What is fatigue (and why does it matter)?
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In the fitness industry (as well as in real life), people often talk about being or feeling fatigued. But what is fatigue, exactly? And why does it matter? In this introductory article to a new series, I provide a usable definition of fatigue, detail the four pathways through which fatigue is produced, and explain why it is important that we are aware of the key mechanisms that cause fatigue in each of these four pathways.
How can we define fatigue?
Fatigue can be defined as a temporary and reversible reduction in exercise performance, as a result of a previous bout of exercise. While most of the terms within this definition are obvious, it is worth mentioning a couple of important points about the use of “exercise performance” as the primary measuring stick for fatigue.
Firstly, in this definition, fatigue is defined objectively, by reference to a reduction in an external measurement (exercise performance). In other words, if we perform a workout and our 1RM is reduced immediately afterwards, then we are fatigued. Similarly, if we go for a bike ride and the time we achieve in a 2km rowing erg is increased immediately afterwards, we are fatigued. The 1RM (which is measured in kilograms) and the rowing erg (which is measured in minutes and seconds) are tests that can be quantified objectively, and then compared to our normal, baseline measurements to get a sense for how much we are fatigued (in percentage terms). Importantly, fatigue is not defined subjectively, by referring to how we feel. Fatigue and the perceptions or sensations of fatigue are actually two, completely separate phenomena, and we need to be careful about our terminology if we want to make sense of this complex area (while it is not fair to say that our perceived level of fatigue is completely unrelated to our actual fatigue in the recovery period after a workout, it is certainly not the best indicator and can often be quite misleading).
Secondly, it is true that some researchers refer exclusively to reductions in maximum strength or maximal force production when defining fatigue (instead of exercise performance more generally). I think this is a mistake, because reductions in exercise performance after a preceding bout of exercise can vary depending [A] on the type of exercise performed in the preceding bout, [B] on the type of exercise performance test that is used, and [C] on the environmental conditions during recovery. At the risk of jumping too far ahead, this occurs because fatigue comprises multiple different mechanisms that work in various ways (including by reducing the maximum shortening velocity of the muscle fiber as well as by reducing the maximum force that it can exert), and these fatigue mechanisms differ depending on the type of exercise that is performed (both in the original exercise bout or in the exercise performance test used to measure fatigue). Thus, some types of exercise cause greater fatigue when measured by one type of exercise performance test than when measured by another.
What causes fatigue?
If fatigue can be defined as a temporary and reversible reduction in exercise performance, as a result of a previous bout of exercise, then what causes it to happen? In many ways, the answer to that question will only appear over the course of this entire series of articles, but we can achieve a fairly quick overview in just a couple of paragraphs.
Exercise performance can be negatively affected by various mechanisms, which we can characterize relatively easily by working backwards from the determinants of exercise performance itself. During any movement, exercise performance is determined by [A] coordination (which in this case also includes inter-muscular interactions between agonists, antagonists, and synergists), [B] agonist voluntary activation (which is determined by the level of central motor command), [C] maximum muscle fiber force production, and [D] maximum muscle fiber shortening velocity.
Therefore, fatigue can cause impairments in exercise performance when it [A] reduces coordination (which is commonly observed as a disruption of normal movement patterns), [B] reduces agonist voluntary activation (which could equally be described as central nervous system [CNS] fatigue), [C] reduces maximum muscle fiber force, and/or [D] reduces maximum muscle fiber shortening velocity. When exercise causes biochemical changes that lead to changes in any of these factors, fatigue (as defined by a reduction in exercise performance) will necessarily occur.
This way of describing fatigue is the opposite way around from the way in which fatigue is most commonly described in the research literature, where mechanisms of fatigue are first assessed, before looking to see how each mechanisms then affect exercise performance. While that approach is more rigorous for the purposes of establishing each mechanism, it is less useful for creating a framework of how fatigue actually works. If we want a unifying framework, we need to start by identifying all of the possible pathways in which exercise performance might be affected, before we then work backwards to detail the various fatigue mechanisms that can produce changes in each of those pathways.
