Nutrition for endurance athletes: the crucial issue of inflammation

Nutrition continues to be a controversial topic; controversy fuelled by the contradictory claims of passionate advocates of specific diets.  Is the major enemy saturated fat or is it carbohydrates; or is a more nuanced answer required?   There is a vast but confusing body of evidence, derived from studies using differing methods, in differing groups of participants and assessing differing outcomes.  But from this confusing body of evidence, there is an emerging pattern that allows an endurance athlete to draw some practical conclusions that are likely to have an impact on performance and on longevity, both as an athlete and as a healthy human.

I am not an expert in nutrition, though I have had a long standing interest in regulation of energy metabolism.  My first scientific papers were focused on a quite different question about energy.  I trained as a physicist and my PhD was concerned with the transmission of electromagnetic energy though ionised gases. This was a topic of interest because in those days controlled nuclear fusion appeared the obvious answer to mankind’s need for energy supplies, and if fusion is to be controlled it will occur in high temperature ionised gas.   Among the lessons I learned from studying ionised gases is that however much we tried to regulate their behaviour to meet our goals, the inanimate gas particles appeared to gang-up to thwart our plans, as if guided by a wilful mind.   Complex systems react to stimulation in ways that sorely challenge our best attempts to predict the outcome.

By the late 1960’s I realised that controlling nuclear fusion was not likely to yield useful energy for mankind in the foreseeable future, so I abandoned the study of ionised gases for biomedical science.   I fairly soon found myself trying to understand the mechanism of the key regulatory enzyme in the glycolytic pathway, phophofructokinase, which regulates the rate of glucose metabolism to meet the energy needs of living cells. In those days we studied isolated enzymes in test tubes.  Although an isolated enzyme gives only a fragmentary glimpse of how metabolism might be regulated in a living animal, I once again encountered the amazing behaviour of a complex system.  But unlike the ionised gases that seemed to strive to achieve instability, I was now dealing with complex systems that sought stability.   As was first appreciated by the eminent though controversial nineteenth century French physiologist, Claude Bernard, living organisms react to changing circumstances in a way that best maintains a stable internal milieu.  The Greco-English word for this adaptive process is homeostasis.   However, as we shall see, sometimes the body’s attempt to adjust to excessive levels in the blood stream of particular molecules involved in energy metabolism, such as the fuel molecule, glucose, or hormones such as cortisol, can lead to adverse consequences.

In my own research career, I subsequently moved on from the study of energy metabolism to the even more complex mechanisms of the human mind and brain.  Here I encountered even more fascinating wilfulness – the ways in which complex systems adapt that are self-serving in the short term but in the long term can be damaging.  But that is a story for another time.  Meanwhile I have retained my curiosity about energy metabolism, and in particular, about homeostasis.

By virtue of homeostasis, the human body can adapt to a wide range of different circumstances, including a range of different diets. On account of the efficiency of homeostasis, the body can cope with demands of everyday life reasonably well on almost any diet provided it includes a few essential ingredients while avoiding overt toxins.  While the body adapts remarkably in the short term, the apparent success in coping with whatever diet we subject our bodies to conceals two problems of special importance to an endurance athlete.  First, the benefits of training are likely to be reduced if nutrition promotes persistent catabolism – the metabolic processes that convert fuel to energy while also breaking down body tissues, rather than promoting anabolism, the rebuilding required during the recovery period. However, if nutrition promotes the prolongation of the acute inflammatory process that facilitates rebuilding of body tissues during recovery, the resulting chronic inflammation has adverse effects on many tissues of the body with potentially serious long term consequences for health.

These two issues are strongly related.   There is an emerging body of evidence indicating that the optimum diet for promoting the benefits of training is similar to the optimum diet for long term good health, though perhaps surprisingly, the optimum nutrition to fuel a race is somewhat different from the optimum diet during training.   In order to understand the logic of these conclusions, it is necessary to understand some of the details of fuel metabolism that are relevant to the way the body adapts to training.  One key issue is the balance between catabolism and anabolism.


