Fitness & Fatigue Model

Article cover image

You are currently exploring the Fundamentals Library , which is designed to provide a basic overview of the topics that are covered in other longer articles. This article is a part of the Physiology section.

Training Process Models

The phenomenon that we get stronger or more muscular over time, as well as the fact that it decreases when we stop training, is very observable. There is a very popular story used to visualise this concept - the ancient legend of Milo of Croton. It's being said that as a child, Milo started carrying a newborn calf on his back. As the bull was growing larger each year, Milo was getting progressively stronger. This story really illustrates the proactive process of increasing physical demands placed on the body - with the goal of acquiring specific adaptations.

milo of croton

The whole point of training is to get better step by step. We get better through different mechanisms, and all of them fluctuate at different rates depending on our training and nutrition.

There are several models that attempt to describe this training process. One of the models that is often used to discuss training is the SRA curve - which stands for Stimulus, Recovery, Adaptation.

This model is a modification of Hans Selye's General Adaptation Syndrome, which explains the stages our body goes through in response to stress.

srv curve

In this context, however, the SRA curve is a framework for understanding how a single dose of training affects our bodies. We do a training session, our performance goes down, and then it recovers to baseline and goes above baseline, which is known as supercompensation. However, as you can see, it represents strength. It does not represent the actual components of that performance.

The more accurate model is known as the fitness-fatigue model. As we train, our fitness (which are adaptations specific to our training) increases, but our fatigue also increases and reduces the effect of fitness on performance.

This way of looking at things is much more accurate, but still a considerable simplification. To understand it more fully, we need to understand what fitness and fatigue are physiologically.

fitness fatigue model

Fitness - Morphological Adaptations

We have already explained that by increasing fitness we mean the degree to which adaptations specific to the stimulus of our training occur. We should not think of strength as the adaptation, because strength is rather the result of different adaptations taking place.

We do a workout that stimulates certain adaptations, and because of those adaptations we become stronger in a certain specific context. This adaptation will continue for some time until it dissipates.

The question then becomes, what is the time course of these processes in all the different adaptations?

In the case of hypertrophy, the main stimulus to increase fiber size is mechanical tension. This stimulus initiates the fitness curve (increase in muscle protein synthesis and the cascade of anabolic processes), which increases for about 24-48 hours and then begins to decline if no stimulus is applied in the meantime.

muscle protein synthesis
Adopted from: A Review of Resistance Training-Induced Changes in Skeletal Muscle Protein Synthesis and Their Contribution to Hypertrophy | Sports Medicine

After this time, muscle protein synthesis elevation ceases and the fibers do not experience relative growth but begin to decrease in size. Obviously, if we continue with our daily activities, only the high threshold fibers used in training will experience this decrease.

So muscle size is an adaptation that will decay quite rapidly if we look at individual fibers. And so if we were to go into space, for example, or if we were to completely immobilize our body, we would probably see a significant loss of total muscle mass, which is called atrophy.

In fact, these studies have been done and they show that 2 weeks of space flight can result in up to 20% loss of muscle mass . In most studies that look at cessation of training, we can see that during a period of detraining as commonly defined, the decrease in muscle size is a much slower and less significant process.

We can certainly hypothesize that this will be different based on our experience. The more advanced we are, the fewer fibers we have that have the potential to grow, and therefore a single training session will give us less overall muscle gain, and detraining will have a greater relative effect.

A beginner can stimulate a lot of new fibers to grow, and therefore that one training session will give him a lot more overall muscle gain. The same period of rest will have a much smaller relative effect.

Unfortunately, other morphological adaptations have not been well studied in the context of adaptation time frames. We might expect that they would follow a similar pattern of adaptation and detraining, and that this time frame might be similar to that of muscle size increases.

Fitness - Neurological Adaptations

The neurological adaptations are actually quite different. Both coordination and motor unit recruitment level fitness curves are likely to rise rapidly as soon as the stimulus appears. For coordination, it's very easy to visualize because sometimes you can learn a pattern or get better at it in a single training session, so the adaptation doesn't take time like hypertrophy, but follows an immediate response.

