J. & WESTERBLAD, H. (1991). Force decline due to fatigue and intracellular acidification in isolated fibres from mouse skeletal muscle. Journal of Physiology 434, 307-322
"If tetany occurs for a long enough period, all of the acetylcholine (the neurotransmitter at the junction between the nerve and the motor unit) will be exhausted.(...) Such a practice, if done infrequently is a great mechanism for improving strength in a given movement. By recruiting as many motor units as possible, and forcing them to fire as rapidly as you can you are "beating a neuromotor dog-trail" that will result in better performance in that movement over time. By exhausting neurotransmitter, I think you might produce a situation where the motor end-plate would act by upregulating its acetylcholine receptors.With more receptors, each motor unit could be recruited more efficiently.(...) If this theory were correct, there would necessarily be a dark side to all of this. The million dollar question is this∑.How long does it take to recover a functional level of neurotransmitter in the fast twitch units? My guess is that in the fast twitch motor units, it may be several days of even weeks. If this is true, that is long enough for those particular motor units to suffering from what I call "functional dennervation".
First, Doug admits he is guessing or postulating a hypothesis. I guess we all do this at some point. Yes, enhancements in neural activation occur with strength training – lots of evidence on this. Some animal research even points to greater adaptations of the neuromuscular junction with higher intensity protocols. See the following:
J Neurocytol 1993 Aug;22(8):603-15
The effects of exercise training of different intensities on neuromuscular junction morphology.
Deschenes MR, Maresh CM, Crivello JF, Armstrong LE, Kraemer WJ, Covault J.
Results indicate that training did induce hypertrophy of the neuromuscular junction that was independent of muscle hypertrophy. Although the HIT and LIT groups exhibited similar hypertrophic responses of the neuromuscular junction, the HIT group displayed more dispersed synapses than the LIT group. Neither exercise training program, however, resulted in altered densities of acetylcholine vesicles or receptors, nor did training significantly change synaptic coupling. Nerve terminal branching was also affected by exercise training. Neuromuscular junctions from the HIT group demonstrated a greater total length of branching, average length per branch, and number of finer, or secondary, branches than those of the LIT group.
However, what Doug seems to be suggesting is that damage to the neuromuscular junction (at least in the larger FG units) may be responsible for an extended recovery requirement. In order for this to occur, one would expect that the neuromuscular junction is the site of fatigue. This is not supported in the scientific literature. Almost all of the exercise physiology / muscle physiology text reference the early work of Merton (1954).
I'm quoting from Brooks et al. (2000). Exercise Physiology, Third Edition: Human Bioenergetics and Its Applications.
“In a now classic series of experiments, Merton (1954) determined that the site of fatigue in the adductor pollicis muscle was peripheral to the neuromuscular junction (i.e., it was within the muscle itself and not the neuromuscular junction)… When the voluntary tension developed by the adductor pollicis decreased to indicate significant fatigue, Merton applied electrical shocks to the ulnar nerve to increase stimulation of the muscle. As indicated, muscle action potentials indicated clear conduction of the signal from the nerve to muscle, but there was no tension response in the fatigued muscle.”
We've discussed this before on the other list. Here is a quote from a previous email I sent regarding this:
“This is in agreement with other references I've seen, suggesting short duration fatigue is peripherally mediated. In "Skeletal Muscle Structure and Function: Implication for Rehabilitation and Sports Medicine", Lieber (1992) cites the early work by Merton (1954) wrt muscle fatigue involving an electrical stimulus superimposed onto an MVC with no increase in force production, suggesting that "CNS fatigue was not the cause for muscle fatigue." Further, "This type of experiment has been confirmed by others, and it is generally agreed that muscle fatigue in highly motivated subjects is not due to CNS fatigue." He also cites work by Bigland-Ritchie (1982) "performed to determine whether fatigue of the neuromuscular junction or sarcolemma occurs during muscle fatigue." He notes that her and "her colleagues demonstrated that almost no change in M-wave occurred in spite of the force decrease", suggesting that "the weak link in fatigue was also not the neuromuscular junction or muscle sarcolemma."
In "Skeletal Muscle Form and Function", McComas (1996) cites evidence suggesting that "impaired E-C coupling is likely to be the most important of the peripheral factors", regarding muscle fatigue. However, the impairment is not a neural event, but due mostly to an interference of the sarcoplasmic reticulum to release CA2+. This is influenced by metabolic by-products, largely the accumulation of the various forms of Pi.”
