Does training with greater fatigue impair gains in speed?

If you enjoy this article, you will like my first book (see on Amazon).

With the arrival of velocity-based training methods, it has become clear that athletic strength training does not need to involve a high degree of fatigue. Indeed, superior results in some high-velocity performance measures seem to be achieved when training with a smaller degree of velocity loss on each set (and therefore less fatigue). So why might fatigue be detrimental for making gains in high-velocity strength?

What is fatigue, and what does it do?

Whenever we exercise, we experience a temporary (and reversible) reduction in strength. This is called “fatigue.” Contrary to popular belief, fatigue is not how we feel after a workout, but the measurable change in performance.

There are many mechanisms that cause losses in strength (fatigue). Broadly speaking, these mechanisms work in one of two ways. They either cause a reduction in the level of motor unit recruitment (central nervous system [CNS] fatigue) or they cause a reduction in the force that the muscle itself can exert, irrespective of the input from the CNS (peripheral fatigue).

Although CNS fatigue is not widely discussed (or if it is discussed, it is usually thought to be the same thing as overtraining), it actually happens during all types of exercise, including both strength training and aerobic exercise. It seems to increase with proximity to task failure, as well as with task duration. CNS fatigue is actually highest in very fatiguing, long-distance exercise like marathon running, and lowest in very short duration tasks like 1RM efforts. The idea that 1RM deadlifts cause large amounts of CNS fatigue (compared to lifting lighter loads) is very much a myth.

When a muscle experiences CNS fatigue during a strength training set, this impairs the maximum level of motor unit recruitment that is reached, and it also reduces the motor unit firing frequency of these motor units (because motor unit recruitment and firing frequency are linked). Since Henneman’s size principle is not violated by fatigue, the process of CNS fatigue must necessarily begin by “switching off” the highest of the high-threshold motor units, before working gradually downwards.

Peripheral fatigue involves a number of different mechanisms, which can occur anywhere between the muscle cell membrane and the actin-myosin crossbridges. When a muscle experiences peripheral fatigue during a strength training set, this impairs the maximum force that each of the working muscle fibers can produce. It does not materially affect muscle fibers that are not working. In addition, some of the peripheral fatigue processes that occur inside the working muscle fibers cause muscle damage (sustained fatigue after the workout), and likely also stimulate certain exercise adaptations (but exactly which adaptations will be the subject of a separate article).

Which fibers are working depends on the motor unit recruitment level throughout the set, which is determined by the level of effort. During normal, recreational strength training, with a self-selected tempo, the muscle fibers of the low-threshold motor units fatigue first, while the fast twitch muscle fibers of the high-threshold motor units are only fatigued at the end of the set, albeit this occurs quite quickly. In athletic strength training, which involves a maximal effort on each rep, muscle fibers of low- and high-threshold motor units fatigue at similar rates to begin with, then the fast twitch muscle fibers of high-threshold motor units fatigue quickly towards the end of the set (fast twitch fibers are metabolically more efficient when moving at fast speeds, so they don’t fatigue as quickly as you might expect early on in the set). The differences in which muscle fibers are fatigued is what causes different shifts in the force-velocity profile with different types of exercise.

Can greater fatigue during a workout impair gains in high-velocity strength?

There is evidence that strength training workouts that involve greater fatigue (either by training with a closer proximity to failure or with higher volumes) can impair gains in high-velocity strength, and this can happen even without impairments in maximum strength. In fact, higher volume training programs can cause greater gains in maximum strength while still causing smaller gains in high-velocity strength than a lower volume of similar training.

Training with different proximities to failure can be explored by comparing (1) programs that involve different numbers of reps in reserve, (2) programs that involve different degrees of bar speed loss over a set, and (3) programs that involve a fixed number of reps for a workout but different amounts of rest between sets.

Velocity-based training studies assess the effects of stopping each set in a workout when the athlete reaches a certain proximity to failure, by reference to a bar speed threshold. The bar speed threshold is set as a certain percentage loss in bar speed loss from the speed of the first rep in the set. Commonly, studies have tested the effects of stopping each set when bar speeds fall by 5–40% from the bar speed of the first rep of the set. Moreover, such studies usually compare the effects of training with smaller (5–20%) and larger (20–40%) bar speed losses, which is essentially the same thing as training with a larger or a smaller number of reps in reserve.