The four fatigue pathways
Out of these four, primary pathways by which fatigue can impair exercise performance, researchers have probably devoted the least amount of time to looking at changes in coordination, although it could potentially be among the most important in certain situations. Indeed, research has shown that the critically important proximal-to-distal sequence of limb movements is actually severely disrupted during throwing by the presence of fatigue, making the movement far less efficient, and thereby reducing throwing performance disproportionately in comparison with the reductions in muscular force at the required movement speed.
In contrast, there is a great deal of literature available regarding reductions in agonist muscle voluntary activation after exercise, which is CNS fatigue. CNS fatigue in exercise science refers specifically to a situation in which the level of motor unit recruitment that can be achieved for a muscle is reduced below the levels that can normally be achieved, due to fatigue mechanisms. While the mainstream fitness industry typically refers to CNS fatigue as some kind of rare, apocalyptic event caused by overtraining, the reality is that it is a perfectly normal and common type of fatigue mechanism that occurs regularly during and after all kinds of exercise.
Researchers have probably devoted more lab time to the effects of fatigue mechanisms on muscle fiber force than on any other single topic in exercise science. Consequently, there is an enormous amount of information that describes the effects of various mechanisms that occur during and after exercise that affect the ability of single muscle fibers to produce force, which are grouped together as “peripheral fatigue” mechanisms. During exercise, the most important peripheral fatigue mechanisms that reduce muscle fiber force are excitation-contraction coupling failure (which is caused by the accumulation of calcium ions inside the muscle fiber) and the production of inorganic phosphates (which is generated by the use of ATP to power the crossbridge cycle, and which is therefore commonly referred to as a metabolite or as metabolic stress). After exercise, the most important peripheral fatigue mechanisms that reduce muscle fiber force are (again) excitation-contraction coupling failure, alongside muscle damage.
Finally, while it is likely the least well-known of all the fatigue mechanisms, there are a number of important studies that have observed large reductions in muscle fiber shortening velocity after exercise, especially after exercise that involves a high degree of metabolite accumulation. Indeed, the main mechanism that causes this reduction in muscle fiber shortening velocity is a peripheral fatigue mechanism involving the accumulation of hydrogen ions, which probably occurs at least in part due to the usage of ATP to power the crossbridge cycle. Therefore, like the accumulation of inorganic phosphates, it is also referred to as a metabolite, metabolic stress, or (as I prefer to call it) metabolite-related fatigue.
Why does it matter what causes fatigue?
Some people might argue that fatigue is just fatigue, and that there is little value in exploring the various mechanisms involved. I disagree, for two key reasons. Firstly, each fatigue mechanism produces a different impact on long-term adaptations, as I will describe in the next couple of paragraphs. This means that when a preceding bout of exercise causes one type of fatigue, this changes the long-term adaptations in one way, while when it causes another type of fatigue, this changes the long-term adaptations in a different way. Secondly, and related to this, the types of fatigue that can be caused by preceding bouts of exercise can differ, depending on the type and duration of exercise that was performed (aerobic, anaerobic, strength training, and so on).
The four fatigue pathways
Coordination can be impaired by fatigue. Indeed, it seems likely that all types of fatigue (both the fatigue that occurs during exercise and also the fatigue that occurs after exercise) disrupt movement patterns. In this case, the exact mechanisms of fatigue do not seem to be particularly important, and all types of fatigue cause a similar effect, which is a reduction in coordination in the movement being performed. This has two important long-term effects. Firstly, it reduces the strength gains achieved through improvements in coordination after the workout. By reducing the coordination during the workout, the ability to improve coordination is impaired, and therefore strength gains due to motor learning are similarly impaired. Secondly, it impairs the ability of future workouts to achieve similar improvements in coordination. Apparently, practicing a movement pattern while fatigued (which typically means using a very inefficient and uncoordinated movement pattern) actually has a negative impact on the ability to learn that movement pattern in future workouts. Thus, not only is practicing a movement while fatigued not helpful, it could actually slow future progress as well. Clearly, this point is of great importance to athletes and powerlifters who want to be very efficient in their movement patterns (so that they can maximize strength and speed in their chosen sporting movements or exercises), while it is likely of much lesser interest to bodybuilders for whom exercise performance is secondary.
