SandCResearch

Figuring out how strength training works

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Central nervous system (CNS) fatigue has been observed during exercise, as well as in the days following exercise. It is often assumed that CNS fatigue that is observed during exercise is the same CNS fatigue that occurs after exercise. However, this is certainly not true, because the CNS fatigue that arises during exercise is caused by a completely different set of mechanisms from the CNS fatigue that arises in the days after a workout. In this article, I explain how CNS fatigue arises during exercise.

What is CNS fatigue (and why does it matter)?

Fatigue refers to a transitory and reversible reduction in maximum strength (or more accurately exercise performance) due to a preceding bout of exercise. Consequently, CNS fatigue refers to a transitory and reversible reduction in maximum strength due to a preceding bout of exercise that is caused by mechanisms inside the brain or spinal cord.

CNS fatigue is not a feeling, nor is it a perception of being tired or fatigued. It is a reduction in the ability to send a sufficiently large electrical signal to the muscle (in the form of a central motor command). By reducing the size of the central motor command for a given level of perceived effort, CNS fatigue prevents maximal levels of motor unit recruitment from being attained, even when we are exerting a maximal effort.

A gradual increase in the amount of CNS fatigue present during exercise causes a gradual reduction in the magnitude of the central motor command, and this steadily reduces the number of high-threshold motor units that are recruited, starting with the highest high-threshold motor unit and working downwards from there. In other words, CNS fatigue affects motor units from the top downwards.

At this point, it is important to recognize that the fitness industry frequently (and incorrectly) refers to CNS fatigue in the context of overtraining. Yet, it is a completely normal part of any fatiguing exercise, including aerobic exercise as well strength training. It really should be discussed more regularly, at least as often as we discuss the role of metabolites in contributing to fatigue. Indeed, CNS fatigue is likely a more common type of fatigue than metabolite-related fatigue, at least if we consider all types of physical activity.

Nevertheless, the presence of CNS fatigue during exercise is not a good thing, because it prevents the recruitment of all of the accessible high-threshold motor units (and in fact preferentially affects the highest high-threshold motor units). Since increasing the ability to recruit high-threshold motor units is a key mechanism that underpins gains in maximum strength and since this adaptation is caused by reaching very high levels of motor unit recruitment during exercise, it is likely that the presence of CNS fatigue during exercise stops this adaptation from happening. Thus, CNS fatigue is a very detrimental phenomenon if we want to stimulate gains in maximum strength. Additionally, since the level of motor unit recruitment during exercise is a key determinant of the hypertrophy that is stimulated (since the higher the level of motor unit recruitment, the more muscle fibers are activated and therefore trained), the presence of CNS fatigue during exercise likely also reduces the amount of muscle growth that is stimulated after a workout. Thus, CNS fatigue is also likely to be detrimental for bodybuilding.

So what causes CNS fatigue during exercise?

Does reaching a high level of motor unit recruitment cause CNS fatigue during exercise?

It is often suggested that CNS fatigue is caused by exercise that involves a high level of effort, and therefore a high level of central motor command. Indeed, some researchers have implicitly assumed that it is the high level of central motor command that causes fatigue within the brain or spinal cord. Similarly, example, have sometimes suggested that CNS fatigue occurs after training with highly-fatiguing drop sets, and powerlifters frequently assume that CNS fatigue occurs after 1RM efforts.

Despite the popularity of these ideas, nothing could be further from the truth.

Indeed, dozens of research studies have shown that CNS fatigue accumulates during low-intensity aerobic exercise that involves submaximal levels of motor unit recruitment, as well as during low-force isometric contractions that do not involve reaching muscular failure. In fact, the amount of CNS fatigue that is present during submaximal contractions is typically much greater than the amount of CNS fatigue present during high-intensity exercise bouts.

This demonstrates that reaching a high level of motor unit recruitment does not cause CNS fatigue, as is often assumed.

These studies also tell us quite a bit about how the process of CNS fatigue works, since it seems that CNS fatigue is actually increased by exercise duration and not by exercise intensity. Indeed, studies that have directly compared different durations of exercise have shown that the amount of CNS fatigue present during exercise increases with increasing exercise duration, and not with increasing exercise intensity. Similarly, when CNS fatigue has been measured at multiple time-points during a long-duration bout of exercise, it has been shown to increase steadily and gradually over time.

Indeed, this gradual increase in CNS fatigue with increasing exercise duration is likely why exercise order matters during strength training. Several studies have shown that muscles that are trained earlier in a workout experience greater gains in strength and size than muscles that are trained later in the same workout. This probably occurs due to the gradual accumulation of CNS fatigue over the course of the workout, such that the later exercises are performed with a higher level of CNS fatigue than the earlier exercises.

So what are the mechanisms that cause CNS fatigue to appear during exercise, and why do they increase with increasing exercise duration?

What mechanisms do cause CNS fatigue during exercise?

CNS fatigue mechanisms all reduce the size of the central motor command that reaches the muscle during maximal efforts. Yet, these reductions can occur at two very different points: the brain and the spinal cord.

Supraspinal CNS fatigue takes place inside the brain. It reduces the size of the central motor command that is created. Spinal CNS fatigue takes place in the spinal cord. It reduces the size of the central motor command that can be transmitted to the muscle (this mechanism still causes CNS fatigue, even if the brain has managed to generate a sufficiently large signal). Although some commentators have denied the existence of one or other of these two types of CNS fatigue, there is evidence that CNS fatigue during exercise can be caused by both supraspinal and spinal mechanisms.

In terms of spinal CNS fatigue, it is usually accepted that the simple act of repeatedly causing a motor neuron to fire is responsible for some kind of fatigue response, such that the longer that the motor neuron spends firing, the greater the spinal CNS fatigue that occurs. While several investigations have been carried out to identify the exact nature of this mechanism, no clear picture has yet emerged. Even so, it does make sense in the context of the observation that increasing exercise duration increases the amount of CNS fatigue that is present.

In terms of supraspinal CNS fatigue, there is evidence that this can be caused by multiple mechanisms.

One important mechanism is afferent feedback. Afferent feedback refers to information that is collected by receptors at various places inside the body, including within the muscles, and which is then sent along afferent nerves back to the brain. This afferent feedback can be produced by several effects inside muscles or within the bloodstream, including metabolite accumulation and inflammatory mediators.