Several velocity-based training studies have found that training with smaller bar speed losses leads to greater improvements in measures of high-velocity strength or athletic performance (such as sprinting or jumping) than training with larger bar speed losses. Moreover, this effect occurs even while gains in maximum strength are similar. This suggests that training with a greater proximity to failure (and therefore more fatigue) in each set might be particularly detrimental for high-velocity strength.

Additionally, a recent study found that strength training with a cluster set configuration caused a shift towards a velocity-oriented force-velocity profile, while traditional set strength training with the same load and number of reps caused a shift towards a force-oriented force-velocity profile. Yet, gains in maximum strength were the same in the two training groups. Cluster set configurations differ from traditional set strength training insofar as they involve fewer reps before a rest is taken, which reduces the proximity to failure (and therefore the amount of fatigue). Indeed, in this study, the cluster set training configuration allowed smaller losses in bar speed during training, which indicates that it caused less fatigue.

Recently, a brand new study discovered that a high volume program of fast eccentric-only training caused greater gains in maximum strength but smaller increases in high-velocity strength than a similar but lower volume training program. The smaller improvement in high-velocity strength when using high volumes was very likely attributable to similar mechanisms as in the velocity-based training and cluster training studies, since the high volume program would be expected to cause more fatigue.

How might fatigue impair high-velocity strength training adaptations?

The ability to produce a force at a high velocity is dependent upon different factors from the ability to produce a force at a low velocity. The ability to exert force at a high speed requires that the muscle fibers can attain that speed, but this is not a requirement at slower velocities. Consequently, athletes who can exert meaningful forces at high speeds are those with the ability to produce the fastest muscular contractions (without regard to force production), and this ability is determined by factors both inside the CNS and inside the muscle that often have little to do with force production.

The main factors that determine the ability to produce fast muscular contractions are (1) coordination, which ensures that any force that is exerted by the working muscle fibers is directed towards the task instead of elsewhere, (2) motor unit recruitment, which determines the number of muscle fibers that are able to produce force at the required speed, (3) motor unit firing frequency, which determines the number of crossbridges that can be formed at a given muscle fiber contraction velocity, (4) antagonist coactivation, which determines the amount of resistance that is provided by the opposing muscles at the joint, while the agonist muscles are trying to produce a movement, and (5) muscle fiber shortening velocity, which determines the maximum possible speed that a fiber can shorten, if all other constraints are removed.

It is actually very difficult to separate out the influence of most of these factors on force and velocity. Only muscle fiber shortening velocity can really be argued to affect velocity exclusively, and even that affects force at submaximal velocities because of the way that the force-velocity relationship works. Ultimately, however, they are all the main contributors to high-velocity strength, which is what is most important.

While it is often said that “a bigger muscle is a stronger muscle,” this aphorism is much less true when we measure strength (force) at fast speeds instead of at slow speeds. Indeed, hypertrophy produces a few negative effects on the ability to exert force at fast speeds (such as increased internal moment arm lengths and increased tissue inertia), which counteract the beneficial effect of adding actin-myosin crossbridges by increasing the total number of myofibrils inside a muscle fiber.

Anyway, let’s look at how fatigue during training might have a negative effect on gains in high-velocity strength through each of these mechanisms.

Improvements in coordination are very likely a major contributor to strength gains at any velocity. However, they have been most extensively researched in the context of fast movements, and there is some indirect evidence to suggest that improvements in coordination may be a bigger contributor to gains in high-velocity strength than gains in low-velocity strength.

Training in a fatigued state is known to impair motor learning, so it is logical that allowing athletes to train closer to failure or with higher volumes will reduce improvements in coordination in the exercise, movement skill, or drill being trained (and hence gains in performance in that exercise, movement skill, or drill, and in any associated movement to which these activities are intended to transfer). Given the greater relevance of coordination to high-velocity strength than to low-velocity strength, this problem may be bigger when training and testing faster movements. Training while experiencing more fatigue could thus preferentially impair high-velocity strength gains.

