Archive for October, 2013

Training in a fasted state

October 19, 2013

Nutrition for the runner is almost as important as training, but it is a topic that many athletes shy away from because it is bedevilled by crankiness.   In recent years, nutritional science has yielded a huge amount of potentially useful evidence about what nutrition is likely to work best in particular circumstances.  But the clamour of enthusiasts who seize upon a particular nutritional notion and assert that it is best for everyone makes it difficult to identify might be useful to a particular individual in particular circumstances.  Endurance athletes, sprinters and sumo wrestlers all practice the art of applying optimum muscular force at the right time, for the right duration, and in the right place.  There are similarities in the training that all must do, but also differences. Likewise, there are similarities in their nutritional requirements but also differences.   Just as with differences in training requirements, the differences in nutritional requirements depend not only on the type of sport but also on the individual’s genes, life history and the particular goal at the present time.  It is a complex topic.

In recent times there has been a great interest in the Paleo diet, a diet supposed to reflect the diet of our primitive ancestors. It is heavily biased towards the protein and fat available in meat, and biased away from carbohydrates, especially from cereals that have only been a staple since humans developed agriculture.   The Paleo diet has been given a little added spice by Tim Noakes’ endorsement of a similar diet, in a rather dramatic reversal of his prior recommendation of carbohydrates in ‘Lore of Running’, the book that has perhaps done more than any other to shape the opinions of runners since its first publication in 1991. It is of interest to note in his statement published in Runner’s World in 2012, Noakes was careful to state that on current evidence he only recommends the diet for individuals suffering what he described as carbohydrate resistance, a metabolic condition predisposing them to diabetes. Furthermore he emphasises that the proposed diet requires a long-term commitment for a life-time

In this post I will not focus on the issue of long term diet. That is an important topic for runners and much good data is now available, which I will return to in future posts.  Meanwhile I want to focus on the question of training in the fasted state, a question that both Robert Osfield and Eternal Fury have raised in their comments on my recent blog posted two weeks ago.   Both Robert and EF are advocates of training in the fasted state, and both are currently running very well.  Their accounts are of course only anecdotal evidence. Nonetheless, there is quite substantial body of relevant scientific research that is worth examining.

The question of training in a fasted state does overlap with the issue of long term diet and in particular, with the issue of the proportion of carbohydrates to fats.  It also raises the issue of differences between different types of carbohydrate: high glycaemic index (GI) carbohydrates which produce a rapid spike in blood glucose levels, and low GI carbohydrates which are absorbed more gradually; and also between different types of fats: especially the difference between omega-6 fatty acids which predominate in the typical Western diet, and omega-3 fatty acids, more abundant in both the putatively healthier Mediterranean and Japanese diets.     So the topic is already complex and the interpretation of the evidence must take account of this complexity

The metabolic requirements of endurance athletes

Our bodies store two main types of fuel: glycogen, which is stored in liver and muscle, and is the precursor of glucose; and fats which are stored in adipose tissue.  Glycogen stores are relatively limited and are typically exhausted by about 2 hours of running. Fat stores, even in the most slender of runners are virtually inexhaustible except in extreme starvation.   Muscle can utilise either fat or glucose when fuel is burned aerobically, but only glucose can be used to provide energy within consuming oxygen.  Hence muscles mainly utilise glucose at high intensities, when the demand for energy exceeds the available supply of oxygen.    For ultra marathon runners, running at aerobic intensities for many hours, fat is the preferable muscle fuel, not only because it is abundant but also because the brain requires glucose, making it crucial to conserve glycogen.   The mitochondrial enzymes that catalyse the combustion of fat are the same enzymes as catalyse the combustion of glucose.  It is therefore important to maximise the development of these enzymes for the effective use of either type of fuel.  However the special requirement for the ultra-marathoner is the ability to promote the mobilization of fats and the transport of fat into muscle cells, thereby promoting preferential utilization of fat.

For shorter endurance event (such as 5K or 10K) the efficient use of oxygen is paramount.  At the pace of these events, adrenalin levels promote mobilization of glucose from the glycogen stores, and glucose contributes a greater proportion to the fuel mix.   It is noteworthy that a little less oxygen is required to produce a given amount of energy from glucose than from fat, and hence the greater mobilization of glucose promotes more efficient utilization of oxygen.   Although the majority of the energy required at 5K or 10K pace is provided by aerobic metabolism, a small amount of anaerobic metabolism occurs, and the accumulation of the lactic acid produced by anaerobic metabolism is a limiting factor, so the 5K or 10 K runner also requires a well developed ability to metabolise lactate to minimise its accumulation.