We demand a great deal of our bodies when we run, though at first sight the answer to meeting that demand is fairly simple. We need to generate large amounts of the energy transfer molecule, ATP, which is the immediate source of the energy required for muscle contraction.    The most straightforward way to sustain the supply of ATP is via the metabolism of glucose.  The apparently simple answer to the question of what we should eat to provide fuel for running is carbohydrates – these are either simple sugars (including  the mono-saccharides, glucose and fructose, and the di-saccharide, sucrose) or complex sugars that are readily converted to glucose in the body.

When I originally started running marathons more than forty years ago, I did not think too deeply about nutrition.   I used to eat potatoes because they are a good source of carbohydrate and lamb’s fry because I believed that it was rich in vitamins and minerals, especially iron, essential for the function of the red blood cells that carry oxygen to muscles. But I also consumed a wide variety of other foodstuffs, including a diverse range of foods containing proteins and fats.   It never occurred to me to consume anything other than water during either training or during a race.  I now believe that failing to consume anything other than water during long races was not the soundest plan.  I might have run faster marathons if I had consumed easily digested carbohydrates during the race.  Nonetheless, I think that in other respects my simple approach to nutrition contained some very sound features that go swept away with the enthusiasm for carbohydrates in the following decades.  ‘Carbo loading’ became an accepted pre-marathon ritual and many runners consumed sugary energy drinks during both training and racing.   Even the all-conquering Kenyans and Ethiopians appeared to rely on a diet with a high carbohydrate content.  So a diet heavy in carbohydrates appears to have a lot to recommend it: it is the simplest way to generate the ATP required for muscle contraction and the world’s best endurance runners appear to rely on it.

But before embracing that simple answer, we need first to recognise that the life-style of an African runner might be quite different from that of a typical European or American, starting with the fact that many African endurance athletes ran to school in childhood thereby producing metabolic adaptations; the daily stresses of life in Africa might differ from those in London or New York; and perhaps the carbohydrates are from a different source.    Simply relying on carbohydrates to provide glucose as the source of energy overlooks the intimate link between glucose metabolism and the hormones that regulate the catabolic processes  that are stimulated to activate the various body systems, including the cardiovascular system, to mobilise the body for action.

The key ‘mobilizing’ hormones are adrenaline, which initiates the ‘fight or fight’ response including an increasing heart rate and depth of respiration, and cortisol, the hormone which prepares the body to deal with for acute stress.  In particular, cortisol stimulates production of glucose and promotes the breakdown of fats and proteins.   Cortisol levels rise steadily during endurance exercise, and typically reaches several times base-line levels by the end of a marathon.  Furthermore, endurance athletes, including dedicated recreational runners, exhibit chronically elevated cortisol levels that persist beyond cessation of exercise.  In addition, ongoing stress for other aspects of life exacerbates the persistence of high cortisol levels

Inflammatory effects and anabolism

Among its many actions, cortisol exerts an anti-inflammatory effect.  Inflammation is the process by which the body initiates repair following trauma, including the traumatic effects of running on body tissues, and potentially re-builds the musculo-skeletal system so that is even stronger after recovery from training than before training.  However, the regulation of inflammation is tricky.  If it becomes chronic it produces serious damage to many tissues, most importantly, promoting the deposition of atheromatous deposits in the walls of blood vessels, eventually creating the risk of blockage.  In the coronary blood vessels that supply the heart, such a blockage can be fatal.   In the short term, elevation of cortisol defers the inflammatory process that is promotes repair and strengthening.  In the long term, its effects can be even more serious.  Sustained cortisol elevation leads to a compensatory decline in receptiveness of the glucocorticoid receptor molecules within cells that act as docking stations for cortisol and mediate its effects.  This decline is an illustration of homeostasis – but the consequences are harmful.  If response to cortisol is blunted, there is an increased risk of damaging chronic inflammation.

While inflammation plays a role in facilitating the short term benefits of training, minimizing the risk of chronic inflammation is crucial not only for long term benefits of training but for long term health.   The need to minimise chronic inflammation leads to two quite clear conclusions regarding nutrition.

  • The first is that carbohydrates that produce a rapid rise in blood glucose levels are potentially very damaging because a rapid rise in glucose stimulates release of insulin and an associated increase in the fatty acid, arachidonic acid, which is pro-inflammatory.
  • The second is that it is important to achieve a good balance between pro-inflammatory and anti-inflammatory fats in the diet.