Improvements in the ability to recruit motor units often (but not always) occur after strength training methods involving a high level of effort, such as heavy (or moderate load) strength training and plyometrics. This adaptation involves bringing additional high-threshold motor units (which were not previously accessible to the motor cortex) under voluntary control for the first time. The adaptation often (but not always) seems to be triggered when the exercise used in training involves a maximal level of effort, and therefore often (but not always) attains a maximal level of motor unit recruitment.

Although we might assume that an improvements in the ability to recruit motor units would affect strength gains at any velocity to the same extent (and I have tended to hold this view previously), it is probably not entirely true, because of the relationship between motor unit recruitment and muscle fiber type. Low-threshold motor units tend to control mainly slow twitch muscle fibers, while high-threshold motor units tend to control mainly fast twitch muscle fibers. The properties of muscle fibers change gradually from the lowest motor units to the highest motor units. They go from being very slow in contraction velocity (and very oxidative) to being very fast in contraction velocity (and very glycolytic).

The maximum contraction velocity of fibers of each type varies a lot. Slow twitch muscle fibers can only shorten at a very slow speed (approximately 0.5–1.0 fiber lengths per second), while fast twitch fibers can shorten much more quickly (approximately 2–6 fiber lengths per second). Consequently, when we test maximum strength at a slow velocity (<1 fiber length per second), all the slow and fast twitch muscle fibers can contribute to force production, at least to the extent that actin-myosin crossbridges can bind at that muscle fiber contraction velocity. However, when we test maximum strength at a fast velocity (>2 fiber lengths per second), none of the slow twitch muscle fibers will be able to contribute to force production. Therefore, high-velocity strength is determined entirely by fast twitch fibers. This simple example can be extrapolated such that only the very fastest muscle fibers can contribute to force during the fastest movements.

Consequently, when new (high-threshold) motor units are made available to the motor cortex as a result of training, they comprise mainly (if not entirely) fast twitch fibers with very fast contraction speeds, and this likely increases high-velocity strength disproportionately to low-velocity strength (note that the fact that even athletic strength training almost always causes greater increases in low-velocity strength than in high-velocity strength suggests that some substantial, different adaptations must be occurring simultaneously, in order to reverse the effects of the increase in voluntary activation on the ratio of high-to-low velocity strength).

Importantly, fatigue may impair the ability to stimulate increases in motor unit recruitment. We know this because light load strength training involves maximal efforts towards the end of a set, which means that the motor cortex is sending a signal to stimulate maximal levels of motor unit recruitment (which should bring additional high-threshold motor units under voluntary control by the next workout), but increases in voluntary activation capacity do not happen after training. This may occur because of the greater CNS fatigue when training with lighter loads, which may prevent the high effort from translating into a maximal level of motor unit recruitment during exercise. Given the greater relevance of motor unit recruitment to high-velocity strength than to low-velocity strength, the negative effects on this adaptation may well be bigger when training and testing with faster movements.

Motor unit firing frequency (MUFR) is the number of pulses sent by the CNS to the muscle every second. Although there is a relationship between motor unit recruitment and MUFR within the motor control scheme, MUFR still seems to be far less important for force production at low velocities than at high velocities (as indicated by the higher level of MUFR in fast contractions than in slow contractions). This is most likely because each new pulse is intended to act at the point of actin-myosin crossbridge release from the previous pulse, and actin-myosin crossbridges release much more rapidly at faster contraction speeds.

Although one recent study did find that MUFR increased after heavy strength training, most previous studies have found that isometric training or heavy strength training does not change MUFR. This is very different from the effects of high-velocity power training, which increases MUFR substantially. Thus, increases in MUFR seem to be an adaptation that is preferentially stimulated after using fast movements, and this is likely because it plays a larger role in high-velocity force production.