When CNS fatigue occurs, this involves an ability to achieve a maximal level of motor unit recruitment despite exerting a maximal effort. Yes, it is entirely possible to believe that a maximal effort is being exerted, and yet the central motor command being sent to the muscle (to produce motor unit recruitment) is lower than it would be in the absence of fatigue. This is very important, because it is likely the magnitude of the central motor command being sent to the muscle to produce motor unit recruitment that stimulates gains in the ability to recruit high-threshold motor units in the future (which is a key mechanism that causes gains in both maximum strength and speed). Therefore, when CNS fatigue is present, this will prevent a workout from stimulating gains in the ability to recruit high-threshold motor units in the future, thereby reducing gains in maximum strength and speed.
When peripheral fatigue occurs that reduces maximum muscle fiber force (as is the case with excitation-contraction coupling failure, reductions in calcium ion sensitivity, reductions in sarcolemmal excitability, and also with the accumulation of phosphates, at least eventually), this can reduce the level of mechanical tension that each muscle fiber experiences. In this way, the amount of hypertrophy that can be stimulated by a muscular contraction reduces. Nevertheless, during normal strength training, these types of peripheral fatigue are delayed in comparison with the type of peripheral fatigue that causes a reduction in muscle fiber shortening velocity, and therefore only take effect in the one or two reps before muscular failure. Therefore, muscular performance during normal strength training is predominantly reduced by muscle fiber shortening velocity and not by muscle fiber force, which is why stimulating reps during normal strength training can be explained by reference to mechanical tension levels. However, in eccentric contractions, whose performance is not limited by muscle fiber shortening velocity, excitation-contraction coupling failure is the main type of peripheral fatigue, and this is why it is not possible to perform dozens of eccentric contractions in a single set and continually achieve more and more stimulating reps. Muscle fiber force is progressively reduced by excitation-contraction coupling failure during successive eccentric contractions, thereby reducing the stimulating effects of each rep by means of mechanical tension (and this is why the stimulating reps during eccentric training are actually at the start of each set, and not at the end).
Note: in addition, the presence of certain peripheral fatigue mechanisms that affect muscle fiber force likely triggers adaptations that underpin increased fatigue resistance, and therefore in muscular endurance and in aerobic exercise performance. In general, these adaptations are of lesser interest to strength and power athletes, but nevertheless are potentially valuable under certain circumstances. Nevertheless, it is important to note that there are also beneficial adaptations produced by fatigue, which relate to fatigue resistance.
When peripheral fatigue occurs that reduces maximum muscle fiber shortening velocity (as is the case with acidosis), this does not reduce the level of mechanical tension that each muscle fiber experiences. This acidosis is the main reason that sets performed with maximal bar speeds display a gradual reduction in bar speed over the course of the set. Similarly, it is the reason that sets performed with a self-selected tempo require an increase in effort (and therefore in central motor command) over the course of a set, if bar speed is to be maintained at the same level throughout. Nevertheless, the levels of mechanical tension experienced by the working muscle fibers are not necessarily reduced by this mechanism, which is why high levels of mechanical tension can still be produced (and experienced) by them, which then stimulates hypertrophy to occur. However, this does not mean that acidosis has no downsides, since a reduction in muscle fiber shortening speed during exercise has two (related) negative effects. Firstly, the reduction in muscle fiber shortening speed means that the muscle fiber itself is not stimulated to alter its contractile properties so as to improve its maximum shortening speed (as occurs after very fast movement training). Secondly, the reduced muscle fiber shortening speed leads to a reduction in motor unit firing frequency, which means that increases in motor unit firing rates are not stimulated, which means that this adaptation (which leads to increased speed and high-velocity force production) does not occur.