In summary, both the ultra runner and the 5K/10K runner require well developed mitochondrial enzymes to enable muscle to burn either glucose or fat efficiently, ultra-marathoners also need to enhance the ability to mobilise fats and transport them into muscle cells, while 5K/10K runners requires well developed ability to metabolise lactate.    The marathon presents a unique combination of challenges. Typical race pace is not far below the level where anaerobic metabolism is appreciable, yet race duration is long enough to deplete glycogen supplies,  Therefore the marathoner requires well developed ability to mobilise and transport fats, highly developed mitochondria enzymes and also the capacity to metabolise lactate.

What role does the nature and timing of nutrition play in the development of these various metabolic capacities, and in particular, what role might training in a carbohydrate depleted state play?

The different goals of training and racing

It should be emphasized that optimum nutrition for training is likely to be different from that for racing.  There is no doubt that for endurance racing whatever the distance, it is crucial to ensure that glycogen stores do not become depleted, both to ensure adequate energy supply for the brain and to fuel increased muscle output required for hills or surges of increased pace.  Glycogen depletion is not likely to be a problem in short races, but beyond 30 Km, it becomes a major issue.  Many studies (reviewed by Burke) demonstrate that both adequate carbohydrate loading before the event and administration of carbohydrate during the event enhance performance, though these studies have not explicitly addressed the question of the timing and amount of carbohydrate that is optimal for an athlete who is well adapted to preferential use of fats.  It is probably best for the fat-adapted long distance runner to augment carbohydrates on race day sparingly to avoid undermining the advantage of preferential utilisation of fats.

Training in a glycogen-deleted state.

The potential benefits of training in a glycogen depleted state with the goal of enhancing fat mobilization, and also possibly enhancing mitochondrial enzymes that are involved in metabolism of either fat or glucose, have been debated for many years.  Various strategies for inducing carbohydrate depletion have been considered.  One strategy is to train twice a day without refuelling between sessions, thereby ensuring that glycogen stores are depleted at the start of the second session.  Perhaps the most impressive study using this strategy was performed by Hansen and colleagues from Copenhagen.  They trained the athletes’ knee extensors, applying different regimes for the two legs.  One leg was trained twice for one hour with a two hour rest between sessions, on alternate days, while the other leg was trained for one hour daily.  Thus both legs did the same total volume of training, but for one leg, half of the sessions were performed in a glycogen depleted state.   After 10 weeks of training, time until exhaustion when working at 90% of VO2 max exhibited a markedly greater increase in the leg that had trained in the glycogen depleted state compared with the other leg.  Mitochondrial enzymes also exhibited a greater increase in the leg trained during glycogen depletion.   Hansen concluded that training twice every second day might be superior to daily training.   Of course, the benefit of training twice on alternate days was not necessarily due to the glycogen depletion. It might have reflected other benefits of thorough recovery between sessions.

The findings from studies in which glycogen deletion is achieved by training after an overnight fast are less convincing.  On balance there is little consistent evidence for improved endurance performance.   There is however consistent evidence for the enhancement of enzymes involved in fat mobilization, and consistent evidence for a decrease in respiratory exchange ratio (relatively less carbon dioxide is produced compared with oxygen consumed) which is characteristic of fat metabolism (see the review by Burke).

The effects on mitochondrial enzymes are less consistent and might depend on the composition of the diet.  For example, Van Proeyen and colleagues from Leuven in Belgium demonstrated that in individuals consuming a carbohydrate rich diet, training in a fasting state improved both ability to utilise fats and also mitochondrial oxidative enzymes compared with training fuelled by carbohydrates before and during training.  However, in individuals consuming a high fat diet, the advantages of training in a fasted state on fat utilization were abolished.  Furthermore, fasted and non-fasted training produced similar improvements in time to exhaustion, while only non-fasted training produced a significant increase in VO2max.  Thus, for individuals on a high fat diet, the advantages of fasted training on ability to utilise fats and on aerobic development are lost; while non-fasted training actually produces a greater increase in VO2max.  It should be noted that the training intensity in the fasted and non-fasted groups was matched.  In light of the strong expectation that fasting would diminish the capacity for high intensity training, even greater gains in aerobic capacity might be expected from non-fasted training if exercise intensity was not controlled.