Let us examine the rationale for each of these conclusions in a little greater detail.

The danger of high GI carbohydrate

The Glycaemic Index (GI) of carbohydrates is a quantity indicating how rapidly and consequently how high the peak blood glucose level after that type of carbohydrate is eaten.   Pure glucose is assigned a GI value of 100%.  A food which produces a peak blood glucose level that is 80% of the level achieve by the same weight of glucose has a GI value of 80%.   A rapid and large rise in glucose causes the pancreas to release a large amount of the hormone insulin. The major role of insulin is the facilitation of transport of glucose into cells, including muscle cells, when it can be utilised to produce energy.  However, excessive or prolonged high levels of insulin has several consequences, including deposition of glucose into fat cells, promotion of subsequent hunger and ultimately resistance of the tissues of the body to the effects to insulin, so that levels need rise even higher to achieve the transfer of glucose into cells.

What does this have to do with inflammation?     The stimulation by glucose of the release of insulin is associated with the production of the fatty acid, arachidonic acid, which belongs to the omega-6 class of fats.    Arachidonic acid plays a key role in inflammation via a complex cellular signalling pathway involving a group of molecules called eicosanoids.  The eicosanoids derived from arachidonic acid are strong pro-inflammatory.  The process of insulin resistance and consequent enhanced increase in release of insulin for the pancreas is associated with increased arachidonic acid production and therefore with inflammation.   Furthermore, insulin also increases another pro-inflammatory molecule, intelukin-6 (IL-6) which is one of the signalling molecules known as cytokines.  Thus, sustained high levels of insulin are associated with activation of several molecular signalling pathways that lead to inflammation.

Regular consumption of substantial amounts of high GI carbohydrates therefore produces the linked problems of insulin resistance, excess production of arachidonic acid and IL-6, and chronic inflammation

Balance between pro- and anti-inflammatory fats

Excess dietary omega 6 fats also lead to high levels of arachidonic acid and the subsequent production of pro-inflammatory eicosanoids.  However, the effects of arachidonic acid and inflammation are not all bad; indeed acute inflammation is probably crucial for recovery and strengthening after training.  The crucial issue is achieving the right balance.  At this stage we need to consider another class of fats, the omega-3 fats,  The omega-3 fats also act as building blocks for eicosanoids, but the eicosanoids derived from omega-3 fats are much less inflammatory than those derive from omega-6 so in effect omega-3 fats reduce the inflammatory effect of omega-6 fats.

The typical western diet contains a large predominance of omega-6 fats over omega-3 fats.  In contrast, the Mediterranean diet, which includes a high proportion of foods rich in omega-3 fats, such as fish and also olive oil, has approximately equally proportions of omega-3 and omega-6 fats, and is associated with lower risk of heart attack and increased life-expectancy.

The high carbohydrate v high fat controversy

The evidence in favour of minimising consumption of high GI carbohydrate and also an approximately equal balance of omega-3 and omega-6 fats is strong, and I believe provide clear guidance regarding healthy selection of types of carbohydrate and of fat.  However, the issue of the relative proportion of fats to carbohydrates in a healthy diet is far more controversial.  An informed evaluation of the evidence regarding this issue requires a more detailed discussion of the catabolic and anabolic metabolic pathways.  I will address this issue in a future post.

9 Responses to “Nutrition for endurance athletes: the crucial issue of inflammation”

  1. EternalFury Says:

    Very interesting information, as always.
    I will take your word of caution seriously.

    I don’t believe in magic nutritional interventions. It could be that, indeed, what produces good results in the short term, also compromises long-term health.
    I wish I had an easy way to measure my cortisol levels.

    I also wonder if it is possible to maintain a high level of HRV while undermining overall health by sustaining chronic inflammation. In other words, I wonder if measuring HRV on a regular basis (before every run) could help in determining when training has become detrimental due to inflammation.

    • canute1 Says:

      Thanks for your comment.