During exercise, working muscles produce metabolites. These metabolites are detected by receptors inside the muscles, and that information is sent to the brain, which causes us to experience burning and fatiguing sensations. Several studies have shown that the presence of these fatiguing sensations can cause supraspinal CNS fatigue. Conversely, blocking these fatiguing sensations can lead to a reduction in the amount of supraspinal CNS fatigue that is present. Therefore, it seems clear that metabolite accumulation can cause CNS fatigue. Even so, a metabolite-based mechanism does not fit well with the observation that CNS fatigue increases with increasing exercise duration, rather than with increasing exercise intensity, because metabolite accumulation is greater during shorter, higher-intensity types of exercise.

Inflammatory mediators are also produced during exercise, and seem to increase with increasing exercise duration. Also, the presence of these inflammatory mediators appears to cause CNS fatigue during exercise, after exercise, and also as a result of sleep deprivation. Based upon these observations, researchers have developed an explanatory model that links the presence of these inflammatory mediators to supraspinal CNS fatigue through two mechanisms. One mechanism involves afferent feedback, since the inflammatory mediators are produced inside exercising muscles, and can be detected by receptors inside the muscles. Another mechanism involves the inflammatory mediators entering the bloodstream and being detected by the circumventricular organs of the brain, which can be accessed without crossing the blood-brain barrier. Even so, both mechanisms probably work in ultimately the same way, which is to increase the perception of effort (I explain how this works in the next section).

In summary, there are therefore at least four different mechanisms that can cause CNS fatigue during exercise: (1) spinal CNS fatigue due to repetitive motor neuron firing, (2) afferent feedback due to metabolites (albeit likely only during high-intensity exercise), (3) afferent feedback due to inflammatory mediators, and (4) inflammatory mediators directly affecting the brain by entering into the bloodstream. It is likely that spinal CNS fatigue and/or inflammatory mediators are the best explanations for how CNS fatigue builds up with increasing exercise duration, since these mechanisms also increase in importance with increasing time.

At this point, it makes sense to take a moment to explain why an increase in the perception of effort causes supraspinal CNS fatigue.

How do changes in the perception of effort bring about supraspinal CNS fatigue?

According to the psychobiological model of exercise, the brain produces a signal that creates movement. As explained above, this signal is called the “central motor command” and it is sent to the muscles to stimulate motor unit recruitment. Large signals create a high level of motor unit recruitment, and small signals create a low level of motor unit recruitment. Importantly, this central motor command also produces a secondary signal (called the corollary discharge), which is what causes our perception of effort.

This perceived level of effort therefore increases progressively as the size of the central motor command (and the level of motor unit recruitment) both increase. Yet, we can only tolerate a certain level of perceived effort for a given bout of exercise (but the exact level might vary according to our level of motivation). In this way, the level of perceived effort limits the maximum level of central motor command.

CNS fatigue therefore arises when either [A] the level of perceived effort is increased by other factors (which do not simultaneously increase the size of the central motor command), or [B] the level of motivation is reduced. When motivation is maintained at a constant level, increasing the level of perceived effort without increasing the level of central motor command causes us to reach our maximum level of perceived effort earlier than we would normally, such that we are unable to achieve maximal levels of central motor command or maximal levels of motor unit recruitment.

Importantly, afferent feedback (and inflammatory mediators exerting direct effects on the brain) increases the perception of effort, without altering the level of central motor command. Therefore, when afferent feedback is present, the level of perceived effort at any given level of central motor command is increased. For this reason, when the level of perceived effort reaches its maximum tolerable limit in the presence of afferent feedback, the level of central motor command is not maximal, which means that the level of motor unit recruitment is also not maximal. We describe this inability to achieve a maximal level of motor unit recruitment despite the production of a maximal effort as CNS fatigue.

But is CNS fatigue during exercise really that important?

How much does CNS fatigue contribute to overall fatigue during exercise?

CNS fatigue has traditionally been shown to be responsible for 50% of the total fatigue that occurs during aerobic exercise, but only 10% of the total fatigue that occurs in strength training. However, until recently, all tests of CNS fatigue have been conducted after a short rest following exercise, and it seems likely that this short rest has been causing us to underestimate the role played by CNS fatigue during exercise to a large extent.

An important recent study compared the traditional way of testing for CNS fatigue with a novel test that did not allow any rest after exercise. The novel test showed that the CNS fatigue after a short bout of maximal effort strength training was responsible for 30% of the total fatigue, and this was much greater than was reported by the traditional testing method, which found that CNS fatigue contributed just 10% of the total fatigue. Previous research has similarly found that CNS fatigue contributes approximately 5–10% to overall fatigue during heavy strength training.

So this suggests that we have been hugely underestimating the contribution of CNS fatigue to overall fatigue during exercise.

Nevertheless, we should have guessed that this underestimation was taking place. Previous research has often shown that when total fatigue is measured by a strength test after long-duration exercise to task failure, the reduction in strength is much smaller than would have been necessary to cause task failure. This suggests that a very rapid recovery of strength is taking place before the measurement is normally taken.

For example, when performing isometric contractions with 10% of maximum force to task failure, it is logical that strength must reduce by 90% during exercise. Otherwise, task failure would not be reached. Yet, when this has been tested, research has found that the reductions in strength (when they are tested a couple of minutes after exercise) are only 50%. Therefore, there is a further reduction in muscular force of 40% during exercise (the reduction is 90%, which is from 100% down to 10%) that is not mirrored by the reduction in strength during the post-exercise strength test.

It seems likely that this additional fatigue is caused by CNS fatigue that dissipates almost immediately after exercise has terminated, and so is not detected by a post-exercise test that is performed a couple of minutes after exercise. Indeed, even the most rapidly-dispersing peripheral fatigue mechanisms take more than several minutes to dissipate after exercise, so it is highly likely that this extra fatigue has a central origin. This suggests that rather than accounting for 5-10% of overall fatigue during strength training and 40–50% of overall fatigue during aerobic exercise, CNS fatigue probably accounts for 20–30% of overall fatigue during strength training, and 60–70% of overall fatigue during aerobic exercise.

So CNS fatigue during exercise is really important!

Which CNS fatigue mechanisms contribute during exercise but not immediately afterwards?

Which particular CNS fatigue mechanism is responsible for the extremely large fatigue effect that is present during an exercise task but which is not present several minutes afterwards is not clear. As I will explain in the next section, it is unlikely to be either inflammation-related afferent feedback or metabolite-related afferent feedback, because neither of those mechanisms dissipate quickly enough.

This suggests that it could be a spinal mechanism. Unfortunately, there is little research to date into the rate of recovery of spinal CNS fatigue after exercise.