Potential disadvantages

At least in the absence of a fat rich diet, training in the fasted state does enhance both the development of fat utilization and the development of mitochondrial oxidative enzymes, but might it have disadvantages?   As already implied, it might impair the ability to perform well and thereby gain maximum benefit from a high intensity training session.  Perhaps even more important is the risk of excessive cortisol release.   Cortisol mobilizes helpful adaptations to stress, but excessive and prolonged cortisol release has adverse effects on many body tissues, and on the immune system.  Furthermore, as discussed in my post two weeks ago, there is evidence that endurance athletes tend to have sustained and potentially harmful increases in cortisol that are proportion to training volume. Hence, it is probably desirable to minimise elevation of cortisol during training.  Gleeson and colleagues demonstrated that exercising at 70% of maximal oxygen uptake for 60 minutes produced greater elevation of cortisol and potential disadvantageous changes in the immune system in individuals in whom glycogen had been depleted by three days of low carbohydrate intake.   Thus, the evidence is indirect, but suggests that training in a glycogen depleted state does create an increased risk of harmful elevation of cortisol.


Training in the fasted, glycogen depleted state is likely to enhance capacity to utilise fats, which is advantageous for an ultra-marathoner and perhaps also for marathoners.  Under some circumstances, it might also produce enhancement of aerobic enzymes.  However, a high fat diet abolishes these advantages of training in the fasted state.  Furthermore, training in a glycogen depleted state increases the risk of excessive elevation of cortisol during either intense or prolonged training sessions.  In addition, training in a glycogen depleted state would be expected to diminish performance in a high intensity training session and might thereby limit the benefits obtained from high intensity sessions.

Overall, I think that training in a fasted state has a very limited role to play, though might be advantageous for ultra-marathoners who wish to maximise capacity to utilise fats.  Although the alternative strategy of a high fat diet might nullify this advantage, it is necessary to evaluate the risks and benefits of a high fat diet.  I will address this issue in detail in a future post, but here, I will merely note that a substantial body of evidence does indicate that moderately high fat diets can be healthy, provided there is an approximately equal balance of omega-3 and omega-6 fatty acids, typical of the classic Mediterranean diet. In contrast, in most Western diets, there is an unhealthy preponderance of omega-6 fatty acids.  Furthermore, Venkatraman and colleagues have shown that increasing fats up to 40% of energy requirements, leads to increased endurance in healthy trained runners.

While there is strong evidence that avoiding glycogen depletion during races is crucial for peak performance, I am inclined to think that in many situations, the mild glycogen depletion achieved by avoiding carbohydrate consumption during training might be advantageous, because it is likely to enhance the capacity for fat utilization and might also promote mitochondrial enzyme development, especially in athletes who consume only moderate amounts of fat in their diet.   Therefore I do not consume carbohydrate during training (except to test strategies for refuelling during a race).  Furthermore, if training in a non-fasted state, it is worth considering what type of pre-training nutrition is optimal.  Sun and colleagues have demonstrated that a low glycaemic index (low GI) breakfast promotes utilization of fat rather than glucose during low and moderate intensity exercise.  A low GI meal minimises the spike in blood glucose but instead produces sustained release of glucose into the blood stream.  Therefore, I consider that a low GI breakfast is optimal for both training and also before a long race.

Too many long runs?

October 3, 2013

A few days reflection, a more detailed examination of my training logs, and an interesting discussion with Robert regarding nutrition in the comments on my recent post about the Robin Hood half marathon, have provided me with food for thought.  I think I have learned some useful lessons, but first of all, I should put that race into perspective.

Although I want to race well, and would like to once again run a creditable marathon, the underlying goal of my running is minimising the inexorable deterioration that accompanies aging.   Six years ago, I decided that I would train systematically for a half marathon.  I had been running regularly since the previous November, though averaging about only 8 Km (5 miles) per week.   At the beginning of March I started systematic training, initially building up volume on the elliptical cross trainer.  After 8 weeks my running pace at the second ventilatory threshold had increased from 6 min per Km to 5 min per Km.  I added increasing amounts of running and by mid-June, did a 5K time trial in 23:27.  I contemplated this ruefully in light of the times of my youth, but decided it was not too bad, and began to speculate whether a half marathon in 105 min might be possible.  I continued to do around 35 (equivalent) miles per week, including some elliptical sessions, and occasional longish runs of 15Km.  Then in August, the arthritis that had afflicted me in my 50’s made an unwelcome return.  At the time, we were on holiday in France, staying in a farm house and sleeping in the loft.  For a few days, I was forced to descend the steep steps from the loft each morning, shuffling on my bottom.   However, the storm abated as quickly as it had arrived, and about six weeks later, I ran the half marathon in 101:24.  That time remains my M60 PB.

