Archive for the ‘Nutrition’ Category

Achieving longevity as a distance runner: twelve principles.

April 27, 2016

In the past seven posts I have addressed the challenge of maximising longevity as a distance runner.  For many of us, age appears to offer the prospect of inexorable decline.  In contrast, a few individuals achieve performances in their 70’s or 80’s that would be a source of great satisfaction for many runners 30 years younger.  Ed Whitlock recorded a time of 2:54:48 in the 2004 Toronto Waterfront Marathon at age 73 and as recently as a week ago, set an M85 half-marathon world record of 1:50:47 in the Waterloo half-marathon.  Even Ed is slowing as the years pass, but he has transformed our understanding of what an elderly distance runner can achieve.

In a previous blog post I attempted to tease out the secrets of Ed’s phenomenal longevity.  I concluded that his remarkably high maximum heart rate, determined largely by his genes, was one of the key elements that made him truly phenomenal, but his life-style and training allowed him to realise the potential offered by his genes. A central feature of his training has been frequent long, slow runs of up to 3 hours duration, often up to four or five times in a week.  This high volume of low intensity running is augmented by moderately frequent races, typically over distances of 5-10Km.

For most of us, merely attempting to emulate Ed’s training would be impractical, either on the grounds of lack of time, or because our bodies could not cope with the volume of training.   However, I believe that if we examine the anecdotal evidence provided by the training of Ed Whitlock and augment this with evidence that is emerging from current scientific studies of aging itself and of the way in which the aging body reacts to training, we can begin to formulate some general principles that will help maximise the chance of achieving the potential longevity offered by our genes.   It is also encouraging that the rapid accumulation of scientific knowledge offers the prospect of even better guidance in the future.

Meanwhile I have assembled a set of 12 principles that encapsulate much of the material presented in the past seven posts.  In this summary, I will not present the evidence justifying these principles. That evidence is presented in the preceding articles. Here are the 12 principles:

  1. Continue to run regularly. The evidence indicates that continuing to run, at least into the seventh and eight decades decreases risk of disability and death. However, by virtue the stressful effect of the impact at foot-strike, and also because running tends to exacerbate the age-related shift of hormonal balance away from anabolism (building up of tissues) towards catabolism (break down of tissues), the risks associated with running are greater in the elderly than in young adults.  Greater care is required to minimise these risks.


  1. Increase training volume gradually. Gradual increase minimises the stress of training and decreases the risk of excessive rise in the stress hormone cortisol, and allows gradual building of resilient less injury-prone tissues.


  1. Recover thoroughly after strenuous training and racing. The major reason is to ensure that acute inflammation resolves rather than becoming potentially destructive chronic inflammation.  However to prevent the development of constrictive adhesions due to the deposition of collagen fibres, it is important to maintain mobility during recovery. This might be achieved by easy exercise – walking, jogging, or elliptical cross training. Perhaps stretching has a role to play though there is little compelling evidence in favour of stretching. There is substantial evidence in favour of massage.


  1. Do a substantial amount of low intensity training. Low intensity training promotes both mitochondrial biogenesis and fat metabolism, while also building the resilience of muscles, tendons, ligaments and bones.  Low intensity training enhances the ability to handle lactic acid by developing the ability to transfer lactate from fast twitch fibres into slow twitch fibres where it is consumed as fuel.


  1. Do a modest amount of high intensity training. High intensity training helps to sustain power (the ability to deliver force rapidly) while also being an effective way to enhance the mechanism for pumping calcium back into muscles. High intensity training enhances the ability to clear lactate from muscle and transport it to other tissues such as liver where it can be utilised.


  1. Optimise cadence. A relatively high cadence at a given pace requires a shorter stride length, thereby reducing peak airborne height (and reducing impact forces) while also reducing braking forces.  Overall, potentially damaging forces are reduced. However high cadence does increase the energy cost of repositioning the swinging leg, so very high cadence is inefficient.  The most efficient cadence increases with increasing pace.  Most runners increase cadence with increasing pace.  Nonetheless for the elderly runner, it might be best to maintain a quite high cadence during training even at low paces because minimising impact forces is more important than maximising efficiency.


  1. Engage in low impact cross training. Although running itself is the most effective way of getting fit for running, running is a very stressful form of exercise on account of the impact forces.  Many of the desired benefits of training, especially cardiac fitness, can be acquired through other forms of exercise. Low impact cross training, (elliptical, cycling, walking) provides substantial benefit with minimum damage.


  1. Do regular resistance exercise. Resistance exercises help maintain strength and power, while promoting anabolism, thereby correcting the age-related tendency towards an excess of catabolism over anabolism. There are many different forms of resistance exercise.  I do regular barbell squats and dead-lifts with quite heavy loads (typically 100Kg) and also do hang-cleans to enhance power in the posterior chain muscles (glutes, hamstrings, gastrocnemius).  These exercises enhance the recruitment of type 2 fibres.


  1. Consume a well-balanced diet. The question of the healthiest diet remains controversial, but there is no doubt that elderly individuals require a higher intake of protein to maximise tissue repair; variety, including bright coloured vegetables, helps ensure adequate intake of micronutrients. At least a moderate amount of omega-3 fats is required to promote repair of cell membranes, but a balance between omega-3 and omega-6 is probably necessary to promote acute inflammation with minimal chronic inflammation.


  1. Get adequate sleep. Sleep is a crucial element of recovery. It promotes a naturally regulated release of growth hormone and encourages tissue repair.


  1. Avoid sustained stress. The body is a dynamic system that requires a degree of challenge, and hence of stress, to prevent atrophy. The body responds to stress of any kind – physical or mental – by increasing release of the stress hormones, adrenaline and cortisol. In the short term this shifts the hormonal balance towards catabolism mobilising the energy required to respond to the stress, but if sustained it damages tissues, not only via break-down of body tissues, but also by promoting more subtle damage to DNA, as discussed in my post on ‘whole body factors’.  To achieve well-being in life and optimum benefit from training, any stress, from whatever cause, should be accompanied by a commensurate amount of recovery.  Measurements such a heart rate, heart rate variability, and blood pressure can provide useful warnings of harmful imbalance.  However, our brains are very well attuned to assessing our level of stress, and sensitivity to one’s own sense of well-being also offers useful guidance.


  1. Develop confidence in control over one’s life.  Scientific evidence from large studies demonstrates that a sense of control over one’s life promotes longevity, while abundant anecdotal evidence illustrates that confidence is a key element in athletic performance.  Good health and optimal performance are facilitated by minimising self-defeating thoughts.  Each individual needs to develop their own strategies for achieving this.


I have been pleased to see from the stats provided by Word-press that many readers from many parts of the world read my blog. There are typically around 30,000 page views per year from over 100 different countries.  I started this blog nine years ago with the aim of encouraging discussion and debate about efficient running and training. Over the years there have been some vigorous debates, mainly about the more controversial issues of running technique.   The challenge of achieving longevity as a distance runner has not aroused the same passions. In part this is because the evidence is less controversial, but nonetheless, some of the evidence could be challenged, and there are many areas in which it could be expanded.  Please let me know if you disagree with these principles or alternatively consider there are other important things to be taken into account.


Cortisol and the stress response

June 2, 2014

Cortisol, a steroid hormone produced by the adrenal gland, plays a key role in mobilizing the body’s resources to cope with stressful challenges, including the challenge of running. Among its many roles is the regulation of blood glucose. When demands are high, cortisol acts to conserve glucose for the brain by minimizing uptake of glucose into other tissues and by promoting the production of glucose in the liver.   Because healing is not a priority when dealing with an acute challenge, cortisol suppresses inflammation and the immune system. In a healthy person, cortisol levels return to normal over a time scale of 30-60 minutes after the stress resolves. However if the transient surge of cortisol required to deal with acute stress is not switched off, cortisol inhibits healing by suppressing the formation of collagen while promoting breakdown of protein, thereby damaging many tissues of the body.