Alternatively, it could be an entirely different mechanism, involving the processing of information gathered from various sources, including the afferent feedback and inflammatory mediators, as well as from cognitive deductions. This is where CNS fatigue starts to require discussion of central governors, which I generally do not discuss, because they are not relevant to testing CNS fatigue by voluntary activation during maximal strength tests.

This psychological mechanism may involve an erosion of self-control. New research has shown that the apparent erosion of self-control (which has traditionally been called “ego depletion”) is probably caused by a task-specific switching of priorities instead of a reduction in resources. This psychological mechanism may bring about a reduction in the ability to exert force during a long-duration task that is not then apparent in a maximum strength test (because the perceived task constraints are different), which then gives the appearance of a rapid recovery of CNS fatigue. It is possible that CNS fatigue is not actually dissipating from the end of the exercise to the strength test, but rather than the CNS fatigue is only apparent in the exercise task, since it involves a longer perceived duration.

Do the various elements of CNS fatigue during exercise recover at different rates?

N.B. Once again, I want to emphasize that the CNS fatigue that is present the following day after exercise is totally different from the CNS fatigue that occurs during exercise, because it is probably caused by the development of muscle damage rather than by the mechanisms listed above. The fact that these CNS fatigue mechanisms recover relatively rapidly should not be taken as an indicator that CNS fatigue is not present in the days following a workout.

There are probably multiple mechanisms of CNS fatigue that are present during exercise. For various reasons, we might expect that these mechanisms will recover at different rates after a bout of exercise. We can identify at least three main elements of CNS fatigue: [A] supraspinal CNS fatigue caused by afferent feedback due to inflammatory mediators or by inflammatory mediators working released into the bloodstream, [B] supraspinal CNS fatigue caused by metabolite-related afferent feedback, and [C] spinal CNS fatigue caused by repetitive motor neuron firing.

  • Inflammatory mediators – since inflammatory mediators take a few hours to dissipate after exercise, they probably contribute to any CNS fatigue that is recorded on the same day as the exercise was performed (typically researchers measure CNS fatigue for 5 – 30 minutes following a workout). Indeed, although it is often claimed that the CNS fatigue that is stimulated during exercise dissipates within minutes, some CNS fatigue is typically present for at least 30 minutes.
  • Metabolites – metabolites dissipate completely within approximately 30 minutes after finishing a bout of high-intensity exercise, but they dissipate more rapidly in the first few minutes, once the venous occlusion caused by muscular contractions has been removed. Therefore, they are probably responsible for the higher level of CNS fatigue that is frequently present at 5 minutes after a strength training workout, compared to after 30 minutes.
  • Spinal mechanisms – although we know very little about the rate of spinal CNS fatigue recovery, spinal CNS fatigue may be one of the mechanisms that dissipates extremely quickly once a bout of exercise has finished. It is possible that this fatigue mechanism essentially disappears as soon as the motor neuron experiences a short break from firing. This would explain the rapid and large recovery from CNS fatigue that often occurs within the first minute of finishing a bout of exercise.

By taking this information into account, we can see that the effects of CNS fatigue are likely underestimated during a bout of exercise itself (because of the rapidly-dissipating spinal CNS fatigue mechanism), that strength training techniques that involve high levels of metabolite accumulation (such as the use of pre-exhaustion, drop sets, and short rest periods) are not a great idea for maximizing adaptations (because of the high levels of supraspinal CNS fatigue caused by afferent feedback), and that long workouts are likely to cause diminishing returns, with later sets and exercises being ineffective (due to the accumulation of supraspinal CNS fatigue due to inflammatory mediators). This is why understanding the mechanisms of CNS fatigue during exercise is so important for strength training programming.

Nevertheless, we can also learn more from these mechanisms.

Does the CNS fatigue that occurs during exercise have a systemic effect or a localized effect?

Although voluntary activation levels are the gold-standard method for assessing the presence of CNS fatigue, CNS fatigue is also often inferred by the presence of non-local fatigue.

Non-local fatigue refers to the existence of fatigue in a muscle that was not used during an exercise bout. This non-local fatigue is frequently used as an indicator that CNS fatigue is present (especially since voluntary activation is very difficult and time-consuming to measure, while non-local fatigue is not). Nevertheless, if we use non-local fatigue to test for the presence of CNS fatigue, we are assuming that CNS fatigue is systemic (insofar as it affects all muscles in the body equally) rather than localized (insofar as it affects only the muscle or motor pathway that was trained).

Interestingly, there is evidence that an element of CNS fatigue may be localized, although much of it is certainly systemic.

When non-local fatigue is measured, there seems to be greater non-local fatigue in muscles that are directly contralateral to the one used during the exercise bout, compared to other muscles in the body. For example, when exercising with the index finger muscle of one arm, there is more non-local fatigue in the index finger muscle of the other arm compared to in the biceps muscles of that other arm. Since contralateral muscles share motor pathways, this suggests that CNS fatigue is greater in those motor pathways that are used during exercise in comparison with those that are not. In other words, there seems to be localized CNS fatigue as well as systemic CNS fatigue.

So what mechanisms might cause this localized CNS fatigue?

What mechanisms might cause a localized CNS fatigue effect (and why does this matter)?

We already know that some of the CNS fatigue mechanisms have systemic effects. Clearly, the inflammation pathway that involves the bloodstream will cause systemic effects, as it works by communicating through the circulation. Similarly, afferent feedback also seems to cause systemic effects. Indeed, recent research has shown that afferent feedback (due to the metabolites produced during exercise) from one muscle causes CNS fatigue in another muscle, as measured during a maximum strength test. Similarly, any indirect CNS fatigue mechanism in the brain caused by a shift in priorities is likely to have systemic effects.

Therefore, spinal CNS fatigue seems to be the only factor that might produce localized effects, since only the motor neurons of the working muscle will be affected by the repeated firing. Cross-over fatigue effects as a result of motor unit firing in the same motor pathway can in this way explain the greater non-local fatigue that seems to occur in the exact contralateral muscles.

Since spinal CNS fatigue likely dissipates very quickly after stopping a bout of exercise, this means that the localized element of CNS fatigue during exercise is probably very short-lived, while the systemic element of CNS fatigue is likely more long-lived. Unfortunately, this means that performing lots of different exercises in a single workout (as during whole-body strength training) will likely not circumvent the problem of increasing CNS fatigue over the course of a strength training workout, since most of the CNS fatigue that builds up over the course of a workout is probably systemic and not localized. It also suggests that when single-leg strength training is performed, appropriate rest periods should be allowed between training each leg, and one leg should not be trained immediately after the other.

