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This article is part of a series:
→ Part 1 — What is fatigue?
→ Part 2 — Do your muscles slow you down?
→ Part 3 — Does your brain slow you down?
→ Part 4 — Why do you slow down?
→ Part 5 — How to resist slowing down.
→ Part 6 — There’s always something left in the tank.
→ Part 1 — What is fatigue?
→ Part 2 — Do your muscles slow you down?
→ Part 3 — Does your brain slow you down?
→ Part 4 — Why do you slow down?
→ Part 5 — How to resist slowing down.
→ Part 6 — There’s always something left in the tank.
Fatigue in runners. Part 2 of 6:
The causes of fatigue — do your muscles slow you down?
Thomas Solomon PhD.
2nd April 2022.
To be the best athlete you can be, you need to resist fatigue for as long as possible during your races. To achieve that, you must arm yourself with knowledge that helps you answer the question: “What causes fatigue?”. Or, in clearer language, “Why do you slow down?”. Stay with me to continue your training in becoming a Jedi of the Fatigue Resistance…
Note: This part and the next part of the series (Parts 2 and 3) go pretty deep into the complexities of fatigue. So, if you wanna get your nerd on then stay tuned. However, if you’re less interested in the why and more interested in the what, then you are welcome to skip ahead to Part 4, in which I summarise all the causes of fatigue during exercise.
Reading time ~20-mins (4000-words).
Or listen to the Podcast version.
Or listen to the Podcast version.
Fatigue during exercise is a failure to maintain expected force (or expected rate of force development, aka power). By dissecting this riddle we will understand how to resist fatigue. But, as with many developments in science, our understanding of fatigue has largely been shaped by the tools available to study it. Muscle fatigue during exercise was first studied in the 1800s and was believed to arise as a consequence of low oxygen and a “fatigue factor”, which could be washed away to get back in the game. In 1889, physiologist Angelo Mosso, author of the famous 1891 textbook La Fatica discovered that repetitive finger muscle contractions led to finger fatigue. He also had participants contract their fingers until fatigue prior to mental tasks showing that pre-task muscular fatigue decreased subsequent cognitive performance. Besides hanging on rigs during an OCR race or competing in the Thumb War World Championships, finger fatigue is of little relevance to running. But Mosso’s work in the 1890s did link the muscles to the brain… an important scientific discovery that was rather neglected for about 80 years.
This neglect was driven, in part, by newly developed tools. In 1912, along came Nobel Laureate August Krogh, who gifted the world a nifty bit of kit — a cycle ergometer and an accurate method for measuring oxygen consumption (aka VO2). Then, in 1962, Jonas Bergström gave us the muscle needle biopsy technique allowing detailed analysis of muscle fatigue but also pushing our attention to fuel depletion in muscle. It wasn’t until the 1980s when multiple aspects of fatigue during exercise began to (re)converge in research labs — the brain met the muscle once again but so too did other environmental inputs like temperature, altitude, and nutrition.
Whatever is the cause, the endgame of fatigue is the same — you slow down and lose seconds, positions, or even medals. But, when we watch sport, commentators will say things like, “their legs are full of lactic acid”, “the next descent will allow them to flush the lactic out of their legs”. Scientists have known for several decades that lactic acid is not a “poison”, is not a “waste product” and is not a direct cause of fatigue. Yet, the narrative that “lactic acid causes fatigue and that we need to flush it out” has become dogma. Because it is a fascinating molecule, I will go deep on lactic acid another time but for now, remember this: the only scenario when lactic acid might directly cause you to slow down is when you are producing massive amounts of it, it dissociates into lactate and hydrogen (H+) ions, and when the concentrations of lactate and hydrogen ions is rapidly escalating. I.e. when you are engaged in a maximal effort for up to a few minutes — think, 200m through to 1-mile races. But even in that scenario, other factors are involved. If you were to believe that lactic acid (or lactate and H+ ions) alone is the cause of your race-day fatigue, you would neglect to focus on the many other “things” and fail in your training to become a Jedi of the Fatigue Resistance.
Because there are many ways to invite a visit from Darth Fader, Sith Lord of Fatigue
, my goal is to show you the many “things” that cause you to slow down. In doing so, I will provide you with several clues paving your route to resisting fatigue.
Now is a good time to acknowledge the following…
Phew.
Once upon a time, the statistician, George Box, pessimistically said that “All models are wrong. Some are useful.”. Fortunately, the more optimistic Stephen Hawking said that “One cannot say that one model is more correct than the other, only more useful”. My advice… Always keep in mind that most research studies are designed to isolate a specific piece of the puzzle in the lab and consequently determine its effect on fatigue. Laboratory studies are rarely a good model for race day. Racing is complex — nothing acts in isolation — because so many “things” are simultaneously smashing your body’s homeostasis and potentially causing fatigue. In the coming sections, I will dig into those “things”...
To start, I want to stratify these models into two halves:
Central fatigue — everything happening in the brain/CNS (central nervous system).
and
Peripheral fatigue — everything happening outside the brain/CNS.
But, I do not intend to convince you that these two “halves” are unrelated. Far from it. Like I said above: nothing acts in isolation.
I will start with aspects of “peripheral” fatigue...
These observations laid the foundations for the everlasting theory that fatigue during exercise is due to metabolite-induced failure of skeletal muscle contractile function (go deep on the history here). But the notion that your heart might get tired of beating so much during exercise is also supported by evidence.