This response is likely to be very complicated in both cases, involving the creation and refinement of neural pathways. It may well be that there is also some delayed adaptation that occurs after the stimulus - for example, during sleep. We don't know much about the exact mechanisms of these adaptations. What we can probably say, however, is that both voluntary activation and coordination are likely to fade slowly compared to morphological adaptations.

In the case of coordination, when we learn a certain pattern, a lot of it stays with us for a very long time. A famous example of this is riding a bicycle. Once we learn this pattern, we don't forget it. It certainly feels rusty when we come back after a break, but it's not like we lose that adaptation completely through detraining.

When it comes to voluntary activation, it also seems to stay with us for a long time. The literature shows that voluntary activation decays much less rapidly than muscle mass during detraining. Again, we can hypothesize that individual factors will play a large role, including age and level of training.

To conclude this part, fitness is the desired effect of our training process. It is the level of a certain adaptation that occurs through the creation of a stimulus that contributes positively to the effect we want to achieve. And since strength and hypertrophy are very much related, the set of adaptations we want to achieve will also be very similar in both cases.

Fatigue

Our fitness level is one half of the equation. The other half is, as we mentioned earlier, fatigue. Fatigue is often associated with how we feel during training. However, in the context of exercise, it is very important to note that fatigue can be objectively measured by a temporary loss of performance.

Let's say I can hold a tuck planche for 5 seconds during a training session and the next day after training I can only hold it for 3 seconds. We already know the fitness curves of different adaptations, and they certainly don't drop that much after 1 day.

However, our performance is not only determined by fitness, but also by fatigue. Typically, fatigue in the context of resistance training is measured by the drop in maximal voluntary contraction or strength in some exercises measured by 1 rep max. However, in the example above, we can safely say that we experienced 2 seconds of fatigue, or 40% fatigue.

CNS Fatigue

Physiologically, there are many different mechanisms of fatigue. A helpful way to look at fatigue mechanisms is to think of them as impairments of the muscle contraction process.

It all starts with signal generation in the brain. The size of the motor command is proportional to the perception of effort. However, there can be a mismatch between the percentage of motor units we can access and the effort we produce, and the size of this deficit will vary from person to person, mainly based on the level of experience in resistance training.

However, there are scenarios where the perception of effort doesn't match the size of the motor command, and the same effort is accompanied by a smaller motor command size, even though that individual is able to access more motor units through voluntary effort. This situation would mean that we feel that we are exerting more than we actually are.

What can cause this is negative sensations coming from the body. For example, burning or inflammation that occurs as a result of activity, or pain that we feel in the area associated with the task.

So this phenomenon basically limits our ability to recruit motor units by altering the perception of effort and therefore affecting neural drive. And so, as long as this negative sensation lasts, it will limit our motor recruitment in all muscles, even if the sensation is coming from the other trained muscle. If we perform an exercise that causes us to feel these sensations, and we do the next exercise right after that, we will limit our motor command and therefore our performance in that exercise as well.

Let's say the motor command is sent and the signal goes through the neurons down the spinal cord. In the unaltered situation, that signal would be the same after transmission through the spinal cord. However, what can happen is that the signal going to the muscle is smaller than the signal that was sent. This probably happens because of desensitization. However, the exact mechanisms are not known.

These two phenomena together can be called Central Nervous System Fatigue. And they basically involve impairments in signal generation and signal transmission to the muscle.

Peripheral Fatigue

Grasping the next part of fatigue requires the understanding of what happens to the signal once it gets to the muscle. When the electrical signal reaches the motor unit and reaches muscle fiber it first goes through the cell membrane until it reaches a transverse-tubule that directs the signal inside the cell. Here, the electrical signal gets converted to a chemical signal and the calcium ions are released to the cytoplasm.

Following the release of calcium ions, actin detects their presence inside the cell and opens its binding side so the myosin can bond and cause the contraction and the cross-bridge cycle. In each part of this pathway fatigue can occur and how that happens is quite complex.

In each individual stage, there are processes that decrease the mechanical tension or velocity of contraction experienced by the muscle fiber. Together this phenomenon can be called peripheral fatigue. What does matter from the practicality standpoint is that the peripheral fatigue will be either caused by metabolite accumulation or the calcium ions overload which has different implications for different structures inside the muscle.