Recent evidence from a study by Skoluda and colleagues indicates that endurance athletes tend to have persistently high levels of cortisol. This increases in proportion to training volume. Thus the regulation of cortisol is potentially of great importance not only for ensuring that an athlete obtains benefits from training, but also for long term health.

The relationship between cortisol and inflammation is complex. In the short term cortisol suppresses inflammation, but sustained elevation of cortisol can lead to a suppression of the receptors that mediate the effects of cortisol on body tissues, and consequently, sustained elevation of cortisol can actually promote chronic inflammation which in turn damages tissues by laying down non-functional fibrous tissue as described in my recent post.

Although excessive cortisol is harmful, reduced ability to generate cortisol when required can be even more harmful. Addison’s disease, a rare condition in which the adrenal gland is damaged by autoimmune attack, is characterised by non-specific symptoms such as weakness and fatigue, and can be result in fatal inability to respond to stress. There is some evidence that sustained stress can reduce the capacity of the adrenal glands to produce cortisol when required, though the concept of adrenal fatigue, popularized by some alternative-medicine practitioners, remains an ill-defined entity.

Cortisol production is regulated by a feedback mechanism that takes account of information about the overall metabolic state of the body. This feedback system acts via the hypothalamo-pituitary-adrenal axis (HPA). The release of cortisol from the adrenal glands is stimulated by a hormone, ACTH, that is produced in the pituitary gland. The release of ACTH is in turn stimulated by a hormone, corticotrophin releasing factor, that is secreted by the hypothalamus. Information about the state of the body is funnelled via the amygdala and hippocampus in the temporal lobe of the brain, to the hypothalamus. This complex feedback system allows a diverse array of neural and hormonal signals to control cortisol release in a way that balances the catabolic effects of cortisol, promoting tissues breakdown, with the anabolic effects of other hormones, such as DHEA (a steroid hormone produced in the adrenal glands) and growth hormone, produced in the pituitary gland, that play a role in promoting the repair and strengthening of damaged tissues.  Thus many complex, interacting processes are involved in ensuring the optimal balance between mobilising body resources to deal with acute challenge and subsequent healing. Factors such as levels of ongoing stress from life circumstances and age contribute to the balance.

 Strategies for optimising the stress response

In summary, an athlete requires healthy adrenal glands which can generate enough cortisol to meet the challenge of stress but then to switch off cortisol production to promote recovery. The simple principle is that for optimum training benefit and long term health, we need to avoid excessive stress. However, the best way of achieving this is likely to determined by individual’s genes and life circumstances. While each individual has to find what works for him or her, there are several issues likely to be relevant to most athletes.

1)      Avoiding over-training. As demonstrated by Skoluda, the sustained excess of cortisol is greater in those who train more. Both volume and intensity matter though it is noteworthy that prolonged duration of exercise promotes increase in cortisol, whereas high intensity promotes hormones such as growth hormone and anabolic steroid hormones that promote strengthening of tissues. Consistent with this, some evidence indicates that the over-training syndrome is more strongly linked to high volume training than to high intensity training.

2)      Recovery from training and racing is crucial.   Not only does inadequate recovery increase the risk of persisting inflammation (as discussed in my previous post) but it impedes the transition from the cortisol induced catabolic state to the anabolic state required to rebuild and strengthen body tissues. This raises the major question of how best to determine if recovery is adequate. Subjective indices such as the Profile of Mood States, and autonomic measures such as resting heart rate and heart rate variability provide a guide, but no single test provides the full answer.  This is an issue I will return to again in the near future.

3)      Resistance training promotes the release of anabolic hormones and has many other beneficial effects on metabolism including increased sensitively to insulin. The major metabolic benefits of resistance training can be achieved by two 15 minute sessions per week.

4)      Life-stress and relaxation. Many of us have relatively limited control over the pressures of work and other responsibilities. However the way we react to these pressures is largely under our own control. Sleep plays a cardinal role. During sleep, cortisol levels fall while release of growth hormone is promoted. During our waking hours we can do a great deal to minimise stress. In recent years, the practice of Mindfulness has been proven to be effective in treating clinical disorders including anxiety and depression. It is a technique derived from Eastern meditative practices in which the aim is cultivation of a calm, non-judgmental awareness of one’s present physical and mental state.   Accumulating evidence indicates that this mental state is the optimum state for individuals such as US Navy Seals for whom remaining calm and focussed under intense pressure is crucial. Some studies show that Mindfulness lowers cortisol levels, while other studies have found evidence of beneficial reduction in stress and improved sleep but did not observe significant reduction of cortisol levels. Mindfulness is a knack that can be acquired by practice. Although the evidence for its effectiveness is still preliminary, my own experience is that it is effective in lowering mental and physical tension. I practice it at any time when I feel pressure is building, and also experiment with employing it while running to promote a constructive focussed mental state.

5)      Fuelling before and during training is a debateable topic. Some evidence indicates that training in a fasting state leads to improved endurance performance, perhaps mediated by the development of increased capacity to utilise fat as fuel, but overall the studies have yielded mixed results, as I have discussed in a previous post. I suspect this is because training in a fasted state also promotes increased cortisol levels that might be harmful. I have made appreciable gains in fitness in the past following training in a fasted state, but suffered one of the few serious muscle strains I have ever experienced after three weeks of high volume training predominantly in a fasted state.   This is mere anecdote, but when combined with the mixed evidence from scientific studies, leads me to conclude that training in a fasted state should be done cautiously, ensuring that overall stress levels are not excessive.

6)      Long term nutrition.  In light of the mechanism by which the hypothalamo-pituitary axis (HPA) adjusts cortisol levels in order to maintain metabolic homeostasis, it would be expected that a diet that promotes healthy energy metabolism would also be expected to promote healthy regulation of cortisol. As discussed in several of my recent posts, there is growing evidence that a Mediterranean diet promotes healthy metabolism. In accord with this, the available evidence indicates that a Mediterranean diet does promote healthy regulation of cortisol. For example a study of Spanish women found that those who chose a dietary pattern closer to the Mediterranean diet, with high mono-unsaturated fatty acid intake, showed more stable regulation of cortisol by the HPA.


The evidence obtaind by Skoluda indicating that endurance athletes suffer sustained elevation of cortisol suggests that taking steps to maintain healthy regulation of cortisol is likely to result not only in a better response to endurance training but also in better long term health. This might be achieved by avoidance of over-training, ensuing good recovery, incorporation of some resistance training into the schedule and a number of life-style adaptations including adequate sleep, stress reduction via strategies such as Mindfulness, and a healthy diet, such as the Mediterranean diet.

Minimising the risks: chronic inflammation

May 24, 2014

In my recent post I summarised the evidence indicating that running, at least in amounts up to 50 minutes of vigorous activity per day, is likely to increase your life expectancy, but nonetheless some endurance runners suffer serious ill-health attributable at least in part to their running. There is unequivocal evidence indicating transient heart muscle damage after endurance event such as a marathon; and unequivocal evidence that endurance athletes are at increased long-term risk of heart rhythm disturbance, such as atrial fibrillation. There is quite strong evidence that many years of marathon training increases the risk of fibrosis of the heart muscle and calcification of the coronary arteries. While the beneficial effects appears to outweigh the adverse effects for the majority, at least some endurance athletes suffer serious adverse effects. On the other hand, the evidence that the benefits appear to outweigh the adverse effects in the majority suggests that is sensible to try to identify what causes the serious adverse effects and take steps to minimise them, thereby increasing the likelihood of being among those who derive more benefit than harm.