      In general, studies reveal that diminished HRV is associated with both increased evidence of inflammation and with increased risk of coronary heart disease. There is debate about whether impaired regulation of the HRV causes inflammation OR alternatively inflammation causes impaired regulation of HRV. In animals, simulation of the vagus nerve (which mediates parasympathetic activity ) protects against inflammation so there are good grounds for proposing that impaired regulation of HRV can play a causal role in inflammation, though I suspect that there is likely to be a reciprocal relations such that inflammation can also cause low HRV. Whichever direction the causal influence occurs, reduced HRV is associated with inflammation so it seems to me sensible to adjust training and other aspect of life, including diet, in the way that maintains fairly large HRV.

      I am a little puzzled about which aspect of HRV matters most. High frequency HRV is mainly caused by parasympathetic activity whereas low frequency HRV is attributed to both parasympathetic and sympathetic activity. However, some of the evidence suggests that low LF HRV is more strongly associated with inflammation than HF HRV. For example, one fairly large study of men in the mid-fifties (actually Vietnam vets studied in 2002) found that low levels of LF and VLF HRV were associated with increased markers of inflammation (interleukin-6 and C-reactive protein). Nonetheless, while the investigators acknowledge that both parasympathetic and sympathetic activity contribute to LF HRV they interpret their findings as indicating that impaired parasympathetic activity is associated with inflammation.

      My own view is that it is worthwhile ensuring that one maintains a fairly high level of HRV, across all three frequency ranges (VLF, LF and HF). The ‘prescription’ for this is: avoid over-training; recover well from races; sleep well, eat a ‘non-inflammatory’ diet, and avoid unnecessary life stresses. I think that the evidence regarding the links between stress, HRV, inflammation and heart disease, supports the hypothesis that endurance athletes can minimise the risks of coronary artery disease by following this prescription, Furthermore, monitoring HRV is potentially a useful guide to adjusting training load to achieve optimum training benefit with minimum risk of long term damage to coronary arteries.

  2. Robert Osfield Says:

    One area I’m curious about is the suppression of insulin during and immediately after exercise and the effect his has on blood glucose and the take up of glucose in the bloodstream to the liver and muscles.

    What hormones are at play here and how much could this effect be used to restock glycogen stores without risking elevating insulin and causing the associated ill effects?

    Where I’m leading is whether we’d be able to time our main carb intake for day to just hour or two after exercise and keep ourselves fat burning for more hours of the day but still have the glycogen stores for when we want to do do high intensity exercise.

    One thing I’m also curious about is the effect of insulin on sleep, as I’ve read that insulin can help one sleep so timing a meal high in carbs as the evening meal can be beneficial to sleep.

    The approach I’ve used in the last six months is to consume moderate amount of carbs for lunch after my pre lunch run and also have them at the evening meal. I do wonder if I should try moving to low carb lunches and then work outs late afternoon and then have a higher carb feast for the evening meal.

    While it’s winter with short daylight hours I’ll stick with pre-lunch runs though as it’s one of my few opportunities to get a dose of sunlight.

    • canute1 Says:

      Thanks for your comment.

      The first point to make is that the rapid uptake of glucose into muscles and synthesis of glycogen that occurs during the first hour after exercise appears to be largely independent of insulin. The early rapid phase of muscle glycogen synthesis is facilitated by the exercise-induced re-location of glucose transporter carrier protein-4 (GLUT4) to the cell surface, leading to an increased transport of glucose across the muscle membrane. In subsequent hours the rate of synthesis of glycogen is largely determined by the regulation of the enzyme, glycogen synthase. The activity of this enzyme is increased by muscle contraction itself; by insulin; and by a low concentration of glycogen.

      The second point is that high GI carbs can cause a substantial rise in insulin after exhaustive exercise. (See for example, Blom et al , Medicine and Science in Sports and Exercise 19(5):491-496). However, I do not think that a moderate rise in insulin after exercise is a cause for serious concern. I think the two main potentially harmful effects of high insulin secretion are increased insensitivity to insulin (insulin resistance, which is the cardinal problem in type 2 diabetes) and the increase in release of pro-inflammatory arachidonic acid that accompanies insulin release. However, exercise itself counteracts insulin resistance so insulin is less likely to produce insulin resistance after exercise. Furthermore, an increase in arachidonic acid might actually be helpful in the post exercise period as acute inflammation is necessary for tissue repair.