This year, I have again been able to train regularly, disrupted only by an episode of arthritis early in the year. I have coped with a greater volume – about 46 (equivalent) miles per week over a period of 6 months.  However, by August, my pace at second ventilatory threshold was slower than 5 min/Km.  I did not attempt a 5Km time trial, but am certain that I would a have struggled to break 25 minutes.  A 105 min half marathon appeared to be an absurd goal.  However, based on previous experience I was hopeful that a few weeks of higher intensity, lower volume training would produce a major improvement.  On the day, this hope was partially justified by the fact that I was comfortably below the second ventilatory threshold while maintaining a pace 4:53 min/Km for the first two Km, on target for a time of 103 min.   But my legs were not coping well.   As described in my recent post, the pace ebbed away and I finished in 107:49, a little more than 6 minutes slower than my time six years ago.  Disappointing, but not really unexpected.  WAVA predicts a loss of a little over 1 minute per year for half marathon time at my age, so in fact I have deteriorated at almost the exact rate that WAVA predicts. Furthermore WAVA predictions are based on the performance of elderly runners who are not only naturally fast, but also are deteriorating less rapidly than average as they age. So this year’s evidence indicates that I have at least slowed my rate of deterioration over 6 years to match that of the WAVA standard setters.  However, the evidence provided by last years time of 101:50, which is my best WAVA graded performance of my 60’s, suggests that I could do better.

This year’s campaign has several other bright spots.  I appeared to cope reasonable well with a volume of  46 miles per week for 6 months.  This bodes well for my plan to train for a marathon next year.  Secondly, I was pleased to find that I can still muster a competitive edge even when nearly exhausted.   With one Km to go, the sight of the swishing ponytail of a young lady who had passed me about 16 Km earlier provided the focus.  I covered the final Km in 4:56, a little faster than I had managed for any Km between 5 and 20 Km.  Having overtaken the young lady with the ponytail with 300m still to run, I subsequently overtook at least four other runners, all younger men, in a spirited run to the line.

105 metres to run and the young lady with the ponytail is now well behind (2nd right). I am in the blue vest and now closing on four young men.

150 metres to run and the young lady with the ponytail is now well behind (2nd right). I am in the blue vest and closing on four young men.

Less than 100 m to go and I am not the only one with an ‘awesome race face’.  The competitive juices are flowing.

Less than 100 m to go and I am not the only one with an ‘awesome race face’. The competitive juices are flowing.

20 m from the line.  The 4 young men are now behind, but I can’t quite catch another young lady, just out of camera view.

20 m from the line. The 4 young men are now behind, but I can’t quite catch another young lady, just out of camera view.

It appears that I am still able to muster the type 2B (fast-twitch) anaerobic fibres when the chips are down.  Unfortunately, type 2B’s can only function at maximum capacity for about 10 seconds.   Nonetheless, at least for a brief period, my type 2B’s were twitching fast enough.  The foot pod recorded a peak stride rate of 216 steps per minute.  But my peak step length was only 118 cm.   Thus, the final sprint confirms that the capacity of my leg muscles to generate a strong eccentric contraction is poor.   This is clearly one of the major limitations imposed by age.   I suspect it is because accumulated fibrous tissue obstructs dynamic stretching of the muscles.  During static stretching I can achieve almost as great a range of motion as I could achieve 55 years ago.    How can I recover my former dynamic range?  As outlined in my previous post, I think hill sprints are probably the best option.

Long runs

But my training log provides further food for thought.  My performance was substantailly worse this year than last year despite a 10% increase in training volume in the final six months.  It is necessary to look at the type of running, not only the volume.   The really striking difference was in the number of long runs.  This year I did 32 runs longer than 15 Km in those six months, many of them in the range 18-21 Km, whereas last year I did 16 runs longer than 15 Km in the corresponding period.  The increase in long runs was the outcome of a deliberate plan to develop better endurance this year.  In fact, I did improve my endurance substantially.  Early in April, one month into my half marathon campaign, I maintained a pace of 6:15 /Km and a heart rate of 740 beats/Km during a typical 16 Km run.  Five months later, I did a 19 Km run at similar effort level and at a pace of 5:43 /Km, with a heart rate of 697 beats/Km.