Although the mechanisms of cardiac damage are not well established, there is a great deal of evidence regarding plausible mechanisms. We are not detached observers who can afford the luxury of waiting until the mechanisms are established beyond doubt, like climate change deniers who prefer to wait until the outcome is certain before acting. Rather, we are each an experiment of one, and we must make our decision for action or inaction based on the current evidence.

Inflammation and myocardial fibrosis

Perhaps the most plausible mechanism for adverse cardiac effects is a mechanism based on inflammation. Prolonged mechanical stress on heart muscle produces damage, which in turn elicits an increase in cytokines, the chemical messengers that circulate in the blood and trigger the events of inflammation which lead to laying down of fibrous tissue. This is the body’s mechanism for repairing damage and increasing the strength of tissues. But the initial deposition of fibrous tissue is slap-dash and unless redundant fibres are removed, the future function of the relevant body tissue is likely to be impaired. In the long term calcium is deposited at the site of damage, making the tissues stiff and inflexible.

In the case of tissues such as the plantar fascia, the misaligned fibres cause the pain of plantar fasciitis and the deposited calcium gives rise to the heel spurs visible on x-ray. In the case of the heart muscle, misplaced fibrous tissue has the potential to interfere with the electrical conduction pathways producing disturbance of rhythm. In the case of the lining of blood vessels such as the coronary arteries, the process is a bit more complex. The accumulation of cholesterol at the sites of damage to the lining of the artery plays a key role in triggering the inflammatory response. The Wellcome Trust have produced an excellent video depicting the sequence of events.

Minimising the risks

From what we understand of the mechanism, there are three key things we can do to minimise the risk of damage:

1)      Allow adequate recovery after heavy training and racing. Studies in animals and humans demonstrate that much of the fibrosis, though perhaps not all, resolves during an adequate recovery period.

2)      Build up training gradually. The tissue trauma that initiates the inflammatory process is less if the tissues have been strengthened by gradual adaptation. This is illustrated by the fact that DOMS is more marked if you suddenly increase training volume.

3)      Consume a diet that minimises chronic inflammation. Current evidence indicates that a Mediterranean diet, in which the pro-inflammatory omega 6 fats prevalent in the Western diet are balanced by omega 3 fats from fish and/or nuts and green leafy vegetables, is a heart-healthy diet.


It is noteworthy that these three strategies not only have the potential to reduce the risk of serious long term adverse effects on the heart, but are also likely to maximises the long term improvement in running performance.

In future posts I will discuss the more complex issue of cortisol and also the exacerbation of rhythm disturbances by excess potassium that is released from damaged muscle cells

The big debates of the past decade: 4) high carbohydrate v Paleo diet

April 26, 2014

Debates about diet for general health and specifically about the optimum nutrition for athletes have raged for many decades, but in the past decade this debate has largely been dominated by the polarization of opinions for or against the Paleo diet, the presumed diet rich in fat and protein consumed by our distant ancestors who hunted on the African savannah.   In recent years, Tim Noakes’ rejection of the high carbohydrate diet that he had advocated in his authoritative ‘Lore of Running’ added momentum to the shift away from carbohydrate towards fat, but on the whole professional dieticians have remained sceptical of fat. The debate is far from over, but I think that there has been substantial progress in assembling evidence regarding optimal nutrition for endurance athletes.   As with virtually all studies of something as complex as human physiology, no single study is definitive. Staunch advocates of either side of the argument can point to the limitations of any single study, but the overall body of evidence does provide a fairly consistent picture. Perhaps it even allows us to speculate on how difference between individuals might account for some for the contradictory findings from studies.

There have also been numerous debates about specific micronutrients, food supplements and ‘super-foods’, ranging from beetroot to chocolate, which I will scarcely touch on here to avoid the post being excessively long. My overall conclusion is that while taking a particular additive might have beneficial effects in some individuals in some circumstances, the unforeseen consequences of many additives often nullify the potential benefits, because the body is a homeostatic system that acts to compensate for any abrupt changes. This is perhaps best illustrated by the antioxidants which have the potential to avert the tissue damage due to free radicals that are a by-product of energy metabolism. Nonetheless, many studies of anti-oxidant supplementation do not show a net benefit. In general, I aim to achieve the required intake of micronutrients via a fairly diverse diet, including a diverse range of fatty acids, rather than by taking supplements.  Despite my general scepticism, I am moderately convinced by the evidence that green tea does have an overall beneficial effect on well-being. It contains moderate amounts of antioxidants along with many other compounds with potential health benefits, including catechins with beneficial effects on cardiovascular health. I myself drink modest amount so green tea as I enjoy it as a beverage.

Nutrition during training and while racing.

There are two aspects of the physiology of running that are established beyond debate and provide the starting point when planning nutrition during preparation for a race and during the race itself.   The first is that the metabolism of glucose (via glycolysis and subsequent oxidative metabolism via the Krebs cycle) produces energy at a faster rate than metabolism of either fat or protein. The second is that the supply of the glucose precursor, glycogen, is limited, whereas even lean runners carry a virtually inexhaustible supply of fat.

Up to the half marathon

The fact that metabolism of glucose generates energy more rapidly makes it essential to burn glucose for events run at speeds near or above lactate threshold pace. Provided we consume enough carbohydrate in the pre-race period  to ensure that glycogen stocks are full before the race, the stored glycogen will last for events lasting up to 90 minutes or even longer. Consistent with this, in a meta-analysis of 20 studies comparing the effects of high carbohydrate with high fat with diet on endurance exercise, Erlenbusch and colleagues found that overall, subjects consuming a high-carbohydrate diet exercised significantly longer until exhaustion, but there was substantial variation in finding between different studies. I myself do a modest amount of carbohydrate loading before a half marathon but consume nothing apart from water during the event itself.


In a marathon, the fact that the store of glycogen is limited comes into play.   To avoid running out of glucose we need to do two things: increase our capacity to utilise fat during the preparatory period and augment our glucose supply by ingestion of carbohydrate during the race.  Irrespective of specific nutritional strategies, training itself – both high volume, low intensity training and also high intensity interval training, enhance the production of the enzymes involved in fat metabolism and thereby increase the ability to utilise fat.

Two other strategies have been studied fairly intensively but with inconclusive overall outcome. First, training in a fasted state might be expected to enhance the ability to utilise fats. Indeed it does, and at least in some studies it enhances endurance performance. However, another factor comes into play. Training in a carbohydrate depleted state encourages the adrenal glands to release cortisol, which acts to ensure that blood glucose is reserved for use by the brain. In the short term cortisol promotes an effective response to stress but if the elevation of cortisol is sustained, it has a damaging effect on many tissues. A study by Skoluda, using measurement of cortisol in hair to assess sustained cortisol levels revealed that many endurance athletes have excessive sustained levels of cortisol. I believe that elevation of cortisol might be one reason why studies of training in a carbohydrate depleted state yield inconsistent findings. My personal conclusion is that as an elderly runner, for me the risks of tissue damage due to sustained cortisol levels are too high. However, for a younger athlete, training in a carbohydrate depleted state might be beneficial provided care is taken to minimize any unnecessary stresses. It is probably useful to monitor for signs of excessive cortisol – though direct measurement is impractical for the recreational athlete. Perhaps assessment of mood via the Profile of Mood States questionnaire provides the most practical proxy measurement.