What is the takeaway?

CNS fatigue is the name given to the types of fatigue that cause reductions in the ability to send a sufficiently large electrical signal to the muscle (in the form of a central motor command) so as to cause a maximal level of motor unit recruitment during exercise. Supraspinal CNS fatigue during exercise can occur in the brain as a result of afferent feedback from metabolites (during high-intensity exercise) or inflammatory mediators (during low-intensity exercise), as well as a result of inflammatory mediators communicating with the brain via the bloodstream (during low-intensity exercise). Spinal CNS fatigue can occur during exercise as a result of the repetitive firing of motor neurons (during exercise of all intensities).

By reducing the size of the central motor command that reaches the muscle to produce motor unit recruitment, the presence of CNS fatigue during exercise likely prevents gains in maximum strength from occurring by means of increases in the ability to recruit high-threshold motor units. Similarly, it likely reduces the amount of hypertrophy that occurs after training. Therefore, it should ideally be reduced or avoided.

By looking more closely at the mechanisms that underpin CNS fatigue during exercise, we can see that avoiding CNS fatigue during exercise involves: reducing the amount of metabolite accumulation during exercise (such as by avoiding short rest periods, advanced techniques such as pre-exhaustion and drop sets), reducing the exposure to inflammatory mediators (by avoiding very long workouts and too many exercises), and by reducing the duration of each set of exercise to avoid long periods of motor neuron firing (by using heavy or moderately-heavy loads, depending on the training goal).

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Decades of research has demonstrated that the focus of attention used during a movement affects its immediate performance, and also affects the long-term improvements that occur in relation to that movement.

Early research in this area focused primarily on the performance of skilled movements, while later research has also included the performance of more strenuous physical tasks. Indeed, recent research has shown that adopting an external focus of attention (immediately) improves performance during skilled movements (including strenuous activity like strength training exercises), and also permits greater long-term improvements to occur in those movements.

What is attentional focus?

Attentional focus refers to what an individual is thinking about (directing their attention towards) during the performance of a movement. When attention is directed externally (towards an object outside of the body), then the focus of attention is said to be an external focus of attention. When attention is directed internally (towards a part of the body), then the focus of attention is an internal one. If no specific focus of attention is used, the state is often said to be a neutral one.

What does an external focus of attention achieve?

During strength training exercises and strength tests, an external focus of attention has sometimes been shown to increase the force that can be produced, even when maximal efforts are being used. An external focus of attention has also been shown to enhance the number of reps that can be done during a set performed to failure. What is more, an external focus of attention increases vertical jump height, horizontal jump distance, throwing distance, and sprint running speed.

For immediately improving strength training exercise performance or athletic performance, an external focus of attention is very effective!

While the majority of the research into the effects of an external focus of attention during physical movements has investigated the immediate effects of using such cues, a small amount of research has also assessed the long-term effects of using external cues during training. It seems that using an external focus of attention produces similar strength gains to an internal focus of attention, but smaller increases in muscle size. Since hypertrophy contributes to gains in maximum strength, this suggests that, for the same amount of hypertrophy, an external focus of attention causes greater strength gains, by means of neural mechanisms.

But what neural adaptations does using an external focus of attention enhance?

What neural adaptations does an external focus of attention enhance? – coordination

Early research into attentional focus identified that an external focus of attention increased the performance of skilled tasks by improving coordination (both immediately and long-term). It therefore seems likely that the same effect occurs during more strenuous physical tasks, like strength training exercises and athletic performances. Yet, this is difficult to assess, because there are few exercises and athletic performances in which coordination can be measured with any degree of objectivity.

Nevertheless, the standing long jump for distance presents a very useful opportunity for coordination to be assessed, because horizontal jumping distance is greatly affected by the angle of take-off, in addition to the impulse that is produced. Research has shown that using an external focus of attention improves this take-off angle by causing it be directed more horizontally, because most individuals employ a take-off angle that is directed too vertically. This observation provides evidence that an external focus of attention improves the coordination of a physical task by altering the movement pattern such that the task is performed more efficiently, and is therefore achieved more successfully. It also suggests that when elements of a physical task involve submaximal effort (such as the early reps of a strength training set performed to failure), then those elements might be performed more efficiently.

Additionally, if an external focus of attention works primarily by improving coordination (both immediately and long-term), then we would expect it to produce increases in athletic performance (which it does), increases in the number of reps in a strength training set (which it does), and even maximum strength (which it does), but without affecting muscle growth (which it doesn’t). Thus, the idea that an external focus of attention works primarily by improving coordination fits well with most other observations.

What neural adaptations does an external focus of attention enhance? – reduced antagonist coactivation

While an external focus of attention clearly enhances exercise performance by improving the coordination of the movement pattern, it also seems to work through an additional (albeit closely related) mechanism. Indeed, some recent research has shown that using an external focus of attention reduces the level of antagonist coactivation in an exercise.

During many movements, the antagonist muscle contracts at the same time as the agonist, albeit to a lesser degree. While this contributes to joint stability and improves control over the movement, it also reduces the external joint torque for a given level of agonist muscle force. For this reason, a reduction in antagonist coactivation improves strength and exercise performance. It seems likely that reductions in antagonist coactivation occur in response to an improvement in the ability to provide the necessary stability at the joint by activating synergist muscles, as well as by improving balance. Indeed, coactivation is often high when unstable exercises are first performed, and it reduces rapidly as these exercises are practiced.

Using an external focus of attention therefore seems to accelerate the processes of learning to use the synergist muscles or of improving balance in order that antagonist coactivation can be reduced safely. This adaptation has essentially the same effect as an improvement in the coordination of the movement pattern.

Indeed, while reducing antagonist coactivation increases strength and exercise performance, it does not affect the ability to increase muscle size. Reducing the level of antagonist coactivation simply increases the amount of external joint torque that occurs for any given level of agonist muscle force. It does not change the conditions that the muscle fibers within the agonist muscle experience, nor does it change the level of motor unit recruitment in the agonist muscle. Thus, while a heavier weight might be lifted for a larger number of reps once antagonist coactivation has reduced, the experience of the agonist muscle in the set will remain unaltered. Consequently, we would not expect any alteration in the level of antagonist coactivation as a result of using an external focus of attention to affect hypertrophy after training. Indeed, this again fits with the current research, which has found no obvious benefit of external focuses of attention for muscle growth.