Studies in trained athletes using echocardiography or cardiac MRI find evidence for exercise-induced cardiac fatigue after cycling road races, high-intensity runs, and ultramarathons. And, spirometry studies show that even your lungs can get “tired” of inhaling during marathons and ultras. Plus, we must acknowledge that low blood oxygen saturation due to hypoxia (“thin air” at altitude) and/or low blood haemoglobin mass (aka anaemia caused by low iron stores and/or blood loss) reduces oxygen delivery to your heart, muscles, and other organs, limiting exercise capacity.
Another way to consider cardiovascular/pulmonary fatigue is to examine to what extent your physiological measures of fitness deteriorate during exercise — for example, how long does it take your heart rate and breathing rate to start “drifting” upwards when working at a comfortably steady pace? (More on that here.) There is also an emerging question of whether better athletes have less deterioration in their high V̇O2max, running economy, and/or lactate threshold during prolonged exercise (physiological values that are typically measured in the “well-rested” state). One way to examine this is to see whether critical speed (or critical power in cycling) — a “fatigue threshold” that represents a metabolic steady-state speed or power (aka rate of energy expenditure) you can maintain for a long time — deteriorates or remains high after a couple of hours of exercise.
So, yes, your heart and lungs can get “tired” during exercise but, of course, you’ve spotted that I’ve now pushed cardiopulmonary fatigue towards something else…
What does this mean?
Essentially, both your race pace and your ability to unleash hell at the end of a race deteriorate when you are fatigued but better athletes better maintain these attributes.
Although the deterioration is not related to depletion of muscle glycogen, carbohydrate feeding during exercise can reduce the loss of critical power during exercise but it does not prevent the loss of anaerobic work capacity (Note: please see veohtu.com/criticalspeed for full info on critical power and anaerobic work capacity).
At low to moderate intensities (easy effort running up to ~marathon pace), you “burn” fuel (predominantly in the form of fatty acids rather than glucose) to produce energy (ATP) “aerobically” (using oxidative/oxygen-requiring metabolic pathways in the mitochondria of your muscle cells). All the while, lactate production is low, lactate concentrations in your blood stay low because your “slow” type 1 muscle fibres can use lactate as a fuel, and your muscles do not accumulate (or are able to rapidly clear) fatigue-causing metabolites (phosphate, hydrogen ions, etc). At such intensities, if you are in a state of adequate energy availability, well-hydrated, and able to stay cool (especially if it is a hot/humid day), all is good and you will keep on trucking.
At higher intensities (e.g. ~½-marathon pace and faster), you burn fuel at a higher rate and you begin to “burn” more glucose than fatty acids to produce more energy (ATP) via “anaerobic” (“substrate-level” nonoxidative/non-oxygen-requiring) metabolic pathways outside the mitochondria in the cytosol of your muscle cells. This results in more phosphocreatine breakdown (to help rapidly resynthesis ATP from ADP) and more glycolysis/glycogenolysis (carb “burning”) leading to more lactate production and the accumulation of fatigue-causing metabolites in and around your muscle cells (hydrogen ions, H+; inorganic phosphate, Pi which directly prevents cross-bridge formation); adenosine diphosphate, ADP; and potassium, K+) plus a loss of sarcoplasmic calcium (Ca2+) release and sensitivity… At higher intensities, you munch through glycogen stores more quickly and you produce more heat, which means you might become more dehydrated and might lose more sodium and you need to stay cool. Fatigue is imminent.
But it is only at very high intensities — e.g. races lasting up to ~5-minutes — when the majority of energy is coming from non-oxidative pathways (phosphocreatine and glycolysis), producing lactate in such large amounts that it cannot be metabolised in muscle cells or taken up elsewhere, thus blood lactate concentrations increase and rapidly accumulating H+ ions cause metabolic acidosis, while other fatigue-causing metabolites (Pi and ADP) go through the roof, causing rapid fatigue.
So, during running, when you go above your critical speed (your fatigue threshold), these are the kinds of “metabolic” things happening in your muscles that cause you to slow down. But, endurance athletes competing in events lasting an hour or more rarely race above their fatigue threshold so not much of this nasty shiz goes down. So, in those circumstances, why do you slow down?
Studies in endurance-trained athletes throughout the 80s, 90s, and 2000s showed that the decline in blood glucose contributes to fatigue during prolonged exercise and that intravenous glucose infusion during exercise can restore healthy blood glucose levels after hypoglycemia has developed and prolong exercise time-to-exhaustion after muscle glycogen has been depleted during long-duration (2-3-hours) low-to-moderate intensity exercise (see here and here ). But, similar studies showed that glucose infusion doesn’t prevent muscle glycogen depletion during exercise (see here and here ) and doesn’t improve high-intensity time trial performance (see here).
Since intravenous glucose infusion is neither allowed (it violates WADAs ethical code) nor practical during a race, some researchers realised that eating glucose is far more sensible for practical application. I went deep on this research at veohtu.com/racedaycarbavailability — during-exercise carbohydrate ingestion prevents hypoglycemia. But, as we all know well, you might still fade on race day even when feeding well.
One study that boldly concluded (and became dogma) that hypoglycaemia does not cause fatigue, was from Philip Felig and John Wahren in 1982. Nineteen untrained regular folks rode to exhaustion at 60-65% V̇O2max. Seven of them developed hypoglycemia but their time to exhaustion was not significantly different (albeit 20-mins slower, on average) than folks who did not develop hypoglycemia (142±15 vs 162±11 minutes). Glucose ingestion (40 or 80-grams) during follow-up trials prevented hypoglycemia but did not affect RPE or time-to-exhaustion. The final sentence of their paper reads: “the so called phenomenon of hitting the wall during marathon running is probably due to factors other than a low blood glucose concentration”. Alas… The main limitation of allowing such a study to become dogma is that subjects consumed their usual diet (so we do not know what their pre-exercise glycogen levels were); they were untrained folks (so the findings are not applicable to athletes); individual data are not presented (so we cannot know if there was a benefit of glucose ingestion for the 7 folks who developed hypoglycemia); and, exercise at 60-65% V̇O2max is a low-to-moderate intensity affair (more akin to an ultra-distance race than a marathon or anything shorter). I am not trying to destroy this specific study but my point is that we cannot conclude from it that “hitting the wall” when giving it large in a marathon does not involve hypoglycaemia.