The other widely studied strategy is consumption of a high fat diet to promote preferential use of fats until a few days before the race and then topping up the glycogen supply via carbohydrate loading.  A few studies have found this to be beneficial in endurance events. For example a study from Noakes’ lab using the nutritional periodization strategy found that high-fat consumption for 10 days prior to carbohydrate loading was associated with an increased utilization of fat, a decreased reliance on muscle glycogen, and improved time trial performance in a 20 Km time-trial following 150 minutes of medium intensity cycling. However, other studies, such as that by Carey and colleagues, have not shown improved endurance performance and overall the results are inconclusive. I suspect that this is because the body is a homeostatic system that adjusts to compensate for any abrupt change in circumstances. Therefore the body is likely to react to thwart any strategy that entails abrupt changes.

My own approach to marathon training is a balanced diet during the period of heavy training (for reasons discussed in the section on healthy nutrition below), moderate carbohydrate loading immediately preceding the event and the consumption of carbohydrate in small amount during the event – though I have yet more experimenting to do to identify the within-race fuelling schedule that suits me best



Developing a high capacity to utilise fats is a high priority in training for an ultra-marathon.  Nonetheless, as in the case of marathon training, I would be inclined to recommend a balanced diet during high volume training, and rely on the high volume of training, augmented by a small amount of high intensity interval training, to maximise the capacity to utilise fat. But it is pre-race and within race nutrition that raises the big issues. An ultra challenges virtually all systems within the body including the brain. The first issue is ensuring an adequate supply of glucose for the brain.  Thus in the pre-race period it is important to ensure that the liver is well stocked with glycogen. Furthermore, because pace is below threshold pace, metabolism of fat is fast enough to provide a large proportion of the energy required by muscles, but at least some glucose metabolism is required. Fat metabolism leads to energy production via the Krebs cycle, but unlike glucose metabolism, fat metabolism cannot restock the pool of Krebs cycle metabolites. This pool gets depleted due to the production of glutamine – an amino acid produced in muscle by an offshoot of the Krebs cycle. Glutamine is transported from the muscle to other organs, most importantly to the gut where it plays a key role in keeping the gut functioning well. So an ultra-runner relies on a modest amount of glucose metabolism within muscle.   What does this tell us about nutrition during an ultra? Clearly a supply of carbs is required but the stomach rejects simple sugars after a few hours. In part this might be a matter of the consistency of the food, but probably even more importantly, the body craves additional things – not only amino acids including glutamine but other things as well. The several possible mechanisms by which augmentation of carbohydrate ingestion with protein might enhance endurance performance has been reviewed by Saunders. In my limited experience of 24 hour events, I have relied on solid food with a fairly high carbohydrate content augmented by protein.


Nutrition for long term health

For the athlete, heart health is of special importance. Not only is heart disease the major cause of mortality in the general population but in addition there is some evidence that extensive endurance training and racing might in fact increase the risk of cardiovascular disease in athletes. Furthermore, most evidence suggests that a healthy diet for the heart minimises cancer. For many years, public health professionals have expressed concern about the unhealthiness of the typical Western diet. Concerns have focussed on the excessive total calories, saturated fats, high salt content, and more recently, high sugar content.

Foods with high sugar content produce a rapid rise in blood glucose that stimulates release of insulin thereby promoting increased resistance to the effects of insulin, while also producing an associated increase in arachidonic acid, an omega-6 fatty acid which is pro-inflammatory.  This exacerbates the problems arising for the fact that the typical Western diet is already unbalanced by an excess of omega-6 fatty acids.  However, the effects of arachidonic acid and inflammation are not all bad. Acute inflammation is probably crucial for recovery and strengthening after training. The crucial issue is achieving the right balance between omega-6 fats and omega-3 fats that are much less inflammatory and reduce the inflammatory effect of omega-6 fats.

The recent comprehensive review of nutritional recommendations for heart health, Eilat-Adar and colleagues reported that both low fat and low carbohydrate diets are a healthy alternative to the typical Western diet. They found that low carbohydrate diets, which typically derive 30%–40% of calories from carbohydrates and are low in saturated fat but higher in monounsaturated fat, are associated with a healthy balance of fats in the blood, with lower levels of potentially harmful tryglycerides and with higher levels of beneficial high density lipoprotein (HDL).   Eliat-Adar also found good evidence that Mediterranean diets, which include high consumption of fruit, vegetables and legumes, together with moderately large amounts of fish but less red meat may improve quality and life expectancy in healthy people, as well as in patients with diabetes, and heart disease. Mediterranean diets are preferable to a low-fat diet in reducing triglyceride levels, increasing HDL cholesterol, and improving insulin sensitivity.

A rigorous meta-analysis of trials by the Cochrane Collaboration also concluded that the evidence suggests favourable effects of the Mediterranean diet on cardiovascular risk factors, though with their usual caution, they stated that more trials are needed.

Because of many confounding effects in studies of self-selected diet, there is special value in large studies in which people are randomly allocated to different diets. One such study is the Spanish Prevención con Dieta Mediterránea (PREDIMED) trial, in which 7,216 men and women aged 55 to 80 years were randomized to 1 of 3 interventions: Mediterranean diets supplemented with nuts or olive oil or a control diet, and followed for a period of approximately 5 years. The Mediterranean diets were healther than the control diet. Nut supplementation was especially protective. Subjects on the Mediterranean diet consuming more than 3 servings/week of nuts had a 39% lower mortality risk than those on the control diet, due to protective effects against both cardiovascular and cancer mortality.

The debate about the merits of saturated versus mono-unsaturated fats has thrown up some surprising evidence contrary to the prominent advice to substitute polyunsaturated fats for saturated fats in worldwide dietary guidelines for reducing risk of coronary heart disease. Recent re-analysis of the large West Sydney Heart study found that replacing dietary saturated fat with omega- 6 linoleic acid, for subjects with known cardiovascular disease, actually led to higher all-cause death rate, and to higher death rate from cardiovascular disease. The most plausible explanation is that the increased death rate was due to the pro-inflammatory effects of omega-6 fatty acids.  Since the typical Western diet contains a high proportion of omega-6 fats, at least a modest intake of omega-3 fats, typically found in oily fish, is likely to be more healthy than increasing omega-6 fats.



There is overwhelming evidence that diet plays a large role in health and longevity, and after many years of confusing debate, there is emerging clarity that the healthiest diet is neither a high fat/low carbohydrate Paleo diet nor a low fat/high carbohydrate diet. Rather, the evidence suggests that a Mediterranean diet is preferable. Augmentation with extra nuts is probably worthwhile. It is also important to achieve a good balance between the pro-inflammatory omega-6 fats and the less inflammatory omega-3 fats, typically found in oily fish. Such a diet is likely to be optimal for athletes during periods of sustained heavy training. For longer endurance events, increased carbohydrate consumption in the immediate pre-race period will ensure that glycogen stores are replenished. During a marathon, regular intake of a small amount of carbohydrate will help maintain the supply of glucose to both brain and muscle, while in an ultra, more complex and palatable food including both carbohydrate and protein is better able to meet the more complex metabolic demands.