Note: again, the presence of certain peripheral fatigue mechanisms that affect muscle fiber shortening velocity is likely also a stimulus for adaptations that underpin improvements in fatigue resistance.
What does this mean for strength training programs?
Hopefully, it should be clear from the above analysis that the production of fatigue during exercise (and also the accumulation of fatigue after exercise, although this was not discussed extensively in the above sections) does not really contribute to long-term adaptations, except to produce increases in fatigue resistance, and thereby contribute to increased muscular endurance or aerobic performance. In most cases, the presence of fatigue has negative effects and actually reduces or impairs adaptations from happening (and this concept will be the subject of a more detailed, follow-up article).
In the wider fitness industry (and even among some researchers), there is an implicit assumption that fatigue during exercise stimulates adaptations or that accumulated fatigue after exercise stimulates adaptations. Indeed, this is often (albeit not always) a tacit assumption during many discussions of periodization and programming methods that involve supercompensation. In such cases, it can be assumed that the presence of a high degree of fatigue in some way stimulates adaptations to occur, when there is in fact little or no evidence for this idea.
In contrast, I would argue that fatigue during exercise most commonly impairs most of the adaptations that we want to create during strength training for athletes and even strength athletes, and that accumulated fatigue is similarly not very helpful. While accumulated fatigue is most commonly visualized as a block of some kind of magic training load that can be accumulated, and which pressurizes adaptations to occur, it is probably better to see it as wear and tear on a vehicle.
Yes, the presence of wear and tear on a vehicle indicates that it has done a lot of mileage, and if that mileage was put to good use, then benefits could accrue. But the benefits are not directly caused by the wear and tear. It is perfectly possible to achieve the wear and tear without any benefits, if the mileage was not directed towards any useful endeavor. What is more, as the wear and tear accumulates, it starts to impair the ability of the vehicle to do the intended journeys.
In the same way, the accumulation of fatigue during (and after a workout) indicates that training is being (has been) performed. If the training is directed towards a useful endeavor, then adaptations can occur. But if the training was not well-programmed, then fatigue can still occur. Moreover, the performance of training in a fatigued state impairs the ability of the lifter to achieve the required adaptations.
What is the takeaway?
Fatigue is a temporary and reversible reduction in exercise performance, as a result of a previous bout of exercise. Contrary to its characterization in the wider fitness industry, fatigue is therefore an objective measure and not a subjective measure. It is a reduction in our ability to produce force, exert force at a specific speed, or exert force for a specific period of time. It is not a perception or a feeling.
Fatigue reduces exercise performance by reducing [A] coordination, [B] agonist voluntary activation, [C] maximum muscle fiber force production, and/or [D] maximum muscle fiber shortening velocity. Each of these types of fatigue can alter long-term adaptations in different ways. Reductions in coordination can prevent motor learning from happening, and may also impair the improvements in coordination produced by future workouts involving the same movement pattern. Reductions in voluntary activation reduce the level of central motor command that is sent to the muscle, which impairs gains in the ability to recruit high-threshold motor units. Reductions in muscle fiber force reduce the magnitude of the mechanical tension that is experienced, which reduces the hypertrophy that is stimulated (this is very common during fatiguing, eccentric training sets). Reductions in muscle fiber shortening speed reduces the bar speed attained during exercise, which reduces adaptations in [A] muscle fiber contractile properties, and in [B] motor unit firing rates, which together underpin gains in speed. Thus, in many situations, certain types of fatigue should be avoided if optimal long-term adaptations are to be achieved. Nevertheless, fatigue resistance can only be improved by experiencing fatigue, and therefore there is always going to be a trade-off between achieving maximum strength or speed and achieving maximum fatigue resistance.
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