      Nonetheless, I tend to consume mainly low GI carbs and some protein after a run. I would anticipate that the blood glucose level produced by low GI carbs is probably enough to achieve adequate re-stocking of the glycogen supply, in light of the enhancement of GLUT4 (facilitating transport into cells) and the increased activity of glycogen synthase (due to recent muscle contraction) and the effect of low glycogen levels, though I do not know of direct evidence that confirms this. While I doubt that elevation of insulin would do much damage in the post exercise period, I nonetheless try to minim unnecessary spikes of insulin.

      With regard to sleep, because insulin promotes the transport of branched-chain amino acids but not tryptophan, into muscle, insulin promotes an increase in the ratio of tryptophan to the BCAA in the blood, and thereby results in preferential transport of tryptophan into the brain. Tryptophan is the precursor of the neurotransmitter serotonin, which tends to induce sleepiness. So insulin does promote sleep. However in view of my overall goal of avoiding unnecessary increase in insulin levels, I favour other strategies that shift the balance from the sympathetic (fight and flight) to parasympathetic (rest and recover) mode. The most straightforward of these strategies, though not always the easiest, is conscious muscular relaxation.

      On the whole, I tend towards three moderate meals during the day (though breakfast is usually the smallest meal) and I avoid high GI carbs to minimise insulin spikes. It might be argued that we evolved to enjoy sporadic feasts after successful hunting, but it seems to me that consuming the food gleaned by gathering (especially low GI carbs) in a more consistent pattern is also likely to have shaped our evolutionary development.

  3. Ewen Says:

    Canute, thanks for your detailed study of the subject. I’ve become a fan of the Mediterranean diet, more so than Paleo, after reading Phil Maffetone’s thorough examination of the subject in his ‘Big Book of Endurance Training and Racing’. Both for good health and support for endurance training. Processed carbohydrates are to be avoided and low Gi carbs form a smaller part of the diet than traditional for endurance athletes.

    • canute1 Says:


      Yes I largely agree with Phil Maffetone on the issue of nutrition. The evidence regarding the effect of nutrition on the ability to benefit from training and on running performance is very ambiguous, but overall, I believe it supports a Mediterranean style diet with moderate amount of carbohydrate (low GI) and moderate amount so fat for endurance athletes. I will review that evidence in my next post.

  4. Robert Osfield Says:

    Canute, do you know of any studies that look at glycogen exhaustion of the liver vs muscles and how this effects cortisol levels?

    I’d guess that if the liver is near glycogen depletion then it’ll not be able to support blood sugar levels and the body will respond by shutting down exercise intensity. What would happen to cortisol levels though as there isn’t any more glycogen to liberate from the liver? How much could gluconeogenesis support the short fall? What are the hormones at play that stimulate gluconeogenesis?

    • canute1 Says:

      I do not know of studies that have specifically examined the effects of depletion of liver glycogen while maintaining muscle glycogen, in healthy individuals. However, in states where liver glycogen is seriously depleted, the tendency for blood glucose to fall would be expected to stimulate cortisol release, since the need to maintain blood glucose to fuel the brain is paramount. This was illustrated in a study by Tabata and colleagues in which healthy young men exercised to exhaustion following a 15 hour fast. Both ACTH (which promotes cortisol release from adrenals) and cortisol itself, were increased.

      Cortisol promotes gluconeogenesis. During intense exercise, gluconeogensis is likely to make a significant contribution to maintaining blood glucose, but the priority is supplying the brain, not the muscles. Cortisol inhibits the transport of glucose into peripheral tissues, including muscle, by keeping the glucose transporter molecules away for the cell surface.

      The increased level of cortisol is likely to result in further reduction of liver glycogen, because cortisol facilitates the action of adrenaline in promoting breakdown of glycogen. Under other circumstances, cortisol can facilitate the action of insulin in synthesis of glycogen, but that is unlikely to apply in states of serious glycogen depletion since the body’s priority will be maintaining blood glucose.

      It should also be noted that in severe glycogen depletion, ketosis is likely to occur. Both fats and amino acids can be broken down to yield ketones which can be used by the brain and also as a fuel for muscle contraction.

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