The five big debates of the past 10 years

February 6, 2014

The past decade has seen a continued growth of distance running as a mass participation sport.   The major city marathons continue to attract many thousands of entrants with aspirations ranging from sub 2:30 to simply completing the distance in whatever time it takes.  Perhaps more dramatically, parkrun has grown from a local weekly gathering of a few club runners in south-west London to an event that attracts many tens of thousands of individuals at hundreds of local parks, not only in the UK but world-wide, on Saturday mornings to run 5Km in times ranging from 15 min to 45 min before getting on with their usual weekend activities. Over this same period, the ubiquity of internet communication has allowed the exchange of ideas about running in a manner unimaginable in the days when distance running was a minority sport pursued by small numbers of wiry, tough-minded individuals whose main access to training lore was word- of-mouth communication.

Not surprisingly, within this hugely expanded and diverse but inter-connected community there have been lively debates about many aspects of running, with diverse gurus proposing answers to the challenges of avoiding injury and getting fit enough to achieve one’s goals.   Pendulums have swung wildly between extremes.  My impression is that the fire in most of the debates has lost much of its heat as the claims of gurus have been scrutinised in the light of evidence.   However, definitive answers have remained elusive.   What have we learned that us useful from this turbulent ten years?

There have been 5 major topics of debate:

1) Does running style matter and if so, is there a style that minimises risk of injury while maximising efficiency?

2) Are minimalist running shoes preferable to the heavily engineered shoes promoted by the major companies?

3) What is the optimal balance between high volume and high intensity training in producing fitness for distance running?

4) Is a paleo-diet preferable to a high carbohydrate diet?

5) Does a large amount of distance running actually damage health, and in particular, does it increase the risk of heart disease.

In all five topics, debate still simmers.  I have scrutinised the scientific evidence related to all five of these question in my blog over the past seven years, and I hope I will still be examining interesting fresh evidence for many years to come.   However whatever answers might emerge from future science, in our quest to determine the answers that will help us reach out running goals we are each an experiment of one and now is the point in time when we must act. I think that the evidence that has emerged in the past decade has allowed me to make better-informed choices in all five of these areas of debate than would have been possible ten years ago.   In my next few posts, I will summarise what I consider to be the clear conclusions for the past decade of debate, what issue remain uncertain, and what decisions I have made with regard to my own training and racing.

For me personally, the greatest challenge as I approach my eighth decade is minimising the rate of inexorable deterioration of muscle power, cardiac output and neuro-muscular coordination that age brings.  Therefore my approach to these debates is coloured by the added complications of aging.  Nonetheless, my goal is not only to continue to run for as many  years as possible, but also to perform at the highest level my aging body will allow during these years.  I hope that the conclusions I have reached will be of interest to any runner aiming in to achieve their best possible performance, whatever their age.

Paleo v High Carbohydrate diet: the evidence for differences in endurance performance; health and life-expectancy

December 15, 2013

Popular enthusiasm for the Paleo diet, including a relatively high proportion of fat and protein presumed characteristic of the diet of our hunter/gatherer ancestors, has re-ignited the long standing debate about the nutritional merits of fat and carbohydrates, especially for athletes.  In recent posts I have compared the effects of a high-fat diet with those of a high-carbohydrate diet on metabolic processes that have the potential to effect endurance performance, health and life expectancy.  We have examined the evidence of these different diets on the development of preferential use of fat rather than carbohydrates for fuel during exercise; on risk of sustained elevation of the stress hormone, cortisol; on insulin resistance and inflammation; and on weight control.   The evidence shows that a high fat diet does promote the use of fats as fuel during exercise, potentially beneficial in warding off disabling glycogen depletion during prolonged exercise.  However both types of diet are associated with risks of sustained elevation of cortisol, insulin resistance and chronic inflammation.  Particular components of each type of diet, specifically high glycaemic index (GI) carbohydrates which produce a rapid rise in insulin after ingestion, and omega-6 fatty acids, which are pro-inflammatory, are associated with high risk.  With regard to weight control, the evidence indicates that low fat and low carbohydrate diets are equally effective.   This post examines the evidence for effects on the ultimate outcomes: race performance, health and longevity.


When it comes to evidence regarding the effect of nutrition on performance, there are conflicting findings.   In a meta-analysis of 20 studies comparing the effects of high fat with high carbohydrate diet on endurance exercise performance, Erlenbusch and colleagues found that averaged across all studies, subjects consuming a high-carbohydrate diet exercised significantly longer until exhaustion, but there were substantial differences between the findings of different studies, probably reflecting differences in the subjects studied and the design of the study.  The benefit of the high carbohydrate diet was relatively large in studies of untrained subjects, but there was very little difference between the two types of diet in studies of trained athletes.  In light of the fact that endurance training itself increases capacity for utilization of fats as fuel, it is plausible that in hitherto untrained subjects, a relatively brief period of high fat consumption is inadequate to produce a substantial capacity for fat utilization, so maximizing efficiency of glucose utilisation might be of greater value in such subjects.

There are some noteworthy studies that have reported greater benefit for a high fat diet in trained athletes.  An early study from Tim Noakes lab in Capetown compared the effects of  2 weeks of high fat (70%) low carbohydrate (7%) diet with a high carbohydrate (74%), low fat (12%) diet in trained cyclists.  The high fat diet led to higher fat utilization and improved performance at moderate exercise intensity, without deterioration of performance at high intensity.   The importance of starting an endurance event with well stocked glycogen stores suggests that greater benefit might be obtained for a periodized nutritional strategy in which high fat diet is followed by a brief period of carbohydrate loading.   A subsequent study from the Capetown lab using the nutritional periodization strategy found that high-fat consumption for 10 days prior to carbohydrate loading was associated with an increased utilization of fat, a decreased reliance on muscle glycogen, and improved time trial performance in a 20 Km time-trial following 150 minutes of medium intensity cycling.

Other studies of trained athletes reported equivocal results.   Carey and colleagues tested the effect of fat adaptation using a nutritional periodization strategy, on performance during a one hour time trial following 4 hours of aerobic cycling.   As expected the fat adaptation resulted in increased fat utilization.  Power output was 11% higher during the time trial and distance covered was 4% greater, but this effect was not statistically significant.  Nonetheless, in 5 of the 7 cyclists, the improvement in performance after fat adaptation was substantial, raising the possibility that the number of subjects was too small to provide adequate statistical power to test for a performance benefit.

Yet other studies indicated no benefit and perhaps even harm from the fat adaptation strategy.  A further study from the Capetown lab by Haverman and colleagues compared 100km cycling time trial performance and also 1 Km sprint performance following 6 days of high fat consumption and 1 day of carbohydrate loading with performance following 6 days of high carbohydrate consumption and 1 day of carbohydrate loading.   The anticipated enhancement of fat utilization was observed, but there was no significant difference between diets in 100-km time-trial performance, while 1-km sprint power output was significantly worse after the high fat diet.  The investigators concluded that despite increasing fat utilization, the strategy of high fat diet followed by carbohydrate loading compromised high intensity sprint performance.  This raises the possibility that the increased fat utilization might reflect impaired ability to use carbohydrates rather than an enhanced ability to utilize fats.

Thus, the tide of evidence has turned against the hope that fat adaptation produced by a period of one or two weeks of high fat consumption might be a worthwhile strategy for improving endurance performance.  In contrast, this strategy might actually impair high intensity performance – an issue that is potentially of some importance even in events lasting several hours in which surges or hills might play a part in race outcome.   The evidence does not rule out the possibility that some individuals might enjoy an improvement in endurance performance, but at this stage, the evidence does not justify a general recommendation of this strategy.

Perhaps improvement in performance from rather drastic dietary adjustments over a period of a few weeks is not the issue of greatest importance to the endurance athlete, for whom training is an undertaking extending over many months or years.  Rather, the question of greater importance is the effect of long term nutrition on long term health.  Although no studies have examined the long term effects of long term nutrition in endurance athletes, recent evidence has provided increasing clarity regarding the optimum diet for long term health in the general population.