Anyway, maintaining blood glucose in the normal range supplies the brain with its prefered fuel: glucose. When blood glucose drops below critical levels (below ~4 mM), the brain fades and you eventually pass out. Low blood sugar (hypoglycaemia) is sensed by the brain but whether liver glycogen and/or muscle glycogen levels are sensed by the brain is unknown. At exhaustion during prolonged exercise, liver and muscle glycogen are often but not always depleted. Similarly, hypoglycemia is not always present in athletes who have reached fatigue. Plus, the onset of hypoglycemia doesn’t always cause fatigue so long as it is resolved.
(Note: if you want to go deep on this topic, please see my Performance Nutrition series, particularly Part 5 at veohtu.com/racedaycarbavailability.)
This is all a bit “it could be this but it might not be”. But, after 100-years of exercise metabolism research, one thing is clear…
And, while we are on the topic of nutrients, it’s also important to know that…
And, to implicate nutrition and hydration with something else important…
To quickly summarise all that into a single succinct statement…
During a long race (or session), glycogen depletion is certainly important but other metabolic factors simultaneously develop, like rising body temperature (heat stress), the onset of hypoglycaemia (low blood glucose), decreasing hydration, and possibly hyponatremia (low blood sodium).
All of these things may explain “metabolic fatigue” at the point of exhaustion.
But
Yep, they are being smashed!
During running your muscles are stretching (eccentric contraction) and pulling (concentric contraction) against load — the stretch-shortening cycle — which naturally causes micro-trauma, aka damage. The longer and/or more intense and/or more technical you go, the more muscle and connective tissue damage will occur. During long races like ½ marathons, marathons, trail races, and ultras, you will accumulate a lot of micro-trauma — thousands of studies have documented this. Whether it’s caused during long-duration running or vigorous electrically-induced contractions or explosive plyometric exercises, muscle damage impairs exercise performance.
During such long races that cause micro-trauma (or damage), it is inevitable fatigue will creep in. But, it is almost impossible to know if these things occur simultaneously. What is clear, however, is that when fatigue creeps in during these arduous races, your biomechanics begin to change — your knee lift drops, your heel kick weakens, and your stride length shortens…
While fatigue is typically defined as a failure to maintain expected work output, fatigue is also characterised by a loss of “complexity” — jargon for the loss of ability to adapt to changing demands (within a race or session). This is seen as a loss of variability in physiological signals (like heart rate, nerve activity, V̇O2) as they reach a plateau but also as a loss of biomechanical complexity. During running, you throw down repeated and rhythmic actions but the variability in these actions alters just before you reach fatigue, causing a loss of stability in your actions and diminished ability to respond to demand — a loss of biomechanical complexity (see examples during 5 km racing here, here, and here). Like I said before, your knee lift drops, your heel kick weakens, and your stride length shortens. Or, on the trails, this might manifest as a loss of ability to raise your foot enough to avoid a rock.
Marathons have become synonymous with “hitting the wall”, at which point (if it happens) there is a clear (sometimes dramatic) change in your biomechanics. From a visual perspective, your running form looks horrible during a race-day detonation. Using video-capture kinematics and movement sensors, studies show steady decreases in foot strike angle, ground reaction force, and time-in-air (aka “flight time”) and gradual increases in ground contact time during a marathon in recreational runners coupled with progressively decreasing stride length throughout the race and drops in running speed at ~25-30 km and/or 35-42 km. Data collected in world-class athletes show that faster marathoners maintain a long step length and longer flight time during the race. Furthermore, a 2022 systematic review found that prolonged running to exhaustion is associated with a decrease in leg stiffness, which may worsen running economy.
Despite changes in biomechanics developing during long-duration and muscle damaging running, some evidence shows that we are rather clever — the changes in gait actually help minimise the energy cost of running as we slow down (see here, here, here & here). This is like a defence mechanism to improve running (and walking) economy to use less energy at a given pace and thereby help dampen “metabolic” fatigue. This sounds great but you’re still slowing down.
All that said, the ultimate consequence of muscle and connective tissue micro-trauma (damage) during exercise is, of course, soreness and pain, which is a perceived “feeling”. You know what that feels like and it doesn’t feel great… To be discussed in Part 3.
So, that’s all you need to know about “peripheral” fatigue.
Now I’d like to “get on your nerves” and start heading towards your brain.
To do so, I first want to consider a simple question…
When you run, you want to produce more force so you can hit the ground harder to propel yourself forward. To produce more force, you need to “recruit” more muscle fibres within a muscle. Having a large “pool” of “recruitable” fibres endows you with a greater potential to produce more force. To move faster, you also want to increase your rate of force development — to increase your power — so you can hit the ground faster, spending more time in the air and less time on the ground — more flying, less plodding. You’ve probably heard about different muscle fibre types: Type 1 (aka “red” or “slow” fibres) and Type 2a/2b/2x (aka “white” or “fast” fibres), blah blah blah. Within each muscle, there are many fibres of multiple types. But the important thing to remember is that you never recruit all fibres within a muscle. They seem to activate in cycles. For example, during prolonged exercise the type 1 “slow-twitch” fibres do much of the work and, as they get “tired”, other “slow” Type 1 fibres take over; when they’re all “tired”, “fast” Type 2 fibres take over.
