Different types of fatigue and how to manage them
We are all familiar with the feelings of fatigue in whatever form they strike: be it by the end of one of a very long endurance ride at a solid Zone 2 intensity, when we are attempting that final 5 minute maximal aerobic power effort and our legs are screaming at us to let them stop, or doing repeated sprintervals and it feels like our muscles are burning. Traditionally, much of this has been put down to lactic acid, but the fact is that lactic acid has no effect on fatigue or burning sensations in the muscles and is quite frankly an outdated term.
In reality, there are many different types of fatigue and understanding what they are can help us combat them and reduce the onset or impact of these various fatigues. In this article, I’m going to do a bit of a deep dive on the subject. It’s worth remembering though that these are all incredibly complex mechanisms, some of which aren’t fully understood yet by researchers. To read more in-depth, I’ve included a list of references at the bottom as to go into big detail on every element here could take tens of thousands of words. So, here is the trimmed down summary.
Hydrogen ions
The first one that we are going to talk about, and the first of the peripheral fatigue mechanisms, is one you would’ve likely heard referred to as lactic acid build-up. However, this is quite a misleading title as lactate is not something that directly fatigues us and, in fact, is something that our body uses as fuel during efforts and can be converted into pyruvate which is then used to make ATP (adenosine triphosphate), which we know to be the energy source of all bodily functions.
The real culprit of fatigue here is something that comes with that lactate production: hydrogen ions. Increased levels of hydrogen ions (H+) create a more acidic environment within the muscles. This, in turn, inhibits the muscles potential to break down substrates using oxidative methods. This can result in greater energy contribution from anaerobic methods and a greater influx of fatigue metabolites. There is also an affect on the muscles cross bridge function, with some studies finding that H+ decreased the capacity for the myosin to release the actin filaments, and reducing the potential for the myosin to bond as strongly, thus reducing peak force capacity and firing rate.
We can reduce the negative effect of H+ by improving our buffering capacity. This can be done by using supplements, such as beta-alanine or bicarbonate of soda. Another means of reducing H+ is to improve our ability to utilise fats as fuel at higher intensity, which reduces the production of lactate and H+ that come with it due to carbohydrate metabolism. As H+ production increases exponentially above the physiological turn point Critical Power, increasing our Critical Power through training will greatly help in reducing the fatigue effect of H+ at certain power levels.
This is why when H+ levels do get so high that they cause fatigue, the best thing to do is to reduce the intensity, which then enables you to clear the hydrogen ions faster than you are producing them. You can also improve your lactate clearance and intramuscular lactate metabolism generally via greater volumes of lower intensity training below the first lactate threshold and improving mitochondrial mass within the muscles and increasing muscle capillary density. I’d recommend reading some of Dr Iñigo San Millán’s work for more detail on this.
Inorganic phosphate
Another cause of peripheral fatigue (and usually the one that leads to the pain we feel in our legs) is something called inorganic phosphate (Pi). This is produced in especially large quantities when we suddenly go from perhaps a very low intensity to a very high intensity. For example, during sprints or micro intervals. Pi is produced during ATP hydrolysis and when using the phosphocreatine pathway to produce energy, which occurs during very high intensity or the initial uptake of high power.
So, when you go from 40 W to 400 W in your micro intervals, the phosphocreatine pathway is how we initially uptake that power. Or, even when starting an endurance ride, the initial energy system working will be the phosphocreatine one, with the aerobic system is kicking in shortly afterwards. This also explains why we feel more fatigue when we have a lot of changes in pace, such as in a criterium or after conducting micro intervals.
The production of inorganic phosphate leads to a reduced cross bridge capacity within the muscles, which is how we produce our power by contracting and releasing the cross bridges (see sliding filament theory) by potentially blocking the uptake of calcium ions (Ca+) which are essential for muscle cross bridge function. It also reduces the potential power from each cross bridge, resulting in a double whammy of power reduction.
We can reduce the impact of inorganic phosphate by pedalling at an easy intensity after the repeated bouts of exercise that produce it or immediately after a large sprint. Studies have found that stopping peddling completely keeps the inorganic phosphate levels high and reduces our capacity to perform sprints again. So, in races, it is a good idea to reduce the amount of surges that we do as that will reduce the inorganic phosphate production.