What neural adaptations does an external focus of attention enhance? – increased motor unit recruitment

Although there are two very obvious neural mechanisms by which an external focus of attention can enhance exercise performance both immediately and also long-term, some researchers and commentators have suggested that an external focus of attention might also increase the level of agonist muscle activation, by means of an increase in motor unit recruitment.

Indeed, this could occur if the external focus of attention increased motivation, since motivation levels limit the maximum level of effort that can be tolerated, and the perception of effort limits the motor unit recruitment that can be achieved. Indeed, it seems logical that providing an external target might be motivating for an athlete.

However, there are two reasons why we must reject this hypothesis.

Firstly, most studies that have compared the levels of muscle activation in the agonist muscles when using an external focus of attention and when using either no focus of attention or an internal focus of attention have found that muscle activation is actually lower with an external focus of attention! While muscle activation is by no means a perfect representation of motor unit recruitment levels, it is still an indicator.

Secondly, when the ability to recruit high-threshold motor units is increased, this causes an improvement in the ability to achieve hypertrophy. Indeed, this is why a block of heavy strength training potentiates the muscle growth produced by a subsequent block of moderate load strength training. Using heavy loads causes greater improvements in the ability to recruit high-threshold motor units, which means that future blocks of training are able to train more muscle fibers in each working set. Since using an external focus of attention does not enhance hypertrophy, we must assume that it does not increase the ability to recruit high-threshold motor units, either acutely or over the long-term.

Why is it important to identify which neural adaptations are enhanced by external cues?

To identify the practical implications of using external focuses of attention, it is important that we know which neural adaptations are enhanced by external cues. Indeed, there are two key takeaways of the above analysis.

Firstly, as noted above, if external cues work by improving efficiency (by increasing coordination and by reducing antagonist coactivation), then they will not affect hypertrophy. Thus, they are of little use for bodybuilders.

Secondly, if external cues work by improving efficiency (by increasing coordination and by reducing antagonist coactivation) and do not increase motor unit recruitment, then although they are of great value to athletes during sporting movements (such as sprinting, jumping, and throwing), they are probably of little use during most strength training exercises. This is because increases in coordination and reductions in antagonist coactivation are very movement-specific, and stimulating these adaptations in one exercise does not lead to similar adaptations in another exercise that involves the same muscle group. In contrast, increases in motor unit recruitment are highly transferable between movement patterns that involve the same muscle group.

What is the takeaway?

It is likely that an external focus of attention improves strength training performance and athletic performance by means of an improvement in movement efficiency (by improvements in the coordination of the movement and due to a reduction in antagonist coactivation). Consequently, this adaptation is unlikely to transfer very far beyond the movement that was practiced. In this way, these adaptations differ quite markedly from an increase in motor unit recruitment levels, which transfers very extensively between movements that involve the same muscle.

In practice, an external focus of attention is therefore likely to be very valuable when an athlete is training with a movement that will be used in sport (such as the powerlifting exercises for powerlifters, and jumping, throwing, and sprinting for many team sports athletes). Yet, an external focus of attention is unlikely to have the same benefits if it is used during an exercise that does not use a movement pattern that is employed during sport (such as a Nordic curl). In such cases, it may be better to employ coaching cues that can increase motor unit recruitment by increasing the level of motivation that is present, which increases the level of effort that the athlete uses. Ultimately, therefore, while an external focus of attention has often been proposed as essential for athletes in all exercises, this is probably not the case. It would be more accurate to say that an external focus of attention is essential for certain movements for certain athletes.

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Plyometrics are often used by strength coaches and sports coaches to enhance high-velocity athletic performance. In addition to improving the high-velocity force production and maximum theoretical velocity of muscles, plyometrics are assumed to produce additional adaptations that alter the stretch-shortening cycle in a useful way. Yet, exactly how they might alter stretch-shortening cycle function has not previously been explained.

What are plyometrics?

Plyometrics can be defined most accurately as unloaded, high-velocity, high effort exercises that involve a definite landing phase and a stretch-shortening cycle (SSC). Consequently, all plyometrics are SSC exercises, but not all SSC exercises are plyometrics. In other words, plyometrics are basically a subset of SSC exercises.

Indeed, many high effort exercises that are in common use among athletes are excluded from this definition because they only involve one or two of the characteristics.

  • Heavy strength training cannot be defined as plyometrics even though it involves an SSC, since it is loaded, low-velocity, and does not involve a landing phase.
  • Power training cannot be defined as plyometrics even though it involves an SSC and is high-velocity, since it is loaded and does not involve a landing phase.
  • Squat jumps cannot be defined as plyometrics even though they are high-velocity and unloaded, since they not involve either an SSC or a landing phase.
  • Countermovement jumps cannot be defined as plyometrics even though they are high-velocity, are unloaded, and involve an SSC, because they do not involve a landing phase.

What is a stretch-shortening cycle (SSC)?

An SSC is a concentric contraction that is immediately preceded by an eccentric contraction. Since the placement of an eccentric contraction immediately before a concentric contraction typically increases the force and velocity of the concentric contraction, this leads to a phenomenon known as the SSC effect. The SSC effect can be quantified by the extent to which either concentric speed, power, or force are increased when the concentric phase is preceded by an eccentric, compared to when the same concentric phase is performed from a standing start.

Although the SSC is often described as a single phenomenon, it is known to be produced by at least five different mechanisms, all of which work in different ways and experience different adaptations after training:

  • the stretch reflex, which is a spinal reflex that increases motor unit recruitment when the working muscle is stretched (the spinal reflex increases the level of central motor command that is sent to the muscle, which in turn increases the level of motor unit recruitment, thereby increasing muscle force, but obviously not affecting single muscle fiber mechanical tension);
  • preactivation, which involves the muscle being activated before the start of the concentric contraction, enabling a higher force to be produced from the outset (in this respect, preactivation does not alter the force produced, but instead alters the timing of the force, and since higher forces are exerted earlier in the contraction, this permits a higher impulse, which in turn generates faster bar speeds and power outputs);
  • the residual force enhancement effect, which involves titin being stretched in the eccentric phase and contributing to force in the concentric phase, very much like an elastic band that is stretched and then released (bearing in mind that this elastic band only functions in this way when the muscle fiber is activated in the eccentric phase);
  • elastic energy storage in tendons in the eccentric phase, which is then released in the concentric phase, and;
  • changes in the force-velocity relationship, due to the tendon lengthening in the eccentric phase, leading to reduced muscle lengthening in the eccentric phase, such that the tendon then provides much of the shortening in the subsequent concentric phase, leading to reduced muscle shortening in the concentric phase. When this happens, the muscle fiber shortening velocity in the concentric phase is disconnected from the joint angular velocity. The more the tendon lengthens and shortens, and the less the muscle lengthens and shortens, the slower the muscle fibers can shorten for the same joint angular velocity, and by shortening more slowly, they can produce much higher forces.