Muscle fibre recruitment is driven by neuromuscular function; that’s jargon for electrical nerve impulses (or action potentials) coming from the brain via the spine to activate (or innervate) your muscle fibres. Electromyographic (EMG) studies show that larger electrical impulses activate more fibres and produce more force but, as you fatigue (slow down), the size of these impulses decreases, you activate less muscle fibres, and produce less force. EMG studies also show that better runners can produce larger EMG signals, recruit more muscle fibres, and can activate muscle fibres more quickly (see here, here and here, but I will cover this in detail elsewhere).
In other words:
If your brain sends more signal, you activate more muscle fibres and produce more force.
That’s pretty cool but, during prolonged intense running, it is intuitive that your brain might get tired of sending electrical signals — your brain might get tired of running. By telling you this, I am trying to get your mighty brain thinking it is involved in the process of fatigue during exercise… Perhaps the reason you slow down is not just due to your muscles, or heart, or lungs, or energy depletion, or environmental extremes?! Perhaps your brain “chooses” to slow down?!
W’oh!
But that’ll have to wait until Part 3. Until that time, stay nerdy and keep training smart.
Thanks for joining me for another “session”. I am passionate about equality in access to free education. If you find value in my content, please help keep it alive by sharing it on social media and buying me a beer at buymeacoffee.com/thomas.solomon. For more knowledge, join me @thomaspjsolomon on Twitter, follow @veohtu on Facebook and Instagram, subscribe to my free email updates at veothu.com/subscribe, and visit veohtu.com to check out my other Articles, Nerd Alerts, Free Training Tools, and my Train Smart Framework. To learn while you train, you can even listen to my articles by subscribing to the Veohtu podcast.
This neglect was driven, in part, by newly developed tools. In 1912, along came Nobel Laureate August Krogh, who gifted the world a nifty bit of kit — a cycle ergometer and an accurate method for measuring oxygen consumption (aka VO2). Then, in 1962, Jonas Bergström gave us the muscle needle biopsy technique allowing detailed analysis of muscle fatigue but also pushing our attention to fuel depletion in muscle. It wasn’t until the 1980s when multiple aspects of fatigue during exercise began to (re)converge in research labs — the brain met the muscle once again but so too did other environmental inputs like temperature, altitude, and nutrition.
Whatever is the cause, the endgame of fatigue is the same — you slow down and lose seconds, positions, or even medals. But, when we watch sport, commentators will say things like, “their legs are full of lactic acid”, “the next descent will allow them to flush the lactic out of their legs”. Scientists have known for several decades that lactic acid is not a “poison”, is not a “waste product” and is not a direct cause of fatigue. Yet, the narrative that “lactic acid causes fatigue and that we need to flush it out” has become dogma. Because it is a fascinating molecule, I will go deep on lactic acid another time but for now, remember this: the only scenario when lactic acid might directly cause you to slow down is when you are producing massive amounts of it, it dissociates into lactate and hydrogen (H+) ions, and when the concentrations of lactate and hydrogen ions is rapidly escalating. I.e. when you are engaged in a maximal effort for up to a few minutes — think, 200m through to 1-mile races. But even in that scenario, other factors are involved. If you were to believe that lactic acid (or lactate and H+ ions) alone is the cause of your race-day fatigue, you would neglect to focus on the many other “things” and fail in your training to become a Jedi of the Fatigue Resistance.
Because there are many ways to invite a visit from Darth Fader, Sith Lord of Fatigue
, my goal is to show you the many “things” that cause you to slow down. In doing so, I will provide you with several clues paving your route to resisting fatigue.
Now is a good time to acknowledge the following…
There are many models of fatigue and scientists argue over them.
There is an “energy supply” model, which is related to glycogen and intramuscular triglycerides (your stored fuel), ingested fuel, and mitochondrial function (how your muscles “burn” fuel to produce energy, aka ATP). There’s a “cardiovascular” model proposing high-intensity exercise is limited by the onset of anaerobic conditions in your muscles due to your heart reaching its maximum ability to pump blood and deliver oxygen. A “biomechanical” model that is related to the elastic recoil of structural proteins in your muscles and their resistance to damage (muscle micro-trauma) caused by prolonged, repeated eccentric contractions. Then there’s the “muscle power” model that proposes that muscles’ contractile capacity to generate force is simply different between different people (due to genetics and/or metabolic adaptations caused by training). And, then there are the models that include the brain: the “central governor” model, which hypothesizes that your brain subconsciously limits your maximal exercise capacity to keep your heart oxygenated, preventing heart damage; the “integrative governor” theory, which includes psychological and physiological homeostatic inputs; and the “psychobiological” model of fatigue, which brings your perception of effort into the mix. (Note: to go deep on these models, I can recommend a 2005 Sports Med narrative review by Abbiss and Laursen.)Phew.
Once upon a time, the statistician, George Box, pessimistically said that “All models are wrong. Some are useful.”. Fortunately, the more optimistic Stephen Hawking said that “One cannot say that one model is more correct than the other, only more useful”. My advice… Always keep in mind that most research studies are designed to isolate a specific piece of the puzzle in the lab and consequently determine its effect on fatigue. Laboratory studies are rarely a good model for race day. Racing is complex — nothing acts in isolation — because so many “things” are simultaneously smashing your body’s homeostasis and potentially causing fatigue. In the coming sections, I will dig into those “things”...
To start, I want to stratify these models into two halves:
Central fatigue — everything happening in the brain/CNS (central nervous system).
and
Peripheral fatigue — everything happening outside the brain/CNS. I will start with aspects of “peripheral” fatigue...
Cardiovascular/pulmonary fatigue happens.