In training, after doing a high intensity sprint, it is important to remain pedalling at a low intensity rather than stopping pedalling entirely. Caffeine has also been shown to attenuate some of the fatigue issues caused by Pi with caffeine increasing increasing Ca+ uptake in the muscles (specifically the sarcoplasmic reticulum). Caffeine has the added benefit of blocking adenosine binding to adenosine receptors an reducing the mental fatigue and perception of effort.
Potassium ions (K+)
So, we’ve had Hydrogen Ions, now it’s time for Potassium Ions. This is an interesting one as an increase of K+ up to a certain level actually can increase the peak force of a muscle. However, once a certain threshold is reached, the peak force capacity of the muscle drops dramatically. The reason for this is that during muscle contractions we have something called the Na+–K+-pump which is essential for muscle contractile function through excitability.
There is an increase in the release of K+ with the onset of exercise, and this increase is linked to exercise intensity, trained state of the individual, and on drugs such as beta-adrenoceptor blockers and caffeine. The way in which elevated K+ impacts muscle contractile function is a complex one, with a very in-depth review of it here: Cairns, S. P., & Lindinger, M. I. (2008). Do multiple ionic interactions contribute to skeletal muscle fatigue?. The Journal of physiology, 586(17), 4039-4054.
The means in which we can reduce the effect of K+ are; caffeine consumption (affects the concentration of K+ interstitially), glucose consumption (prevents the deterioration of electrical properties of the muscle fiber membrane) and training state with more trained individuals better able to restore the Na+–K+ balance in reduced periods of time or at reduce intensities.
Reactive Oxygen Species (ROS)
There is a continual battle going on in our bodies at all time, the generation of ROS, and the generation of anti-oxidants to neutralise them. At rest and low exercise intensities, this battle is controllable, the same way that H+, Pi and K+ all are. ROS are generated as byproducts from the mitochondria and mitochondrial oxidative phosphorylation and actually play a useful role in physiological adaptation and signal transduction when maintained at homeostasis.
However, as we exercise more, use more oxygen, and oxidative phosphorylation rates increase, homoeostasis is broken and there is an imbalance of ROS. They then cause inflammation in the body via various different means along with acting on myofibrillar proteins to inhibit calcium sensitivity and depress musclar force.
We can reduce the impact of ROS via ingestion on antioxidants in out diet or via supplements such as cherry and blackcurrant juices, as well as turmeric consumed with black pepper and olive oil. We can also increase our bodies generation of antioxidants via Myogenic cells through training adaptations. However, it is worth noting that although ingesting antioxidants could improve recovery day to day in training, it could also reduce the training adaptations and benefits from the training itself.
Our bodies are clever, and a certain level of ROS is required for adaptations to occur in the body, one of those being the ability to generate more antioxidants ourselves. For stage races or before a key event, antioxidant consumption may be helpful both in the short run and the long run. However, in day to day training, it is probably best to avoid antioxidant supplements and focus on a varied diet of fruit and veg.
Muscle Afferents
Our body is incredibly clever, and we have parts of our muscles called Afferent Fibres. These afferents play a very important role in exercise as they monitor the state of the muscle and interact with the central nervous system (CNS). The afferents we are concerned with here are Group III and IV as they mediate cardiovascular and ventilatory reflexes.
Essentially, they help regulate the CNS to control some degree of blood and oxygen delivery to the working muscles. They are essential, as studies have found that blocking these receptors from signalling the CNS reduced the blood/oxygen delivery to the working muscles by reducing blood flow and also pulmonary ventilation.
However, they also play a role in Central Fatigue and are linked in a way to some of the peripheral fatigue mechanisms (H+ and Pi). Up to a certain critical threshold these afferents assist in muscular contractile performance and delivering oxygen to the muscles.
However, once this threshold is crossed, the afferents provide inhibitory feedback to the CNS to reduce the central motor drive, basically our voluntary capacity to produce greater muscular force is reduced. The suggested reason for this inhibitory feedback is to limit the body from spending time above this critical threshold and producing excessive peripheral fatiguing metabolites.
This is to try and protect the body and muscles from associated damage due to these metabolites. Studies have tested with inhibiting the afferents above the critical threshold, and although blood oxygen levels were slightly reduced, this negative affect was outweighed by the increased central motor drive. In the test, cyclists were able to perform at a higher power output over a 5km time trial than those without afferent inhibition.