By considering these mechanisms carefully, we can identify which of them are the most important during plyometrics, and subsequently also identify what adaptations they might experience such that plyometrics performance can be improved by training.

Which SSC mechanisms are most important during plyometrics?

Introduction

Some SSC mechanisms are more important in some types of muscular contraction, while other SSC mechanisms are more important in other types. To understand more about plyometrics, it is helpful to consider which of the SSC mechanisms are most important for high-velocity, high effort movements with a pronounced SSC.

The stretch reflex

While the stretch reflex is probably the most famous mechanism that underpins the SSC effect, it is unlikely to contribute much to the SSC effect during a plyometric exercise. When a movement is performed with a high effort, it is already employing a high level of motor unit recruitment. Thus, the stretch reflex, which works by increasing motor unit recruitment, has little scope to enhance force production in a SSC action (compared to a similar concentric-only action), because there is little capacity for increasing motor unit recruitment beyond a level that is already very high (and in some cases may already be maximal).

Preactivation

The preactivation effect is likely a key SSC mechanism during plyometrics, since the relatively high eccentric force produced in the landing phase means that the muscle is strongly activated before the start of the concentric phase. In this way, preactivation is also an SSC mechanism during heavy strength training. For this reason, preactivation is not that interesting for understanding plyometrics, since it occurs similarly in most high-effort contractions.

Residual force enhancement

The residual force enhancement (RFE) effect has been carefully described by many studies. When titin is stretched inside an activated muscle fiber, it produces a very high force. In this way, titin also explains why eccentric contractions produce much higher forces than either isometric or concentric contractions. Nevertheless, the force that titin produces is caused by its stretch, in the same way as an elastic band. Thus, as the muscle fibers begin the concentric phase, they still experience this elastic force pulling them back to their starting length. Consequently, titin can contribute to force production in the concentric phase of SSC movements, and this is called the RFE effect.

The magnitude of the RFE effect is dependent upon two factors.

Firstly, it is dependent upon the number of muscle fibers that are activated in the eccentric phase, because titin only produces this high force when it is inside an activated muscle fiber. Secondly, it is dependent upon the extent to which the muscle fibers are lengthened while they are activated, in the same way as an elastic band produces force in proportion to the extent to which it is elongated. Consequently, it is easy to see that the RFE effect is an important contributor to the SSC effect during heavy strength training exercises.

During heavy strength training, a large number of muscle fibers are activated for a large proportion of the lowering phase of the exercise, which means that the RFE effect can contribute substantially to the force production in the subsequent lifting phase.

During plyometrics, there is also a large number of muscle fibers activated in the lowering phase, due to the relatively high eccentric forces that are exerted upon landing. Yet, the RFE effect is limited by the extent to which muscle fibers lengthen in this phase, because this lengthening is much smaller than in heavy strength training, for two reasons. Firstly, plyometrics typically involve a shorter joint angle range of motion than strength training exercises. Secondly, tendons are viscoelastic, and this means that they tend to lengthen very little during heavy strength training. This means that the muscle fibers that are in series with the tendons can lengthen a long way (which produces a large RFE effect). In contrast, tendons lengthen a lot during plyometrics, which means that the muscle fibers cannot lengthen anywhere near as far (which produces a limited RFE effect). Thus, while the RFE effect probably does contribute to the SSC effect during plyometrics, it does not contribute to the same extent as during heavy strength training.

Elastic energy storage in tendons

Whether the storage of elastic energy in tendons during the eccentric phase of an exercise can enhance velocity, power, or force during the subsequent concentric phase is currently unclear, although it does seem to play an important role in increasing energy efficiency, which makes it a very important mechanism during aerobic exercise.

Changes in the force-velocity relationship

The final SSC mechanism involves an alteration in the force-velocity relationship of the working muscle fibers. This occurs due to the lengthening and shortening of the tendons that are in series with the muscle. When a tendon lengthens in the eccentric phase of an SSC movement, it allows the muscle fibers to lengthen less. When the tendon shortens in the subsequent concentric phase, it allows the muscle fibers to shorten less. When muscle fibers shorten less (over the same joint angle range of motion), they shorten slower for the same joint angular velocity. This means that they produce a higher force, due to the force-velocity relationship. The greater the tendon lengthening in the eccentric phase, the greater the tendon shortening in the concentric phase, and the less that the muscle fibers lengthen and shorten. Thus, the more that the tendons lengthen and shorten during the SSC, the greater force that the muscle fibers produce.

We might expect that this final mechanism would be more important for plyometrics than for heavy strength training, because tendons tend not to lengthen and shorten very much during heavy strength training, while they do lengthen and shorten quite a lot during plyometrics, and other light load exercises.

Comparing SSCs in heavy strength training and plyometrics

When comparing heavy strength training and plyometrics, we can identify that the working mechanisms in both activities are: [A] preactivation, [B] the residual force enhancement effect, and [C] changes in the force-velocity relationship due to tendon lengthening and shortening.

Moreover, we can see that the contribution of preactivation will probably be fairly similar in both types of exercise, while the residual force enhancement effect will be greater during heavy strength training, and the effect of changes in the force-velocity relationship due to tendon lengthening and shortening will be greater during plyometrics.

The magnitude of the SSC effect can be measured by comparing the athletic performance, force or bar speed of a non-SSC exercise variation with the athletic performance, force or bar speed of an SSC exercise variation. For example, we might compare jump heights during squat and countermovement jumps. Alternatively, we might compare concentric bar speeds in bench presses or back squats involving both eccentric and concentric phases with those same exercises performed as concentric-only exercises from a static starting point. The percentage increase in performance that occurs as a result of using a SSC exercise variation instead of a concentric-only exercise variation can be defined as the SSC effect.

The magnitude of the SSC effect is greater when performing light load exercise (like plyometrics), compared to when doing heavy load exercise (like heavy strength training). This suggests that the overall contribution of changes in the force-velocity relationship due to tendon lengthening and shortening is greater than the overall contribution of the residual force enhancement effect, and also that the SSC effect is a very important aspect of plyometrics.

What causes the SSC effect to increase after plyometrics?