In the 1920s, Nobel Laureate, AV Hill, observed that fatigue during short-duration high-intensity exercise occurs when the oxygen requirement of contracting muscles exceeds cardiac output (the heart’s capacity to deliver oxygen). During such exercise, VO2 reaches a maximum causing an inadequate supply of oxygen to the heart (myocardial ischaemia), limiting maximal cardiac output. In this model, Hill proposed that since energy can only come from “anaerobic” sources during short-duration high-intensity exercise, lactic acid accumulates, “poisoning” the muscle, impairing muscle relaxation, and ultimately terminating exercise.These observations laid the foundations for the everlasting theory that fatigue during exercise is due to metabolite-induced failure of skeletal muscle contractile function (go deep on the history here). But the notion that your heart might get tired of beating so much during exercise is also supported by evidence.
Studies in trained athletes using echocardiography or cardiac MRI find evidence for exercise-induced cardiac fatigue after cycling road races, high-intensity runs, and ultramarathons. And, spirometry studies show that even your lungs can get “tired” of inhaling during marathons and ultras. Plus, we must acknowledge that low blood oxygen saturation due to hypoxia (“thin air” at altitude) and/or low blood haemoglobin mass (aka anaemia caused by low iron stores and/or blood loss) reduces oxygen delivery to your heart, muscles, and other organs, limiting exercise capacity.
Another way to consider cardiovascular/pulmonary fatigue is to examine to what extent your physiological measures of fitness deteriorate during exercise — for example, how long does it take your heart rate and breathing rate to start “drifting” upwards when working at a comfortably steady pace? (More on that here.) There is also an emerging question of whether better athletes have less deterioration in their high V̇O2max, running economy, and/or lactate threshold during prolonged exercise (physiological values that are typically measured in the “well-rested” state). One way to examine this is to see whether critical speed (or critical power in cycling) — a “fatigue threshold” that represents a metabolic steady-state speed or power (aka rate of energy expenditure) you can maintain for a long time — deteriorates or remains high after a couple of hours of exercise.
So, yes, your heart and lungs can get “tired” during exercise but, of course, you’ve spotted that I’ve now pushed cardiopulmonary fatigue towards something else…
Metabolic fatigue can also slow you down.
Several studies show that prolonged exercise deteriorates athletes’ critical power and anaerobic work capacity compared to when they are fresh (see here and here). We also know that being able to “resist” this deterioration is what separates world-class from sub-elite athletes.What does this mean?
Essentially, both your race pace and your ability to unleash hell at the end of a race deteriorate when you are fatigued but better athletes better maintain these attributes.
Although the deterioration is not related to depletion of muscle glycogen, carbohydrate feeding during exercise can reduce the loss of critical power during exercise but it does not prevent the loss of anaerobic work capacity (Note: please see veohtu.com/criticalspeed for full info on critical power and anaerobic work capacity).
At low to moderate intensities (easy effort running up to ~marathon pace), you “burn” fuel (predominantly in the form of fatty acids rather than glucose) to produce energy (ATP) “aerobically” (using oxidative/oxygen-requiring metabolic pathways in the mitochondria of your muscle cells). All the while, lactate production is low, lactate concentrations in your blood stay low because your “slow” type 1 muscle fibres can use lactate as a fuel, and your muscles do not accumulate (or are able to rapidly clear) fatigue-causing metabolites (phosphate, hydrogen ions, etc). At such intensities, if you are in a state of adequate energy availability, well-hydrated, and able to stay cool (especially if it is a hot/humid day), all is good and you will keep on trucking.
At higher intensities (e.g. ~½-marathon pace and faster), you burn fuel at a higher rate and you begin to “burn” more glucose than fatty acids to produce more energy (ATP) via “anaerobic” (“substrate-level” nonoxidative/non-oxygen-requiring) metabolic pathways outside the mitochondria in the cytosol of your muscle cells. This results in more phosphocreatine breakdown (to help rapidly resynthesis ATP from ADP) and more glycolysis/glycogenolysis (carb “burning”) leading to more lactate production and the accumulation of fatigue-causing metabolites in and around your muscle cells (hydrogen ions, H+; inorganic phosphate, Pi which directly prevents cross-bridge formation); adenosine diphosphate, ADP; and potassium, K+) plus a loss of sarcoplasmic calcium (Ca2+) release and sensitivity… At higher intensities, you munch through glycogen stores more quickly and you produce more heat, which means you might become more dehydrated and might lose more sodium and you need to stay cool. Fatigue is imminent.
But it is only at very high intensities — e.g. races lasting up to ~5-minutes — when the majority of energy is coming from non-oxidative pathways (phosphocreatine and glycolysis), producing lactate in such large amounts that it cannot be metabolised in muscle cells or taken up elsewhere, thus blood lactate concentrations increase and rapidly accumulating H+ ions cause metabolic acidosis, while other fatigue-causing metabolites (Pi and ADP) go through the roof, causing rapid fatigue.
So, during running, when you go above your critical speed (your fatigue threshold), these are the kinds of “metabolic” things happening in your muscles that cause you to slow down. But, endurance athletes competing in events lasting an hour or more rarely race above their fatigue threshold so not much of this nasty shiz goes down. So, in those circumstances, why do you slow down?
Glycogen depletion can slow you down.