Metabolite accumulation occurs much faster and it is much faster to dissipate. The calcium ion overload is a much more long lasting process, the longest one of which is excitation contraction coupling failure lasting roughly from 2-4 days. Excitation contraction coupling involves the transfer of electric signal to the chemical signal, and the damage of triadic junction causes failure of the mechanism. This damage is primarily caused by certain enzymes, produced as a response to calcium overload.

Because of this, the calcium ions are not getting released in response to the sensed action potential, which likely disrupts the forming of cross-bridges and therefore reduces the active tension experienced by a muscle.

The next mechanism that causes reduction in performance is muscle damage, which is the actual destruction of myofibrils. The process of muscle damage is not fully understood, and it is sometimes considered to be the mechanism for hypertrophy. There is evidence suggesting that the damage is primarily caused by the same biomechanical reactions. The enzymes whose production is triggered by calcium overload continue to disrupt the myofibrils even after the training session. As the damage occurs and preserves, there is an inflammatory response.

And this is where it gets very interesting, because as we remember, central nervous system fatigue is dependent on negative sensations coming from the body, including the inflammation. As you can probably tell, this means we will still experience CNS fatigue after the workout, not as a result of the workout itself, but the muscle damage that was followed by inflammation that happens after the workout.

Interestingly, muscle damage can be maintained for an extremely long time, up to even a couple of weeks after a training session. Actually, in the most severe cases, the damage can be so strong that muscle will be put to necrosis. When that happens, our body will try to rebuild that fiber which can take weeks to occur.

Fatigue Mechanisms Timeframe

So if we want to put these things into a single time frame, it's like this. When we do a set, a few minutes after the set, the central fatigue dissipates as the negative sensation coming from the body dissipates.

The peripheral fatigue continues after the workout. Some of the peripheral mechanisms will dissipate the same day, some mechanisms will take longer, and the longest of them will last up to about 2-4 days. The muscle damage caused by this workout, depending on the characteristics of the workout and individual factors, can take up to a couple of weeks to resolve, obviously in the most severe examples. Typically it will likely follow the 2-4 days pattern as well.

As the inflammation develops after this workout, there is also an additional CNS fatigue due to inflammation that will be present as long as this inflammation is present. This means that when we talk about fatigue, we need to look at each of the mechanisms individually and see how they respond to different training variables. From this, we will be able to tell how long fatigue will last and what will be negatively affected by fatigue, which is what is important from a training programming standpoint.

So, while peripheral fatigue seems to be a bottleneck for repeating the workout, remember that the actual magnitude of fatigue will depend largely on the characteristics of a workout. If we are performing high rep eccentric deadlifts with a large emphasis on stretching position to failure - the damage from that workout will be greater than if we were doing an easy set of ring rows. If you have not already done so, be sure to check out our Calisthenics Skills Fatigue Index Chart, where we have broken down how fatiguing the popular calisthenics skills are.

fatigue timeline

Acute Mechanisms of Fitness & Fatigue

Since fitness is directly responsible for performance increases, we must mention that, in addition to the adaptations mentioned, there are also certain short term mechanisms that acutely improve or impair our performance and are not the result of a previous training session.

The first of these is Post-Activation Potentiation, known as PAP. This mechanism increases the tension produced by the muscles and is one of the effects of warming up on performance.

A similar effect can be produced by any intervention that temporarily increases our muscular activation (either by increasing the motor command signal or by improving the efficiency of its transmission). This intervention could be increasing arousal (increasing the activity of the sympathetic nervous system) or motivation through caffeine consumption, listening to music, or the presence of other people.

At the same time, things like dehydration, reduced glycogen levels or pain can acutely impair our performance as long as they are present, even though they are not the effects of the previous training session.

Repeated Bout Effect

The concept worth mentioning is that just as our fitness depends on the experience of the athlete, so does fatigue. The phenomenon partially responsible for this is called the Repeated Bout Effect - the situation where the single bout of training makes the fatigue after subsequent training of the same type smaller.

Repeated Bout Effect in literature is used both in the context of DOMS as in the context of actual fatigue (performance reduction). This effect is not very long lasting, as each subsequent training session will have less of an impact on subsequent sessions.