Long term health and life expectancy

We will focus on evidence related to heart health because heart disease is the greatest cause of mortality in the general population and in addition there is some evidence that extensive endurance training and racing might in fact increase the risk of cardiovascular disease in athletes.  Furthermore, most evidence suggests that a healthy diet for the heart minimises risk of cancer, though there are instances where foods that appear healthy for the heart have been linked to increased risk of cancer.  Although depression is associated with only a modest risk of premature death, it is the illness causing the greatest degree of disability world-wide (according to the World Health Organization).  Furthermore, mental state is of substantial importance in athletic performance.  Therefore, I will also briefly address the evidence regarding the association between diet and depression.

Cardiovascular disease

In a recent comprehensive review of nutritional recommendations for cardiovascular disease prevention Eilat-Adar and colleagues found that both low fat and low carbohydrate diets are a healthy alternative to the typical Western diet.  They note that low carbohydrate diets are associated with lower levels of potentially harmful tryglycerides and with higher levels of beneficial cholesterol in high density lipoprotein (HDL).   Low-carbohydrate diets, which include 30%–40% of calories from carbohydrates and are low in saturated fat but high in mono-unsaturated fat, were found to be safe in healthy and overweight individuals at follow-up for up to 4 years.   We will return to the controversial issue of saturated fat later.  Eliat-Adar also found good evidence that Mediterranean diets, which include high consumption of fruit, vegetables and legumes, together with moderatley large amounts of fish but less red meat, may improve quality and life expectancy in healthy people, as well as in patients with diabetes, and heart disease.  Mediterranean diets are preferable to a low-fat diet in reducing triglyceride levels, increasing HDL cholesterol, and improving insulin sensitivity.

A meta-analysis of trials by the Cochrane Collaboration – an organization which does extremely rigorous and conservative reviews of medical treatments – also concluded that evidence suggests favourable effects of the Mediterranean diet on cardiovascular risk factors, though with their usual caution, they stated that more trials are needed.

One trial that warrants special mention is the Spanish Prevención con Dieta Mediterránea (PREDIMED) trial, in which 7,216 men and women aged 55 to 80 years were randomized to 1 of 3 interventions: Mediterranean diets supplemented with nuts or olive oil and control diet. During a follow-up period of near to five years, nut consumption was associated with a significantly reduced risk of all-cause mortality.  Subjects consuming more than 3 servings/week of nuts had a 39% lower mortality risk.  A similar protective effect against cardiovascular and cancer mortality was observed.

With regard to the issue of saturated versus unsaturated fats, a recent re-analysis of the large and well conducted West Sydney Heart study found that replacing dietary saturated fat with omega- 6 linoleic acid, for subjects with known cardiovascular disease, actually led higher all-cause death rate, and higher death rate from coronary heart disease and cardiovascular disease.  The authors also performed a new meta-analysis of previous studies and found that the pooled data also provided a strong trend towards higher death rate when saturated fat was replaced by omega-6 linoleic acid.  This finding is contrary to the prominent advice to substitute polyunsaturated fats for saturated fats in worldwide dietary guidelines for reducing risk of coronary heart disease.   The most plausible explanation is that the increased death rate is due to the pro-inflammatory effects of omega-6 fatty acids.


The frequent reports in both popular press and the medical literature linking various foodstuffs to cancers of various types makes this topic a mine-field.  In part this situation reflects the heterogeneity of cancer and the multiplicity of different factors that might contribute to the cause in different cases.  Nonetheless, in general, the evidence indicates that diets that are healthy with regard to weight control and cardiovascular outcome tend to be associated with lower risk of cancer.  For example, a recent large review found that adherence to the Mediterranean diet was associated with lower risk of certain cancers, especially cancers of the digestive tract, consistent with the finding from the PREDIMED study mentioned above.  However, in light of the fact that a key difference between typical Western diets and the Mediterranean diet is the  larger relative amount of omega-3 fats in the Mediterranean diet, it is noteworthy that some studies have reported that omega-3 fats are associated with increased rate of prostate cancer, while others have reported a decreased rate.  This should encourage caution against simplistic conclusions that a food item is invariably healthy in all amounts and all circumstances.


Many studies using relatively low quality methodology to assess diet and/or mental state have reported an association between adherence to a ‘healthy’ diet and decreased risk of depression.  More recently, several studies have addressed this issue using more rigorous methodology.  A meta-analysis by Psaltopolou and colleagues of studies examining the association between Mediterranean diet and risk of various neurological and mental disorders found that the Mediterranean diet was associated with a decrease in risk of depression of approximately 30%.  This reduction was very similar in magnitude to the reduction of risk of stroke and for cognitive impairment.  However, association cannot establish cause, and it is possible that other life-style factors associated with adherence to a healthy diet account for the better physical and mental health.   The most conclusive evidence comes for randomized controlled trials in which individuals are randomly allocated to different diets.  In the PREDIMED trial, the group who were allocated to the Mediterranean diet augmented with extra nuts experienced a 20% lower rate of depression over a period of 3 years, compared with those on a low fat diet.  This was not a statistically significant reduction.  However, in those who had type 2 diabetes, the Mediterranean diet with extra nuts produced a 40% reduction in occurrence of depression which was significant.  Thus the balance of evidence does suggest that a Mediterranean diet augmented by nuts produces a reduction which is significant at least in those who already show other evidence of adverse metabolic effects.


There is overwhelming evidence that diet plays a large role in health and longevity, and after many years of confusing debate, there is emerging clarity about the type of diet that is healthiest.  This is neither a high fat/low carbohydrate Paleo diet nor a low fat/high carbohydrate diet.  Rather, a substantial body of evidence suggests a Mediterranean diet is preferable, especially when augmented with extra nuts.

There is some variability between studies in what is taken to be the Mediterranean diet, but the consistent features include high consumption of fruits, vegetables and legumes (beans, nuts, peas, lentils); low consumption of red meat and meat products but substantial consumption of fish; near equal proportions of omega-3 and omega-6 fats;  moderate consumption of milk and dairy products; and low  to moderate red wine consumption.   The status of grains and cereals is ambiguous. The Mediterranean diet adopted in PREDIMED included a high consumption of grain and cereals. In general, whole grains and cereals appear healthy though gluten sensitivity is an issue for at least some individuals.

While the evidence for the Mediterranean diet is largely based on studies of the general population with emphasis on heart health, rather than being focused on athletes, the disconcerting evidence that male athletes who have run numerous marathons over a period of many years are at risk of atherosclerosis (as discussed in detail in my post of 30th May, 2012) suggests that a ‘heart-healthy’ diet should be a high priority for endurance athletes.

When it comes to endurance performance, there is no clear evidence in favour of any particular diet.  However the consistent evidence that a high fat/low carbohydrate diet promotes preferential utilization of fats during exercise appeared promising at first.  It is disappointing that this apparently beneficial adaptation is not reflected in enhanced performance, even in ultra-endurance events.  On contrast, there is actually evidence that it can harm high intensity performance, such as 1 Km cycling time trial performance.   However, the fact that at least some individuals do appear to show an endurance performance benefit from a high fat diet (followed by brief duration carbohydrate loading) as observed in the  study by Carey and colleagues, makes me reluctant to dismiss the potential value of at least moderately high fat consumption.  One crucial issue is to identify why the clear evidence of improved fat utilization does not generally lead to enhanced performance.  It appears that the fat adaptation strategy, at least in the form of a rapid increase in proportion of fat to a quite high level over a periods of a few weeks, is in some way harming the utilization of carbohydrates as much as it might be improving the utilization of fats.