Whether fatigue during exercise might impair potential increases in MUFR is not clear, but it would seem logical. The MUFR does not reach as high levels in a maximal effort contraction at a slow speed compared to in a similar, maximal effort contraction at a fast speed (likely because a greater MUFR is simply unnecessary to achieve optimal actin-myosin crossbridge formation). Given that fatigue involves a slowing of muscle fiber contraction velocity, it is possible that this could reduce the level of adaptations in MUFR that occur.

Until recently, the literature indicated that reductions in antagonist coactivation (causing increased strength) were predominantly a feature of high-velocity training, and did not occur after low-velocity strength training. Moreover, these adaptations seemed to be velocity-specific, and only applied to tests of high-velocity strength. More recently, it has been shown that reductions in antagonist coactivation may also occur after very long periods of heavy strength training, although this does not negate fact that larger, velocity-specific adaptations still occur after high-velocity training.

Whether fatigue during exercise might impair potential adaptations that lead to reductions in antagonist coactivation is not clear. Fatigue might alter the level of antagonist coactivation during a bout of exercise, and such a change might be reasonably expected to affect any long-term neural adaptations (most likely in a negative way).

Contrary to popular belief, muscle fiber contraction velocity actually changes by way of two different mechanisms after training.

Firstly, the contraction velocity of a muscle fiber obviously changes if its fiber type changes. In this respect, exercise (of any kind) causes a reduction in the contraction velocity of a single muscle fiber, as that fiber shifts from a type IIX fiber to a type IIA fiber (or as that fiber shifts from a hybrid type containing more glycolytic isoforms to pure types with more oxidative isoforms). Importantly, more fatiguing exercise (either in the form of a greater proximity to failure or a high training volume) causes a larger shift in muscle fiber type from type IIX to type IIA. This is likely a key way in which more fatiguing training can impair gains in high-velocity strength, given that only the fastest muscle fibers are relevant for the highest speed contractions.

Secondly, the contraction velocity of a single muscle fiber can be altered irrespective of its type. This is very important, because high-velocity training methods (albeit not normal strength training) can enhance single fiber contraction velocity. While it is not well-understood, it seems likely that single fiber contraction velocity is increased by the stimulus of a fast contraction velocity during exercise, in much the same way as high levels of mechanical tension are the stimulus that causes adaptations that lead to individual muscle fibers increasing in strength. Given that fatigue involves a slowing of muscle fiber contraction velocity, it is possible that it could prevent such adaptations within the muscle fiber from occurring.

What does this mean in practice?

Hopefully, it should be clear that athletic strength training (and any high-velocity training such as jumping and plyometrics) should [1] use maximal efforts on every rep, [2] avoid excessive fatigue in each set, and [3] only use sufficient volumes to make progress from one workout to the next. In practice, all of these features can be implemented by using velocity-based training methods, although that is not to say that cluster training and reps in reserve are not viable alternatives, so long as appropriate cues are provided. By training in this way, changes in high-velocity strength might track gains in maximum (low-velocity) strength, instead of lagging substantially behind.

What is the takeaway?

Strength training workouts that involve greater fatigue (either by training with a closer proximity to failure or with higher volumes) can impair gains in high-velocity strength, and this can happen even without impairments in maximum strength. In fact, higher volume training programs can cause greater gains in maximum strength while causing smaller improvements in high-velocity strength than a lower volume of similar training.

Direct research suggests that the main factor causing the negative effect of more fatiguing training on high-velocity strength is a shift from fast (type IIX) to moderately-fast (type IIA) muscle fiber proportion, since type IIX and type IIA muscle fibers have very similar maximal force per unit cross-sectional area, but type IIX muscle fibers are clearly faster than type IIA muscle fibers. Since muscle fiber contraction velocity is a key determinant of high-velocity strength but is largely irrelevant for maximum (low-velocity) strength, this makes sense.

Even so, arguments can be made that smaller improvements in coordination, motor unit recruitment, motor unit firing frequency, antagonist coactivation, and single muscle fiber contraction velocity (regardless of muscle fiber type) might also contribute to the inferior gains in high-velocity strength that occur when allowing more fatigue to accumulate in a strength training workout.

If you enjoyed this article, you will like my first book (see on Amazon).

Figuring out how strength training works. See more of what I do: https://www.patreon.com/join/SandCResearch