In practice, repeated bout effects will have a pretty big influence when we start a certain new activity or exercise. However, it is not something that will make us fatigue resistant and double or triple the amount of training we can do in a span of a training week.

DOMS (Delayed Onset Muscle Soreness)

The already mentioned DOMS is a very common phenomenon of muscle soreness that occurs after exercise. DOMS usually appears about 8 hours after training, peaks 1 or 2 days later, and subsides within 7 days after exercise, although sometimes it can take even longer to go away.

In the course of this article, you may have thought that the muscle damage or peripheral fatigue I'm talking about manifests itself in the soreness that pretty much all resistance training enthusiasts are familiar with.

However, it appears that DOMS is still a very unknown phenomenon and while there are several hypotheses, including fascia inflammation or nerve compression, it is still not fully understood what causes the sensation. It is certainly not the lactic acid though, which is the popular hypothesis.

What we do know is that they have too many differences in timing and pattern of occurrence with fatigue (performance decrease) to be considered closely related. On the other hand, since pain has been shown to decrease voluntary activation, DOMS could also have this direct effect on performance.

Needless to say, these are not completely useless pieces of information from a training programming standpoint, but they cannot be used alone to guide our decisions.

Enjoyed the article?

Share it with others!

Don’t Miss
Next Articles

Sign up to Calintellect newsletter and get new articles delivered to your inbox whenever we publish!

loading...

Credits

  1. A Review of Resistance Training-Induced Changes in Skeletal Muscle Protein Synthesis and Their Contribution to Hypertrophy | Sports Medicine

References

  1. Chris Beardsley on Twitter: “IMO, the fitness-fatigue model still has a role to play in describing the adaptations to training, but this proposed revised version is better than the traditional one.” https://twitter.com/sandcresearch/status/981109230286655489
  2. General Adaptation Syndrome (GAS): Stages and Triggers. https://www.verywellhealth.com/general-adaptation-syndrome-overview-5198270
  3. Williams, D., Kuipers, A., Mukai, C., & Thirsk, R. (2009). Acclimation during space flight: Effects on human physiology. CMAJ, 180(13), 1317–1323. https://doi.org/10.1503/cmaj.090628
  4. Ivey, F. M., Tracy, B. L., Lemmer, J. T., NessAiver, M., Metter, E. J., Fozard, J. L., & Hurley, B. F. (2000). Effects of strength training and detraining on muscle quality: Age and gender comparisons. The Journals of Gerontology: Series A, 55(3), B152–B157. https://doi.org/10.1093/GERONA/55.3.B152
  5. Jackson, M. (2014). Evaluating the role of Hans Selye in the modern history of stress. Stress, Shock, and Adaptation in the Twentieth Century, 21–48. https://doi.org/10.1515/9781580468350-003
  6. Koolhaas, J. M., Bartolomucci, A., Buwalda, B., de Boer, S. F., Flügge, G., Korte, S. M., Meerlo, P., Murison, R., Olivier, B., Palanza, P., Richter-Levin, G., Sgoifo, A., Steimer, T., Stiedl, O., van Dijk, G., Wöhr, M., & Fuchs, E. (2011). Stress revisited: A critical evaluation of the stress concept. Neuroscience and Biobehavioral Reviews, 35(5), 1291–1301. https://doi.org/10.1016/J.NEUBIOREV.2011.02.003
  7. Palygin, O., Mamenko, M., & Sonkodi, B. (2022). Delayed onset muscle soreness and critical neural microdamage-derived neuroinflammation. Biomolecules, 12(9), 1207. https://doi.org/10.3390/BIOM12091207
  8. Salomoni, S., Tucker, K., Hug, F., McPhee, M., & Hodges, P. (2016). Reduced maximal force during acute anterior knee pain is associated with impaired muscle activation and corticospinal excitability. Pain, 157(1), 158–166. https://doi.org/10.1097/j.pain.0000000000000333
  9. Damas, F., Phillips, S., Vechin, F. C., & Ugrinowitsch, C. (2015). A review of resistance training-induced changes in skeletal muscle protein synthesis and their contribution to hypertrophy. Sports Medicine, 45, 801–807. https://doi.org/10.1007/s40279-015-0320-0