The SSC effect is a good way to assess SSC function, or the extent to which the SSC can enhance performance. It can be quantified as the extent to which either concentric speed, power, or force are increased when the concentric phase is preceded by an eccentric, compared to when the same concentric phase is performed from a standing start.

To the extent that the SSC effect increases after plyometric training, then this would be a very important contributor to increased athletic performance. Moreover, given that the main contributor to the SSC effect during plyometrics seems to be the changes in the force-velocity relationship due to tendon lengthening and shortening, it seems likely that any increase in the SSC effect would involve an improvement in this mechanism.

For tendon lengthening during the eccentric phase of a plyometric movement to increase, the muscle would have to increase its eccentric strength relative to the stiffness of the tendon. In this way, the muscle would be better able to resist lengthening during the eccentric phase, and the tendon would have to lengthen more instead.

While it has traditionally been assumed that increases in tendon stiffness contribute to the increases in athletic performance that occur after plyometric training, this is probably not true. In fact, not all studies have revealed increases in tendon stiffness after plyometric training. Moreover, when plyometric training is compared with other types of exercise, such as heavy strength training and isometric training, it almost always produces smaller increases in tendon stiffness. Consequently, if the mechanism by which plyometrics improved SSC function was an increase in tendon stiffness, then heavy strength training would be superior at producing this effect, and plyometrics would be largely unnecessary. Since this is not true, it is likely that other adaptations are involved.

In contrast to the effects on tendon stiffness, there is good evidence that plyometrics improve the eccentric strength of the muscle to a greater extent than other types of exercise, including isometric training. In the context of plyometrics research, eccentric strength is sometimes measured and described as “active muscle stiffness” to make it clear that the muscle is working in series with the tendon, and that the muscle must overcome the stiffness of the tendon.

By increasing eccentric strength to a greater extent than tendon stiffness, plyometrics enhance the size of the SSC effect. After plyometric training, the tendons tend to lengthen more and the muscle fascicles tend to lengthen less in a high-velocity, SSC contraction. Thus, the traditional idea that plyometrics cause an improvement in athletic performance by means of increases in tendon stiffness is not correct. Rather, plyometrics improve athletic performance by increasing eccentric strength more than tendon stiffness. In contrast, isometric training (and heavy strength training) cause greater increases in tendon stiffness than in eccentric strength (since eccentric strength often lags concentric strength these types of training, while increases in tendon stiffness are quite pronounced. Thus, the SSC effect is likely reduced after these types of training, which is likely one of the reasons that these types of training are much less effective for improving athletic performance than plyometrics.

What is the takeaway?

In addition to improving high-velocity force production and speed, plyometrics improve SSC function, leading to an increase in the size of the SSC effect. This probably occurs by means of a greater increase in eccentric muscle strength than in tendon stiffness, such that muscles are able to lengthen less during landing (eccentric) phases and tendons are forced to lengthen more. By lengthening less in the eccentric phase, muscles necessarily shorten less in the following concentric phase. By shortening less, they shorten less quickly for the same joint angular velocity, and this allows them to produce higher forces owing to the force-velocity relationship.

In this way, plyometrics differs from heavy strength training, which likely produces greater increase in tendon stiffness than in eccentric muscle strength, such that muscles are forced to lengthen more during landing (eccentric) phases and tendons are able to lengthen less. It seems likely that extended periods of time spent performing heavy strength training likely reduce SSC, but that subsequent blocks of plyometrics may be able to reverse this adverse effect. In this way, the success of traditional periodization models involving blocks of heavy strength training followed by blocks of plyometrics can be explained.

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Eccentric overload training tends to produce similar hypertrophy to normal strength training. This is strange, because we might expect the combination of eccentric training and concentric training within the same set to cause greater muscle growth compared to normal strength training. Why does this superior muscle growth not happen?

What is eccentric overload training?

In this article, when I refer to “eccentric overload,” I am talking about strength training that involves maximal efforts in the lowering (eccentric phase) of the exercise, in the same way that eccentric training involves maximal efforts in the lowering (eccentric phase) of the exercise. This is an important point, because the term “eccentric overload” is often incorrectly used to refer to slowing down the lowering (eccentric) phase during normal strength training. Yet, these types of training are fundamentally different from each other, at least from a physiological point of view.

Eccentric overload involves maximal efforts on every rep, and this means that it involves a very high level of motor unit recruitment on every rep. This in turn means that a lot of muscle fibers are activated on every rep, and are therefore stimulated to grow. In contrast, slow lowering (eccentric) phases during normal strength training involve submaximal efforts on each rep (and therefore a low level of motor unit recruitment). This means that only a relatively small proportion of the fibers in the muscle are activated and stimulated to grow.

How does fatigue develop during sets performed with different contraction types?

#1. Introduction

In my view, the reason why eccentric overload training does not produce greater hypertrophy than normal strength training is because of differences in the way that fatigue develops during [A] normal strength training, and [B] eccentric overload training. While it is often assumed that the fatigue that occurs in concentric and eccentric contractions is very similar (and therefore has similar effects), this is not actually the case.

#2. Normal strength training

During normal strength training, lifters perform stretch-shortening cycle actions comprising both lifting phases (concentric contractions) and lowering phases (eccentric contractions). At the start of the set, the level of motor unit recruitment (and therefore the number of activated muscle fibers) is necessarily much higher in the lifting phase than in the lowering phase, because of the extra passive tension that muscle fibers exert when they are actively stretched (more force per muscle fiber means fewer muscle fibers need to be activated to produce a given force).

Since the fast twitch muscle fibers of higher threshold motor units are more easily-fatigued than the slow twitch muscle fibers of lower threshold motor units, fatigue develops more quickly during the lifting (concentric) phase than in the lowering (eccentric) phase.

In concentric contractions, the formation of crossbridges is relatively inefficient, which leads to a high energy usage, and this in turn causes metabolite accumulation to occur quite quickly. The accumulation of metabolites primarily causes muscle fiber shortening speed to slow down, by means of acidosis (the effects of phosphate ions on force production are delayed by comparison). Importantly, this slowing down of the muscle fiber does not reduce the force that it produces, which means that the fiber continues to experience mechanical tension (which is the factor that stimulates muscle fibers to increase in size).

Obviously, acidosis has no fatiguing effect on eccentric contractions, because these involve muscle fiber lengthening, and not muscle fiber shortening. Reducing the speed at which the muscle fiber shortens cannot really influence the force that is produced while the same muscle fiber lengthens. Therefore, the primary type of fatigue that is generated by concentric contractions in the lifting phase of normal strength training does not affect the ability of muscle fibers to produce force in the lowering phase. Consequently, while effort (and therefore also motor unit recruitment) will increase due to increasing fatigue in the lifting phase as proximity to failure approaches, the same increases in effort (and motor unit recruitment) do not occur in the lowering phase.