Because muscle glycogen levels are typically low when athletes reach exhaustion after giving it medium or medium-large until failure (a lab model of fatigue), it is natural to assume that muscle glycogen depletion causes fatigue in long races. Historical studies in the 1960s from folks like Jonas Bergstrom, Eric Hultman, and Bengt Saltin, found that subjects receiving a low-carb diet had lower pre-exercise muscle glycogen levels and poorer exercise time-to-exhaustion. These folks also found that higher pre-exercise muscle glycogen levels were associated with longer exercise time-to-exhaustion (see here , here, and here — I went deep on this history at veohtu.com/carboloading). Many moons on, these findings have been replicated many times (I went deep on this topic at veohtu.com/racedaycarbavailability.) BUT we also know that muscle glycogen is not always depleted when trained endurance athletes reach exhaustion during exercise (the historical data on this topic reviewed here), suggesting that the depletion of accessible stored fuel in muscle is just a small piece of the puzzle. Furthermore, your currency of chemical energy, ATP (the thing that is ultimately produced when you “burn” “fuel” so you can move forward), is never depleted (see here & here) even at exhaustion when other things like muscle glycogen are empty — there is always energy available but your body kinda chooses not to use it.Hypoglycaemia (low blood sugar) can slow you down.
In 1924, Sam Levine and colleagues found that runners completing the Boston marathon had lower blood glucose levels than when they started and noted that their level of physical weakness, pallor, and collapse was associated with their blood glucose levels. The following year, many of the same runners were asked to eat a high-carbohydrate diet for 24-hours before the race and to start eating candy after about 24 kms (15 miles) into the race, finding that their “condition” was better at the finish line, their post-race blood glucose was higher than baseline and their race times improved. Similarly, in 1939, Erik Christensen and Ove Hansen found that if “sugar water” (aka sucrose aka glucose + fructose) was given at the point of fatigue during cycling, low blood glucose levels were restored and subjects could ride for longer (note: you will need to learn German or have your German-speaking wife help you translate this paper).Studies in endurance-trained athletes throughout the 80s, 90s, and 2000s showed that the decline in blood glucose contributes to fatigue during prolonged exercise and that intravenous glucose infusion during exercise can restore healthy blood glucose levels after hypoglycemia has developed and prolong exercise time-to-exhaustion after muscle glycogen has been depleted during long-duration (2-3-hours) low-to-moderate intensity exercise (see here and here ). But, similar studies showed that glucose infusion doesn’t prevent muscle glycogen depletion during exercise (see here and here ) and doesn’t improve high-intensity time trial performance (see here).
Since intravenous glucose infusion is neither allowed (it violates WADAs ethical code) nor practical during a race, some researchers realised that eating glucose is far more sensible for practical application. I went deep on this research at veohtu.com/racedaycarbavailability — during-exercise carbohydrate ingestion prevents hypoglycemia. But, as we all know well, you might still fade on race day even when feeding well.
One study that boldly concluded (and became dogma) that hypoglycaemia does not cause fatigue, was from Philip Felig and John Wahren in 1982. Nineteen untrained regular folks rode to exhaustion at 60-65% V̇O2max. Seven of them developed hypoglycemia but their time to exhaustion was not significantly different (albeit 20-mins slower, on average) than folks who did not develop hypoglycemia (142±15 vs 162±11 minutes). Glucose ingestion (40 or 80-grams) during follow-up trials prevented hypoglycemia but did not affect RPE or time-to-exhaustion. The final sentence of their paper reads: “the so called phenomenon of hitting the wall during marathon running is probably due to factors other than a low blood glucose concentration”. Alas… The main limitation of allowing such a study to become dogma is that subjects consumed their usual diet (so we do not know what their pre-exercise glycogen levels were); they were untrained folks (so the findings are not applicable to athletes); individual data are not presented (so we cannot know if there was a benefit of glucose ingestion for the 7 folks who developed hypoglycemia); and, exercise at 60-65% V̇O2max is a low-to-moderate intensity affair (more akin to an ultra-distance race than a marathon or anything shorter). I am not trying to destroy this specific study but my point is that we cannot conclude from it that “hitting the wall” when giving it large in a marathon does not involve hypoglycaemia.
Anyway, maintaining blood glucose in the normal range supplies the brain with its prefered fuel: glucose. When blood glucose drops below critical levels (below ~4 mM), the brain fades and you eventually pass out. Low blood sugar (hypoglycaemia) is sensed by the brain but whether liver glycogen and/or muscle glycogen levels are sensed by the brain is unknown. At exhaustion during prolonged exercise, liver and muscle glycogen are often but not always depleted. Similarly, hypoglycemia is not always present in athletes who have reached fatigue. Plus, the onset of hypoglycemia doesn’t always cause fatigue so long as it is resolved.
(Note: if you want to go deep on this topic, please see my Performance Nutrition series, particularly Part 5 at veohtu.com/racedaycarbavailability.)
This is all a bit “it could be this but it might not be”. But, after 100-years of exercise metabolism research, one thing is clear…
Low carbohydrate availability can cause fatigue.
Starting a long race with low carbohydrate availability will make you slow down sooner (because your small “fast” fuel store — glycogen — will deplete and your blood glucose will drop). And, doing nothing to remedy low carbohydrate availability during a long race will also make you slow down sooner. (By “long”, I mean, anything longer than ~1-hour). Having a high muscle (and liver) glycogen at the onset of exercise and feeding carbohydrates regularly during prolonged vigorous exercise helps athletes resist fatigue for longer. But, this is not to say that glycogen depletion and/or hypoglycemia are the sole reasons you slow down. And, of course, you’ve fatigued during long sessions and races even when you’ve regularly consumed carbohydrates.And, while we are on the topic of nutrients, it’s also important to know that…
Dehydration can cause fatigue.
I won’t go deep on this topic because I’ve done so already… Starting a race in a dehydrated state might make you slow down sooner, especially in the heat (most likely due to a poorer ability to cool down through sweat). Furthermore, becoming excessively dehydrated during a race in hot conditions will also make you slow down sooner (again due to poorer cooling).And, to implicate nutrition and hydration with something else important…
Environmental extremes also cause fatigue.