In my opinion, one candidate mechanism by which high fat consumption might harm carbohydrate metabolism in muscle is the elevation of cortisol associated with the fat adaptation strategy used in the studies.  One immediate effect of high cortisol is the decrease in accessibility of the glut4 transporter molecules that transport glucose into muscle.   Furthermore, sustained elevation of cortisol can produce a decrease in sensitivity of glucocorticoid receptors that mediate the various effects of cortisol, including its anti-inflammatory effects, thereby possibly leading somewhat paradoxically to chronic inflammation.  This is speculation on the basis of what is known about mechanisms rather than direct evidence of beneficial or harmful effects in practice.  Nonetheless, it appears to me plausible that a gradual introduction of a higher proportion of fats, at least up to the modest levels in the Mediterranean diet, over a more sustained period might produce promote preferential utilization of fat during exercise in a manner that translates into improved endurance performance.

In light of the evidence that glycogen depletion during training can enhance training effects, I consider that during normal training, consumption of carbohydrates is potentially counter-productive, in most instances.  Exceptions might include high intensity sessions; very prolonged sessions; or for the purpose of testing the planned strategy for race day in the final few long runs of marathon/ultra-marathon preparation.  However, the need to start an endurance event with glycogen stores well stocked suggests that at least a brief period of carbohydrate loading, and ingestion of carbohydrates during long events, is highly desirable.

In summary, I consider that the emerging evidence provides strong support for the proposal that the optimum nutrition for most endurance athletes is a Mediterranean diet, but with carbohydrate loading immediately prior to long races.

Paleo v High Carbohydrate diet: the evidence for metabolic differences affecting health and endurance performance.

December 13, 2013

The recent surge of interest in the Paleo diet, based on the speculation that evolution has equipped humankind to thrive on a diet relatively rich in fat and low in carbohydrate, has added new spice to the long-standing debate over the optimum proportion of fat and carbohydrate in our diets.  This debate is of substantial importance for anyone seeking to live a long and healthy life, and is of particular importance for endurance athletes who subject their bodies to the rigours of extensive training and require those long-suffering bodies to function with peak efficiency on race day.  There are five related mechanisms by which diet is likely to affect health, longevity, response to training and race performance.  These five mechanisms are: the capacity to utilise fat in preference to carbohydrate; minimization of sustained elevation of cortisol; avoidance of chronic inflammation; prevention of insulin resistance; and control of body weight.  In the post, I plan to examine the evidence regarding the influence of the proportions of fat and carbohydrate in the diet on these five related mechanisms.  In my final post in this series, I will examine the evidence for effects on the ultimate outcomes: race performance, health and longevity.

The metabolic challenges facing the endurance athlete

I will start with a brief review of an issue covered in my most recent post: the metabolic challenges that the runner faces if glycogen becomes depleted in the final stages of a marathon.   The body’s paramount goal in these circumstances is ensuring adequate glucose to fuel the activity of the brain.  Secretion of the stress hormone, cortisol, increases dramatically, with three immediate consequences: cortisol promotes gluconeogenesis in the liver thereby replenishing glucose; it inhibits the function of the glut4 transporters that transport glucose across the cell membrane into muscle cells and other peripheral tissues; and it promotes beta-oxidation of fatty acids which become the main energy source for muscle.  This response averts disaster for the brain, but it is not ideal.

Not only does excessive elevation of cortisol have potential adverse long term effects, but there are immediate undesirable consequences.  Reliance of fat as the main fuel for muscle have a dampening effect on power output because fat metabolism requires oxygen making it difficult to  exceed the limit achievable aerobically, but in addition, as we saw from an examination of the central role that the Krebs cycle plays in both catabolic and anabolic processes, there are multiple other metabolic consequences.  Reduced production of pyruvate from glucose in muscle makes it necessary to utilize glutamine to keep the level of the intermediate metabolites of the Krebs cycle topped up.  Muscle is the main source of glutamine for other organs and body systems. Depletion of glutamine in muscle leads to a fall in blood levels of glutamine which has adverse effects in the gut, liver, kidney and immune system.  In the gut, glutamine serves a diverse range of essential metabolic functions.  In the liver, glutamine is a major source of the oxaloacetate required for gluconeogenesis, when low levels of glycogen limit the generation of oxaloacetate via pyruvate derived from glucose.   In the kidney, glutamine is the source of ammonia needed for the excretion of acids.  Glutamine also plays crucial catabolic and anabolic roles in the cells of the immune system, and a fall in glutamine will exacerbate the direct adverse effect of cortisol on the immune function.  Although the body appears prepared to tolerate some loss of immune function during vigorous exercise, overall, it is undesirable to allow glutamine level to fall too far.  Therefore, not only is it crucial to start an endurance event with well-stocked glycogen stores, but one of the key goals of endurance training is developing the capacity to utilise fats in preference to glucose at aerobic paces thereby avoiding a state of serious glycogen depletion in long races.

Effect of nutrition on capacity to metabolise fats during exercise.

Many studies, reviewed by Burke and Hawley, demonstrate that a high fat diet promotes the utilization of fats during exercise.   However, on race day, the endurance athlete requires not only a well developed ability to utilise fats, thereby minimising the depletion of glycogen stores, but also  needs to start the race with glycogen stores fully topped up. Fortunately, the evidence reviewed by Burke an Hawley indicates that switching from a high fat diet to a high carbohydrate diet in the period immediately before the race does not undermine the ability to utilise fats.   As an illustration, Staudacher and colleagues demonstrated that a short term high fat diet (6 days; 69% fat) followed by a high carbohydrate diet in the day preceding exercise produced a 34% enhancement of ability to utilise fats during submaximal cycling in a group of highly trained endurance athletes, whereas 6 days of high carbohydrate intake (70% carbohydrate) followed by a further high carbohydrate day, resulted in a 30% reduction in fat utilization.  This has encouraged the hope that a  “fat adaptation” strategy in which a high-fat, low-carbohydrate diet is consumed for up to 2 weeks during normal training, followed by high-carbohydrate diet during a brief taper in the few days before a key race, might improve performance.

However despite the consistent evidence that such nutritional periodization can achieve the desired enhancement of fat utilization, there is less clear evidence of enhancement of race performance.  This might simply be that may other factors influence performance, so large, well-controlled studies are required to allow any benefit for this nutritional strategy to emerge clearly from the inconsistencies due to other sources of variance.  Alternatively, it might be that this nutritional strategy has hidden adverse effects.  For example, it is plausible that the nutritional strategy might upset hormonal balance is an adverse manner.  I will return to the issue of effects on performance in my next post, but first we need to consider the possible effects of nutrition on hormones such as cortisol and insulin.

Effect of nutrition on sustained cortisol levels

The balance of evidence indicates that a very low intake of carbohydrate and high fat consumption, for either a few days or for longer periods, leads to sustained elevation of cortisol.  For example, Langfort and colleagues compared the effects of 3 days of a high fat and protein diet (50% fat, 45% protein and 5% carbohydrates) with three days of a mixed diet.  They observed no difference in maximal aerobic capacity, but did observe a significant increase in both adrenaline and cortisol before and after exercise.  Furthermore, several studies have shown sustained elevation of cortisol after longer periods of high fat diet.  For example, in a comparison of three different diets, each administered for 4 weeks to overweight young adults, Ebbeling and colleagues found that twenty-four hour urinary cortisol excretion was highest with the low-carbohydrate, high fat diet (10% from carbohydrate, 60% from fat, and 30% from protein.)  Similar effects are seen with more moderate amounts of fat.  For example, in a study of runners, Venkatraman and colleagues observed greater pre-test cortisol after 4 weeks at 40% fat compared with 15% fat, but in other respects, the outcome tended to be more favourable, including greater time to exhaustion in the 40% fat group.