#3. Concentric-only training

In concentric-only training, fatigue progresses in very much the same way as in normal strength training. Metabolite accumulation occurs, which reduces muscle fiber shortening speed. When the strength training set is being done with a self-selected tempo, this then requires an increase in motor unit recruitment such that additional muscle fibers are activated to compensate, and the desired tempo can be maintained. Again, this slowing down of the muscle fiber does not reduce the force that it produces, which means that the fiber continues to experience mechanical tension (which is the factor that stimulates muscle fibers to increase in size).

#4. Eccentric-only training

In eccentric-only training, fatigue progresses differently compared to in normal strength training and in concentric-only training, for two important reasons. Firstly, eccentric contractions are very efficient, and do not require the same amount of ATP as concentric contractions in order to produce force, partly because of the large role played by the passive elements (which do not require energy), and partly because each crossbridge requires less energy to be pulled open than it does to form in the first place. For this reason, metabolite accumulation is fairly minimal during eccentric contractions. Secondly, the stretching of muscle fibers while they are activated opens stretch-activated ion channels, which cause a large number of calcium ions to enter the muscle fiber from the surrounding area. This causes calcium ion-related fatigue mechanisms to occur much more quickly than they do during isometric or concentric contractions.

The main types of calcium ion-related fatigue are [A] excitation-contraction coupling failure, and [B] reductions in sarcolemmal excitability. These types of fatigue do not cause a reduction in muscle fiber shortening speed. Rather, they both cause a dramatic reduction in muscle fiber force by preventing the crossbridges inside the muscle fiber from forming in the first place. This is why eccentric-only training causes much larger reductions in strength after a set than concentric-only training (but causes smaller changes in maximum muscle shortening speed). It is also why continuing to perform more and more reps of eccentric contractions in a set doesn’t continue to produce more and more hypertrophy. The calcium ion-related fatigue suppresses the ability of muscle fibers to produce force (and therefore experience mechanical tension) in a way that metabolite-related fatigue does not.

#5. Eccentric overload training

During eccentric overload training, the level of effort (and therefore the level of motor unit recruitment) is high in both the lifting and lowering phases of an exercise. Hence, the easily-fatigued, fast twitch muscle fibers experience fatigue from both sets of mechanisms (metabolite accumulation in the lifting phase and calcium ion-related mechanisms in the lowering phase).

This has a very interesting effect.

Although the primary fatigue mechanism that occurs during concentric contractions (metabolite accumulation) does not affect force production in eccentric contractions, the reverse is not true. Calcium ion-related fatigue mechanisms that are provoked during eccentric contractions absolutely do reduce force production during concentric contractions.

Consequently, during eccentric overload training, the muscle fibers of the high-threshold motor units start to experience excitation-contraction coupling failure from the very first rep of the set. This is not a major problem for any adaptations that are stimulated by the lowering phase, since that happens during eccentric-only training anyway. However, it is a big problem for any adaptations that might be stimulated by the lifting phase, because it causes reductions in muscle fiber force that would not occur in normal strength training or in concentric–only training (where metabolite accumulation is the primary mechanism of fatigue).

How does hypertrophy occur after training with different contraction types?

#1. Introduction

One interesting feature of strength training is that it causes different types of hypertrophy depending on the extent to which passive tension is experienced by the activated (and responsive) muscle fibers. When muscle fibers experience a lot of passive tension due to titin being stretched, they tend to grow by increasing in length. When they experience mechanical tension without passive tension, they tend to grow by increasing in diameter. We can use this observation to draw inferences about how hypertrophy is stimulated after different types of strength training.

#2. Normal strength training and concentric-only training

After normal strength training and concentric-only training, most (if not all) muscle fiber growth occurs in the form of increases in muscle cross-sectional area. Unless the concentric phase starts from a stretched position (which causes passive tension), there is no substantial increase in fascicle length. This tells us that the muscle fibers that belong to the high-threshold motor units (which are the ones that respond to strength training) do not experience very much passive tension during these types of training.

This is logical if we take into account the fact that concentric-only training does not involve a lowering phase, and therefore cannot experience passive tension (unless each concentric phase starts from a stretched position). It is also logical if we take into account the fact that normal strength training involves a relatively low level of muscle activation in each lowering phase, such that only a relatively small proportion of the fibers in the muscle are activated and stimulated to grow longitudinally.

#3. Eccentric-only training and eccentric overload training

After eccentric-only training and eccentric overload training, most muscle fiber growth occurs in the form of increases in muscle fiber length. In contrast, there are comparatively small increases in muscle cross-sectional area (and probably even smaller increases in muscle fiber diameter, since some increases in muscle cross-sectional area can arise due to increases in muscle fiber length).

This tells us that both eccentric-only training and eccentric overload training mainly cause muscle fiber growth due to experiencing passive tension in the eccentric phase. While this may be obvious for eccentric-only training, it is perhaps surprising for eccentric overload training, because it implies that the concentric phase doesn’t really do very much for hypertrophy.

Why might this happen? There is an obvious explanation.

Unlike in normal strength training, considerable fatigue is produced in the eccentric phase of eccentric overload strength training. While the metabolite-related fatigue produced in concentric phases does not affect eccentric muscle fiber force production, the calcium ion-related fatigue produced in eccentric phases does affect concentric muscle fiber force production.

In fact, by the time a set of eccentric overload training reaches the final few reps of the set (in which concentric phases are able to stimulate hypertrophy), the level of calcium ion-related fatigue is has reduced muscle fiber force to the point where the mechanical tension cannot stimulate much muscle growth. Thus, only the eccentric phase is able to trigger hypertrophy in eccentric overload training, which is why it mainly increases muscle fiber length, in the same way as eccentric-only training.

What is the takeaway?

Eccentric overload training does not cause more hypertrophy than normal strength training, and this probably happens because of the different type of fatigue that develops in the eccentric phase of each rep, which impairs the level of mechanical tension that is produced (and therefore experienced) by muscle fibers in each concentric phase to a greater degree than occurs during normal strength training. This reduces the stimulus that is experienced in the concentric phase, and thus most of the hypertrophy is actually caused by the eccentric phase (which we can see must be the case, because the hypertrophy that occurs after eccentric overload training is mainly in the form of increases in fascicle length, the same as after eccentric-only training).

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