Again, I won’t go deep on this because I’ve done so previously or plan to do so in the future. But, racing in cold conditions can make you go slower and slow down sooner (due to low muscle temperature, hypothermia, and faster fuel store depletion). Similarly, racing in hot conditions can also make you go slower and slow down sooner (due to heat stress, faster fuel store depletion, and elevated RPE). And, racing at a high altitude can also make you go slower and slow down sooner because the lower partial pressure of atmospheric oxygen — “thin air” — reduces oxygen saturation in your blood, making it harder to deliver oxygen to your muscles, heart, and other organs, an extra special problem for athletes with asthma or vascular diseases (note: a deep-dive on altitude is coming soon). Plus, combining such environmental conditions — “hot and high” (Western States) or “cold and high” (Beijing Winter Olympics) — may have additive negative effects on your performance.To quickly summarise all that into a single succinct statement…
During a long race (or session), glycogen depletion is certainly important but other metabolic factors simultaneously develop, like rising body temperature (heat stress), the onset of hypoglycaemia (low blood glucose), decreasing hydration, and possibly hyponatremia (low blood sodium).
All of these things may explain “metabolic fatigue” at the point of exhaustion.
Although metabolic fatigue can happen and might happen, it doesn’t always explain fatigue during exercise.
The plot thickens, but we’re not done yet…
Changes in biomechanics can slow you down.
Imagine you are deep into a long race and are probably getting warm, probably running out of accessible glycogen, possibly becoming hypoglycaemic and perhaps becoming dehydrated. Now think about what has been happening to your muscles and connective tissue each time your foot has struck the ground…Yep, they are being smashed!
During running your muscles are stretching (eccentric contraction) and pulling (concentric contraction) against load — the stretch-shortening cycle — which naturally causes micro-trauma, aka damage. The longer and/or more intense and/or more technical you go, the more muscle and connective tissue damage will occur. During long races like ½ marathons, marathons, trail races, and ultras, you will accumulate a lot of micro-trauma — thousands of studies have documented this. Whether it’s caused during long-duration running or vigorous electrically-induced contractions or explosive plyometric exercises, muscle damage impairs exercise performance.
During such long races that cause micro-trauma (or damage), it is inevitable fatigue will creep in. But, it is almost impossible to know if these things occur simultaneously. What is clear, however, is that when fatigue creeps in during these arduous races, your biomechanics begin to change — your knee lift drops, your heel kick weakens, and your stride length shortens…
While fatigue is typically defined as a failure to maintain expected work output, fatigue is also characterised by a loss of “complexity” — jargon for the loss of ability to adapt to changing demands (within a race or session). This is seen as a loss of variability in physiological signals (like heart rate, nerve activity, V̇O2) as they reach a plateau but also as a loss of biomechanical complexity. During running, you throw down repeated and rhythmic actions but the variability in these actions alters just before you reach fatigue, causing a loss of stability in your actions and diminished ability to respond to demand — a loss of biomechanical complexity (see examples during 5 km racing here, here, and here). Like I said before, your knee lift drops, your heel kick weakens, and your stride length shortens. Or, on the trails, this might manifest as a loss of ability to raise your foot enough to avoid a rock.
Marathons have become synonymous with “hitting the wall”, at which point (if it happens) there is a clear (sometimes dramatic) change in your biomechanics. From a visual perspective, your running form looks horrible during a race-day detonation. Using video-capture kinematics and movement sensors, studies show steady decreases in foot strike angle, ground reaction force, and time-in-air (aka “flight time”) and gradual increases in ground contact time during a marathon in recreational runners coupled with progressively decreasing stride length throughout the race and drops in running speed at ~25-30 km and/or 35-42 km. Data collected in world-class athletes show that faster marathoners maintain a long step length and longer flight time during the race. Furthermore, a 2022 systematic review found that prolonged running to exhaustion is associated with a decrease in leg stiffness, which may worsen running economy.
Despite changes in biomechanics developing during long-duration and muscle damaging running, some evidence shows that we are rather clever — the changes in gait actually help minimise the energy cost of running as we slow down (see here, here, here & here). This is like a defence mechanism to improve running (and walking) economy to use less energy at a given pace and thereby help dampen “metabolic” fatigue. This sounds great but you’re still slowing down.
All that said, the ultimate consequence of muscle and connective tissue micro-trauma (damage) during exercise is, of course, soreness and pain, which is a perceived “feeling”. You know what that feels like and it doesn’t feel great… To be discussed in Part 3.
* * *
So, you can see how depletion of your body’s fuel stores and/or body water stores play a role and become emphasised when racing under environmental extremes. Plus, you can see how these things feed into aspects of “metabolic fatigue” (e.g. phosphocreatine/glycogen depletion and/or hypoglycaemia and/or acidosis). Furthermore, a lack of power caused by metabolic fatigue may exacerbate the consequences of biomechanical fatigue. For example, lacking energy to contract a “tiring” hip flexor enough to raise your knee to avoid a rock will change the mechanics of your gait, perhaps putting unfamiliar load and greater energy demand on other muscle groups. W’oh, how complicated!
So, that’s all you need to know about “peripheral” fatigue.
Now I’d like to “get on your nerves” and start heading towards your brain.
To do so, I first want to consider a simple question…
What actually happens in your muscles when you slow down?