The way to overcome this afferent feedback induced central fatigue, is to reduce intensity and decrease Group III/IV stimulus. Once that critical threshold is passed, the cascade of fatigue mechanisms, both central and peripheral, increases until intensity is reduced. We can increase the threshold at which the afferents start to provide inhibitory feedback the same way we can reduce the presence of H+ and Pi, by increasing the physiological turn point known as Critical Power.
Respiratory Muscle Metaboreflex
When we exercise at a high intensity, our muscles fatigue and lose the capacity to work as well as we’d like. However, for some muscles, loss of function is a lot more dangerous than for others. If we lost function in the respiratory muscles, we’d be in a dire situation, and as we exercise and breathe heavily and frequently, we use a lot of muscles to inhale and exhale.
As these muscles fatigue, the body starts to redirect blood flow from the locomotor muscles (legs for the majority in cycling) and redirect it to the respiratory muscles so that their function can be maintained. The result of this is that the locomotor muscles start to reduce in function and capacity to produce force, while the respiratory muscles maintain function, and as exercise intensity decreases, the balance can stabilise.
There are two main ways to counter this metaboreflex. Firstly, we can train, improve our capacity to transport oxygen to the muscles, break down substrates to be oxidised, and increase the level of substrates that we can oxidise. So mitochondrial density and capillary density. This will mean that less oxygen is required by the legs at a given power output, and the metaboreflex won’t occur until a higher output, but likely a similar relative intensity to training status.
The other way we can potentially reduce the impact of the metaboreflex, is respiratory muscle training (RMT). Altitude masks, although useless for altitude training, actually serve a purpose for RMT as they increase the resistance we encounter when we breathe in and out. This can increase the time to when our respiratory muscles fatigue, and therefore delay the metaboreflex so that blood flow is not redirected from the locomotor muscles to the respiratory muscles and therefore time to exhaustion should be increased.
Substrate availability
Another form of fatigue comes from substrate availability. Simply put, this means having the fuel available to conduct the work. Higher intensity work requires carbohydrates in order to complete it, but our carbohydrate stores are not indefinite. With our muscles and liver saturated in carbohydrates (muscle glycogen when it’s in the muscles), we have perhaps enough carbohydrates to fuel 90 minutes of high intensity exercise.
This is why consuming carbohydrates is vital to allow for prolonged high intensity work. When we do not consume enough carbohydrates, we are unable to complete exercise at higher intensities, as even with a lot of fuel in even a very learn person’s fat stores, fat metabolism requires more oxygen to break down than carbohydrates so can’t be done when oxygen demands are very high such as high intensity exercise.
This means the only way that we can continue to exercise is to reduce the intensity dramatically. This is likely the feeling you will have encountered if you’ve ever suffered the dreaded bonk. Your legs go heavy and there is no intensity that you can produce other than one that is essentially just turning the legs very, very easily.
Fortunately, this one is probably the easiest form of fatigue to combat. We simply must ensure that A) we’ve consumed sufficient carbohydrates in both the day leading up to, and on the morning of, exercise, and B) for exercise sessions longer than 90 minutes that we consume carbohydrates during the session as well. The amount of carbohydrates that you can consume depends on your ability to process them.
Traditionally, we’ve been told that 60 g an hour was the maximum we could consume. This then increased to 90 g an hour when a mix of fructose and glucose was consumed. Nowadays it is considered that up to 120 g of carbohydrates can be consumed per hour when mixing different carb sources – as long as our gut has been trained to deal with the high carbohydrate load.
It’s important to consume the carbohydrates before we feel that we need them. Once we hit the point of fatigue due to lack of fuel, it’s too late as the time required to get the carbohydrates into the working muscles means we’ll have to spend a period of time working at a very low intensity in order to recover.
For those just starting out with carbohydrate fuelling, it’s best to start with maybe 40-60 g an hour. After that, you can train with increasingly higher carbohydrate loads to improve your body’s tolerance to carbs and ability to utilise them.
Heat fatigue
Heat fatigue affects us in several ways. The main one we’re going to talk about is heat production itself and how that affects both the muscles’ ability to contract and also our ability to utilise fuel sources. When we work in hot environments and our core temperature increases to around 40 degrees, we become less able to use fats as fuel and more reliant on carbohydrates, which itself causes greater H+ production and therefore quicker onset of fatigue.