The type of fat might matter: in a study of Spanish women, García-Prieto and colleagues found that high saturated fat intake was associated with an unfavourable loss of the normal daily variability in cortisol levels while women who dietary pattern was closer to the Mediterranean diet, with high consumption of monounsaturated fatty acids, showed healthy regulation of cortisol levels.  However, it perhaps important to emphasize at this point that when it comes to other long term health outcomes (which we will examine in the next post) there is relatively little evidence that saturated fats are especially harmful. There is little basis for the long-standing demonization of saturated fats in comparison with unsaturated fats.  The recent pressure by the UK government on the food industry to reduce saturated fat content of foods is scarcely justified.

Nonetheless, the association between a high proportion of dietary fat and sustained elevation of cortisol is a potential concern.  Epidemiological studies demonstrate that sustained high cortisol levels may promote adiposity, insulin resistance, and cardiovascular disease. For example, in a 6-year prospective, population-based study of older adults, individuals in the highest third of 24-hour cortisol excretion had a 5-fold increased risk of cardiovascular mortality, compared with the lowest third.

Insulin resistance

One of the important mechanisms in adverse long term cardiovascular outcome is insulin resistance, the cardinal feature of type 2 diabetes.  The claims regarding the relative harmfulness of fats and carbohydrates in regard to insulin resistance remain a source of controversy.  Consistent with the evidence that high blood and tissue levels of fatty acids are associated with insulin resistance a substantial body of historical evidence indicates that high fat diet impairs glucose tolerance.  On the other hand, ingestion of carbohydrate leads to increased levels of blood glucose which triggers insulin release, which in turn can result in insulin resistance.  It is likely that the answer is not to be found simply in the proportion of energy derived from carbohydrate or fat, but rather in the type of carbohydrate or fat.  In the case of carbohydrates, it is likely that high glycaemic index (GI) foods promote insulin resistance.  Brand-Miller and colleagues demonstrated that in lean young adults, a meal with a high glycemic load (the mathematical product of the amount of carbohydrate by the glycemic index of the carbohydrate-containing foods) result in higher insulin concentration, than a meal with similar total calories but low glycemic load.  At least in individuals at genetic risk, high insulin secretion promotes insulin resistance.  Consistent with this evidence suggesting that a diet based on low glycaemic load might reduce insulin resistance in those at risk, Barnard and colleagues demonstrated that a low fat vegan diet with a high proportion of low GI carbohydrates improved the control of blood glucose in individuals with type 2 diabetes more effectively than a low carbohydrate diet.

A large body of evidence, reviewed by Grimble and colleagues, reveals an association between insulin resistance and chronic inflammation.  Grimble concludes that the evidence regarding the direction of the causal relationship favours chronic inflammation as a trigger for chronic insulin insensitivity.



Endurance athletes are at particular risk of chronic inflammation, in part on account of the repeated trauma to muscle and other connective tissues associated with training, making the effect of nutrition on inflammation a crucial issue.   The issue is complex.  On the one hand, as discussed in my recent post on inflammation, a high carbohydrate load can promote inflammation due to the release of the pro-inflammatory fatty acid arachidonic acid in association with insulin secretion from the pancreas.  Furthermore, some carbohydrates, especially cereals containing gluten, can impair the lining of the gut, leading to chronic inflammation.  However, a high fat diet also carries risk.  Omega-6 fatty acids are pro-inflammatory, making it important to have a good balance of omega-3 and omega-6 fats in the diet, yet the typical Western diet is much richer in omega-6 fats.

Thus, both a high carbohydrate diet and a high fat carry risk of inflammation, with evidence suggesting that identifiable components of these diets account for much of the risk.  High  GI carbohydrates and a -6 to omega-3 fats appear to generate the greatest risk.    The traditional Mediterranean diet, containing a moderately high level of fat with near equal proportions of omega-3 ad omega-6 fats; and vegetables with a relatively low glycaemic index, appears to offer a near optimum combination.  In a comprehensive review association of dietary patterns with inflammation and the metabolic syndrome (whose key feature is insulin resistance), Ahluwalia and colleagues concluded that healthy diets such as the Mediterranean diet can reduce inflammation and the metabolic syndrome.

Body weight

While control of body weight is one of the major preoccupations of dieting non-athletes, it is not usually the main preoccupation among endurance athletes simply because endurance training itself promotes weight loss.  Nonetheless, even a modest excess of weight has serious implications for endurance race performance, because the energy required to accelerate the body to compensate for the inevitable braking during every stride, and to elevate the centre of mass in order to become airborne, is proportional to body mass.  Therefore, the weight of any body tissue that is not performing a useful purpose is a handicap.  However, the issue of what tissues perform a useful purpose for the endurance athlete is not entirely straightforward.  Muscle that does not contribute to propulsion might be a handicap, while at least some fat is required to sustain balanced hormonal function.  The ideal weight for endurance athletes is likely to vary between individuals, but observation of elite athletes suggests it is likely to correspond to a body mass index range between 20 and 23.  Alternatively, since excess fat is likely to be a greater handicap than excess muscle, a body fat percentage in the range 5-11 percent for males and a somewhat higher proportion for females, might be a more relevant guide.

While an excess of the ratio of total calories consumed to total calories expended is an important factor in determining the likelihood of weight gain, there has been much debate about the relative merits of low fat or low carbohydrate diets.  A recent meta-analysis of 23 trials including almost three thousand participants concluded that both types of diet improved weight and metabolic risk factors, with no significant differences between the two in the reductions in body weight or waist circumference.  Nonetheless there were slight but significant differences in some of the metabolic risk factors, with low carbohydrate diets producing a potently healthier increase in high density lipoprotein cholesterol and reduction in triglycerides, but a lesser reduction in potentially harmful low density lipoprotein cholesterol.  The authors concluded that low-carbohydrate diets are at least as effective as low-fat diets at reducing weight and improving metabolic risk factors.


Nutrition does indeed have an appreciable impact on the five metabolic mechanisms that are likely to influence both endurance performance and long term health.  There is unequivocal evidence that a high fat diet produces an increase in the utilization of fats in preference to carbohydrate, which is potentially beneficial for endurance performance.  However, there is also evidence that consumption of a high fat diet over a period ranging from a few days to 4 weeks, results in a sustained increase on cortisol, which is potentially harmful in the medium and long term.

Nutrition also plays an important role in insulin resistance and inflammation.  For these two issues, the type of fat or carbohydrate appears to be especially important.  High GI carbohydrates and high total glycaemic load promote inflammation and insulin resistance.  However high levels of fat in blood and in body tissues are associated with insulin resistance, while omega-6 fats are pro-inflammatory.  With regard to weight control, either low fat or low carbohydrate diets can be effective.

Overall, these observations do not provide any simple answer to the question of the optimum proportion of fat to carbohydrate, but do suggest that both fats and carbohydrates can carry risks.  It is noteworthy that much of the evidence demonstrating adverse effects is based on studies in which there was an abrupt change to a high proportion of either fat or carbohydrate. In the next post, we will examine the evidence regarding the influence of proportion of fats and carbohydrates on endurance performance and on long term health, before finally drawing practical conclusions based on a synthesis of the evidence.