As you’ve learnt, there are physiological events involving the lungs, heart, blood vessels, and muscle metabolism that occur during fatigue and are sometimes (but not always) found at the point of exhaustion. They all relate to oxygen and fuel delivery, fuel “burning”, and ATP (energy) production to keep the muscles producing force.When you run, you want to produce more force so you can hit the ground harder to propel yourself forward. To produce more force, you need to “recruit” more muscle fibres within a muscle. Having a large “pool” of “recruitable” fibres endows you with a greater potential to produce more force. To move faster, you also want to increase your rate of force development — to increase your power — so you can hit the ground faster, spending more time in the air and less time on the ground — more flying, less plodding. You’ve probably heard about different muscle fibre types: Type 1 (aka “red” or “slow” fibres) and Type 2a/2b/2x (aka “white” or “fast” fibres), blah blah blah. Within each muscle, there are many fibres of multiple types. But the important thing to remember is that you never recruit all fibres within a muscle. They seem to activate in cycles. For example, during prolonged exercise the type 1 “slow-twitch” fibres do much of the work and, as they get “tired”, other “slow” Type 1 fibres take over; when they’re all “tired”, “fast” Type 2 fibres take over.
Muscle fibre recruitment is driven by neuromuscular function; that’s jargon for electrical nerve impulses (or action potentials) coming from the brain via the spine to activate (or innervate) your muscle fibres. Electromyographic (EMG) studies show that larger electrical impulses activate more fibres and produce more force but, as you fatigue (slow down), the size of these impulses decreases, you activate less muscle fibres, and produce less force. EMG studies also show that better runners can produce larger EMG signals, recruit more muscle fibres, and can activate muscle fibres more quickly (see here, here and here, but I will cover this in detail elsewhere).
In other words:
If your brain sends more signal, you activate more muscle fibres and produce more force. W’oh!
But that’ll have to wait until Part 3. Until that time, stay nerdy and keep training smart.
Thanks for joining me for another “session”. I am passionate about equality in access to free education. If you find value in my content, please help keep it alive by sharing it on social media and buying me a beer at buymeacoffee.com/thomas.solomon. For more knowledge, join me @thomaspjsolomon on Twitter, follow @veohtu on Facebook and Instagram, subscribe to my free email updates at veothu.com/subscribe, and visit veohtu.com to check out my other Articles, Nerd Alerts, Free Training Tools, and my Train Smart Framework. To learn while you train, you can even listen to my articles by subscribing to the Veohtu podcast.
Disclaimer: I occasionally mention brands and products but it is important to know that I am not affiliated with, sponsored by, an ambassador for, or receiving advertisement royalties from any brands. I have conducted biomedical research for which I have received research money from publicly-funded national research councils and medical charities, and also from private companies, including Novo Nordisk Foundation, AstraZeneca, Amylin, A.P. Møller Foundation, and Augustinus Foundation. I’ve also consulted for Boost Treadmills and Gu Energy on their research and innovation grant applications and I’ve provided research and science writing services for Examine — some of my articles contain links to information provided by Examine but I do not receive any royalties or bonuses from those links. These companies had no control over the research design, data analysis, or publication outcomes of my work. Any recommendations I make are, and always will be, based on my own views and opinions shaped by the evidence available. My recommendations have never and will never be influenced by affiliations, sponsorships, advertisement royalties, etc. The information I provide is not medical advice. Before making any changes to your habits of daily living based on any information I provide, always ensure it is safe for you to do so and consult your doctor if you are unsure.
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About the author:
I am Thomas Solomon and I'm passionate about relaying accurate and clear scientific information to the masses to help folks meet their fitness and performance goals. I hold a BSc in Biochemistry and a PhD in Exercise Science and am an ACSM-certified Exercise Physiologist and Personal Trainer, a VDOT-certified Distance running coach, and a Registered Nutritionist. Since 2002, I have conducted biomedical research in exercise and nutrition and have taught and led university courses in exercise physiology, nutrition, biochemistry, and molecular medicine. My work is published in over 80 peer-reviewed medical journal publications and I have delivered more than 50 conference presentations & invited talks at universities and medical societies. I have coached and provided training plans for truck-loads of athletes, have competed at a high level in running, cycling, and obstacle course racing, and continue to run, ride, ski, hike, lift, and climb as much as my ageing body will allow. To stay on top of scientific developments, I consult for scientists, participate in journal clubs, peer-review papers for medical journals, and I invest every Friday in reading what new delights have spawned onto PubMed. In my spare time, I hunt for phenomenal mountain views to capture through the lens, boulder problems to solve, and for new craft beers to drink with the goal of sending my gustatory system into a hullabaloo.
Copyright © Thomas Solomon. All rights reserved.
I am Thomas Solomon and I'm passionate about relaying accurate and clear scientific information to the masses to help folks meet their fitness and performance goals. I hold a BSc in Biochemistry and a PhD in Exercise Science and am an ACSM-certified Exercise Physiologist and Personal Trainer, a VDOT-certified Distance running coach, and a Registered Nutritionist. Since 2002, I have conducted biomedical research in exercise and nutrition and have taught and led university courses in exercise physiology, nutrition, biochemistry, and molecular medicine. My work is published in over 80 peer-reviewed medical journal publications and I have delivered more than 50 conference presentations & invited talks at universities and medical societies. I have coached and provided training plans for truck-loads of athletes, have competed at a high level in running, cycling, and obstacle course racing, and continue to run, ride, ski, hike, lift, and climb as much as my ageing body will allow. To stay on top of scientific developments, I consult for scientists, participate in journal clubs, peer-review papers for medical journals, and I invest every Friday in reading what new delights have spawned onto PubMed. In my spare time, I hunt for phenomenal mountain views to capture through the lens, boulder problems to solve, and for new craft beers to drink with the goal of sending my gustatory system into a hullabaloo.
Copyright © Thomas Solomon. All rights reserved.