"Perhaps this mechanism that Dr. Mcguff describes can explain, as he himself suggests, what for instance Drew and other people (including myself) have experienced with certain applications of SS, with regard to size gains (or lack thereof). In my opinion Dr. Mcguff's article is much less an argument for rest/pause at failure as it is an argument against the use of the deep inroad technique. Since the strongest correlation with hypertrophy is, as I understand, mechanical stress and not neurotransmitter exhaustion, if what Dr. Mcguff suggests is correct, deep inroad technique may perhaps be the best possible protocol for performance gains in absence of size increases, but of course also the worst for hypertrophy. In pushing beyond failure, with all available fast twitch fibers already recruited and fatiguing at an accelerated rate, especially if in a state of tetany, we get a situation where there is a disproportionate amount of neural activity for very little mechanical stress, since deep inroad technique is performed primarily as an isometric action. This may overstimulate the neural component of strength gains and at the same time understimulate, or more likely, as Dr. Mcguff suggests, short-circuit the structural adaptations (hypertrophy) because of "functional dennervation" of the motor units. This of course is complete speculation on my part, but I think it's possible that the extent of the exhaustion of neurotransmitters in a single set taken to failure and beyond, with deep inroad technique, may equal that of multiple sets not taken to failure. As Drew has pointed out in his website, the total TUL of a SS workout, with sometimes over 120 seconds of uninterrupted loading in every set, may easily exceed the total TUL of a multiple set workout. But with a good percentage of the that TUL spent under deep inroad technique, with increased rate of neurotransmitter release, the toll on some components of the nervous system may be even greater."
Again, failure / fatigue of the neuromuscular junction regarding muscle fatigue is not supported in the scientific literature. Although I have a great deal of respect for Doug, his theory regarding “functional denervation” is based on a guess. The experimental evidence shows this not to be the case. Even in sustained tetanic isometric contractions, the latest evidence suggests that reduced force output (fatigue) is due metabolic factors. On the site's file section, I will post two very good reviews on this.
Journal of Physiology (2001), 536.3, pp. 657-665
Role of phosphate and calcium stores in muscle fatigue
D. G. Allen and H. Westerblad
Conclusion:
Failure of SR Ca2+ release has been shown to be a major contributor to muscle fatigue. Increasing evidence supports the hypothesis that precipitation of CaPi in the SR contributes to the failure of SR Ca2+ release. We suggest that this mechanism may be important in high intensity activities which lead to fatigue in > 1-2 min but other mechanisms are probably more important in lower intensity activities which cause fatigue in > 1 h.
News Physiol Sci 17: 17-21, 2002
Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause?
Håkan Westerblad, David G. Allen and Jan Lännergren
"But look at the example of (drug free) powerlifters, Olympic weightlifters, gymnasts, etc. They rarely if ever train to failure, load intermittently and use very high volume. And despite all that there's no denying that they're able to achieve great physiques and very impressive strength levels. If we are to explain why SS is productive, this model must also explain why these people also get such good results in spite of using improper training methods by our standards. And genetics can't explain everything..."
We will have to agree to disagree on this. The more I see regarding myostatin deletion and the genetic over-expression of local muscle IGF-1, the more I'm convinced that genetics explain most of this. If you have not seen the latest article concerning myostatin deletion in the New England Journal of Medicine, I suggest you take a look. These genetic mutations are being identified in infants and children, as well as their families. It's quite amazing.
"The mechanism that Dr. Mcguff describes in "Grist for the mill" appears to be something along those lines, only the component of the nervous system that "burns out" would be peripheral."
Again, not supported in the scientific literature.
"Yes, but you seem to use fatigue and failure interchangeably. In my opinion they're entirely different animals and cannot be confused: -Fatigue is the physiological process you described that explains the decrease in maximal force output (strength) secondary to continued high intensity exertion. -Failure is the physical consequence of trying to continue moving a constant weight despite the strength decrease caused by fatigue. But where I'm trying to get at is, that one thing is fatigue with submaximal loading (before failure) and another quite different may be fatigue with maximal loading (after failure)."
Fatigue and failure are not entirely different. I use them interchangeably because one (failure) is caused by the other (fatigue), at least in most strength training protocols. Sure, failure is the inability to lift a given load. But this happens because of muscle fatigue. We fail because we fatigue, not the other way around.
"I insist, there's the general physiological process (fatigue) that explains the decrease in momentary strength. But then there's failure itself, which in my view, is simple newtonian physics: net force equals momentary strength plus opposing resistance. When momentary strength drops below the opposing resistance, the net force applied to the weight becomes negative, and movement slows down to a stop. This is the moment of failure and it is, in my opinion, pure physics."
Yes. I agree with the above.
"However, at a physiological level, this represents a turning point -- from a state of submaximal loading to a state of maximal loading. This may have, as Dr. Mcguff suggests, repercussions in terms of neurotransmitter release rate, which may lead to eventual neurotransmitter exhaustion. Or am I getting it all wrong?"
No. “Neurotramitter exhaustion” is not supported in the literature (as per the previous references), at least not in the references I've seen. Again, even during maximal tetanic isometric contractions this has not been shown to be the case.
I hope this answer some of your questions.
Ryan A. Hall