But is it possible to do too many long runs, even at an easy pace?  Dudley’s well known study of rats training on a wheel for various durations and intensities, demonstrated that aerobic capacity increases with increasing duration of running, but only up to a certain limit, that depends on intensity.  The duration for optimal gain was greatest at low intensities, at paces where most of the work is done by slow twitch fibres.  But even at low intensity, there was no additional gain in aerobic capacity beyond about 90 minutes of training.    The physiology of muscle fibres in humans is quite similar to rats, though proportions of fibre types differ both within and between species.  Nonetheless, despite probable small differences, it is unlikely in either rats or man, that training beyond around 90 minutes will produce further improvement in aerobic capacity.  There might of course be other benefits, including conditioning of connective tissues and improving the balance between consumption of fat and glucose.  But could there be penalties?


For several years the debate between cross-fit enthusiasts and endurance runners has focussed on the potentially harmful effects of cortisol. In the short term, increase in cortisol mobilizes the body’s resources to deal with stress. In particular, it mobilizes glucose to fuel brain and muscle; and limits inflammation.  It should be noted that the brain is the higher priority; although blood glucose levels are increased, cortisol inhibits access to the glut4 transporter molecules in muscle cell membranes that transport glucose into the muscle, thereby ensuring preferential supply to the brain.   But perhaps more importantly for the rpesent discussion, sustained increase in cortisol has a range of harmful effects, including destruction of muscle and weakening of immune defences.  Cortisol rises steadily during long duration exercise.  Typically the level increases to around 220% of normal levels during a marathon.  The crucial issue is: how long is this increase sustained?  In a fit person, the level returns near to baseline within a few hours.  However, in the presence of other stresses, it can remain appreciably elevated for several days.  Until recently, the debate between cross-fitters and endurance runners has remained stalemated over the issue of whether or not typical endurance training programs produce a significant sustained increase in cortisol.

However in 2012, Skoluda and colleagues published the results of a thought-provoking study.  They measured cortisol levels in hair samples in athletes.  Levels of cortisol in hair, unlike levels in blood or saliva, provide a good index of sustained levels.  They found that in a sample of 304 endurance athletes, fairly representative of committed recreational runners, levels of cortisol, in hair were almost 50 % greater than in a reasonably well matched control group.   Furthermore the magnitude of the increase was greater in those with greater weekly training volume.  The increase was greater in marathon runners than in half marathoners, though both groups had values that were significantly increased compared with controls.  Typically a training volume of 70 Km/week (a little lower than my average of 74 Km/week) was associated with a 1.8 fold increase in sustained level of cortisol.  The health consequences of an increase of this magnitude are unclear though such an increase might plausibly result in greater risk of upper respiratory tract infections and even perhaps add to the risk of atherosclerosis and myocardial infarction.   There is evidence for increase in atherosclerosis among male multi-marathoners, as I have discussed previously.  Furthermore, the elevated cortisol levels might inhibit protein synthesis in muscles and limit any gain in strength.

It should be noted that increases in cortisol during exercise are usually less in well trained athletes, suggesting that problems due to cortisol might by ameliorated by a gradual increase in training volume. On the other hand, running in a glycogen depleted state would be expected to increase cortisol levels.  Therefore, I remain sceptical of the wisdom of training in a carbohydrate-depleted state.  In the discussion following my most recent post, Robert has raised some interesting points related to his positive experiences following changes in both the type and timing of his nutrition, including doing long runs without breakfast.  He is running very well at present, though it is perhaps noteworthy that his total training volume has been relatively low this year compared with previous years, and hence, sustained cortisol levels would not be expected.

Total volume or length of long runs?

Although Skoluda did not attempt to disentangle the effects of total weekly training volume from length or frequency of long runs, the evidence that cortisol rises steadily during a long run raises the possibility that it is the length and frequency of long runs that is the main contributor to sustained elevation of cortisol.  When taken together with the evidence that gains in aerobic capacity are likely to be small after 90 minutes of training, I think it is quite plausible that the large number of long runs in my program this year not only contributed to a relatively slow gain in aerobic fitness, but might also have produced a sustained increase in cortisol that impeded the development of strength.   Although I intend to prepare for a marathon next year, I will be more judicious in planning the frequency of long runs.