When our core temperature increases, a lot of enzymes in the body are unable to function properly and therefore we experience impairments in certain functions such as the ability to break down fuel.
The other way in which heat causes eventual fatigue is by dehydration. When we become dehydrated, we experience a reduction in our salt balance as salt is required to move water from within the body to outside the body to allow evaporation to cool us down: this is sweating.
With salt levels reduced (Sodium Na), we lose some of the contractile signalling capacity which is how our muscles contract and release. You may feel particularly bad cramps after being dehydrated, for example when your calf muscles tense up without any conscious intention to do so, although there is a lot of debate about cramps and dehydration.
This potentially happens due to electrical signals not been passed properly to the muscles through the sarcoplasmic reticulum. As all muscle cross bridges by nature are contracted (the myosin filaments grabbing onto the actin) we get the involuntary contractions.
We actually release the muscle cross bridges with energy so dehydration, often accentuated by heat, can cause cramping by failure to release – or relax – the muscles. You will also likely see an increased heart rate for a given intensity as reduced fluid means lower blood volume and decreased stroke volume, this in itself can increase the RPE and affect mental fatigue.
There are various ways to reduce the impact of heat fatigue. One method is heat acclimatisation which involves training in a hot environment more regularly and increasing our ability to sweat in order to reduce body temperature as well as increase tolerance to greater fluid losses while maintaining peak athletic performance. The old saying about 2% loss of fluids results in 10% loss of athletic performance has been disproven as marathon runners often finish marathons with significantly higher percentages of fluid loss while maintaining peak marathon pace.
Additionally, it has been found that making sure the hypothalamus section of the brain is cool has a significant effect on core body temperature. An easy way of doing this is by putting an ice pack on the back of your neck. Ensuring that you have a good quality fan in your turbo room, as well as maybe a dehumidifier, will also go quite a long way to reducing the impact of heat on your performance.
Another very simple way to combat dehydration is not only to consume enough water but also to ensure that enough salt is being consumed, both to allow replenishment of salts, but also to allow water to travel through the cell walls and avoid hyponatremia (further reduction of intracellular sodium). This is hard to get exactly right unless you have your sweat tested for the amount of salt per millilitre and then also have your sweat rate tested. However, the amount of salt required is often higher than you would expect when exercising hard in the heat.
Hopefully you found this piece interesting. Let us know any stories of how fatigue has really hit you and how you combatted it.
Other references:
Westerblad, H., Allen, D. G., & Lannergren, J. (2002). Muscle fatigue: lactic acid or inorganic phosphate the major cause?. Physiology, 17(1), 17-21.
Amann, M., Wan, H. Y., Thurston, T. S., Georgescu, V. P., & Weavil, J. C. (2020). On the influence of group III/IV muscle afferent feedback on endurance exercise performance. Exercise and sport sciences reviews, 48(4), 209.
Lindinger, M. I. (1995). Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle. Journal of molecular and cellular cardiology, 27(4), 1011-1022.
Clausen, T. (2003). Na+-K+ pump regulation and skeletal muscle contractility. Physiological reviews.
Reid, M. B. (2008). Free radicals and muscle fatigue: Of ROS, canaries, and the IOC. Free Radical Biology and Medicine, 44(2), 169-179.
Lian, D., Chen, M. M., Wu, H., Deng, S., & Hu, X. (2022). The role of oxidative stress in skeletal muscle myogenesis and muscle disease. Antioxidants, 11(4), 755.
Chan, J. S., Mann, L. M., Doherty, C. J., Angus, S. A., Thompson, B. P., Devries, M. C., … & Dominelli, P. B. (2023). The effect of inspiratory muscle training and detraining on the respiratory metaboreflex. Experimental Physiology, 108(4), 636-649.
González-Alonso, J., Teller, C., Andersen, S. L., Jensen, F. B., Hyldig, T., & Nielsen, B. (1999). Influence of body temperature on the development of fatigue during prolonged exercise in the heat. Journal of applied physiology, 86(3), 1032-1039.
Mohr, M., Nielsen, J. J., & Bangsbo, J. (2011). Caffeine intake improves intense intermittent exercise performance and reduces muscle interstitial potassium accumulation. Journal of applied physiology, 111(5), 1372-1379.
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