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Plans for 2019

January 1, 2019

Happy New Year.

Thanks to all who have continued to read my posts during the past year.   Despite the fact that I posted only twice in 2017 and 5 times in 2018, it appears that you, my valued readers, have not given up.  There were 36,139 page views  in 2017 and 33,733 in 2018, placing these two years among the top three since I started blogging 11 years ago.

In part the paucity of my posts in recent years has been because the energy invested by the running community in the vigorous debates of the preceding decade about issues such as running style and running shoes has almost fizzled out. Meanwhile other interesting aspects of science have continued to advance. In particular, the evidence that exercise is one of the most effective ways to enhance health and wellbeing has become increasingly compelling. Much of this evidence is relevant not only to health and well-being but also to training to achieve optimum performance.   Therefore, there is much to write about.  I hope that in 2019 I will find time to post more frequently.

In my posts in the final months of 2018 I compared and contrasted performances and training of Ed Whitlock and Gene Dykes.   The differing career paths followed by Ed and Gene have prompted me to review again the question of the optimum way to achieve longevity as a distance runner

This is a topic I have discussed at length on this blog in recent years.  It is time to return to it, not only because of the different trajectories of Ed and Gene, but also because the past few years have been a fertile period in the study of relevant basic biology.   I anticipate covering the topic in a series of several posts:

  • The role of genes
  • The role of satellite cells
  • The role of inflammation
  • Hormones and the autonomic nervous system
  • The enigmatic role of mind and brain

While I hope this intricate scientific story will prove fascinating in itself, I will nonetheless attempt to remain anchored to the evidence presented by the stories of great distance runners, not only the veterans, Ed Whitlock and Gene Dykes, but also some of the ‘younger’ runners who set the standards for distance running in the 21st century, especially Haile Gebreselassie and Paula Radcliffe.

Threshold training: integrating mind and body

February 5, 2017

There is little doubt that ability to minimise acid accumulation in muscle and blood while running at race pace is a major determinant of performance at distances from 5K to marathon.  However the question of how best to train to achieve this ability is less clear.

This ability depends on several different physiological capacities. On the one hand, there are capacities such as cardiac stroke volume, capillary supply to muscles, and aerobic enzymes in the mitochondria that contribute to the overall capacity to generate energy aerobically, and thereby minimise production of lactic acid.  On the other hand are the physiological capacities that determine the ability to transport and utilise lactic acid. These include the transport molecules located in cellular membranes that transport lactic acid out of the fibres, especially type 2 fibres, where it is generated.  After transport out of type 2 fibres it can be taken up into type 1 fibres with the same muscle where it can be used as fuel, or carried via the blood to other organs such as the heart where it can be also used as fuel, or to the liver, where it can be converted by the process of gluconeogenesis into glucose and thence stored as glycogen.   All of these physiological capacities contribute to the ability to minimise lactic acid accumulation at race pace and all can be trained, to at least some extent,  by sustained running at threshold pace.


Specificity v Variety

Many coaches and athletes, including renowned coach Jack Daniels, have argued that the optimum form of training to minimise lactic acid accumulation at race pace is threshold training (i.e. sustained running at a pace in the vicinity of the threshold at which lactic acid begins to accumulate rapidly) or cruise interval sessions, in which epochs of moderate duration at a pace a little above lactate threshold alternate with recovery epochs at a lower pace to allow some dissipation of the acidity.  Threshold training is consistent with the principle of specificity: namely that the most efficient way to enhance the ability to sustain race pace is to train at a pace near to race pace.

However, there are several reasons to question the principle of specificity  Perhaps most important is the likelihood that if you rely on running near threshold pace as the main way to enhance this ability, your body will make use the physiological capacities that are already well developed to achieve the target pace during training sessions.    If some of the required physiological capacities are less well developed, it might be more efficient to spend time training is a manner that challenges those less developed physiological capacities.  For example, if ability to transport and utilize lactic acid is relatively weak, high intensity intervals will generate large surges of lactic acid and will challenge the mechanism for transporting and utilizing lactic acid.

As discussed in a recent post, many different types of training session, ranging from long runs at a moderate aerobic pace; threshold runs; to high intensity intervals can help develop the various physiological capacities required to minimise acid accumulation while running at race pace.  In general, it is likely to be best to employ a varied training program that utilises all of these types of training to promote that all of the required physiological capacities.  The proportion of the different types of training should be adjusted according to the athlete’s specific needs and also to the goals of the phase of training. During base building, when a substantial volume of training is required to build overall resilience while also building a large aerobic capacity, it is best to place the focus on lower intensity running to avoid accumulation of excessive stress. Nonetheless, some more intense training should be included in the phase, in part because it is an efficient way to develop aerobic capacity (as demonstrated by the many studies of high intensity interval training) and also because a judicious build-up of intensity develops the resilience of tissues to cope with high intensity in the pre-competition and competitive seasons.

To minimise risk of injury, there should be a gradual build of the intensity of the sessions training during base-building; intense training should generally be avoided when tired; and within any intense session, thorough warm up is crucial.  As discussed in my recent blog post, there are some grounds for proposing that risk of injury might actually be higher during sustained running at threshold pace than during more intense interval sessions provided you take adequate precautions to minimise risk of injury.  Nonetheless, there is little doubt that threshold sessions have an important part to play in the training of a distance runner. But rather than regarding such sessions as the universal answer to the question of what session to do to enhance the ability to sustain race pace, it is more sensible to utilise these sessions to achieve more specific goals.

One of the truly specific roles of the threshold session is training the body to integrate all of the physiological capacities required for distance racing.   The human body is a multi-organ system in which each individual organ, especially heart, lungs, muscles and brain, but also other organs such as liver and adrenal glands, plays a specific role in distance running performance.  Threshold training promotes the required integration of this diverse orchestra of organs.  For the most part, this integration occurs unconsciously.  We do not need to think about it.  This truly amazing integration of different physiological processes occurring in different organs is achieved by an intricate network of nerves, hormones and other signalling molecules, without the need for conscious intervention.  Indeed attempts to intervene consciously often led to less efficient integration, as is indicated by the finding that in some instances, runner who focus on internal processes such as breathing run less efficiently than runners who focus on things in the external world.

Brain and mind

The brain via its role as the central processing unit of the nervous system and also as a high level regulator of the endocrine system, plays a cardinal role in this integration.  For the most part, the brain carries out its integrating role non-consciously, but we would be missing out on two of the very valuable features of threshold training if we ignored its value in training conscious brain processes.

The first of these is the development of the confidence that butresses the self-talk that is sometimes necessary to overcome a self–defeating internal dialogue during a hard race.   In general I try to avoid doing demanding threshold sessions when I am tired or stressed because of the risk of injury at such times, but sometimes a scheduled hard session cannot reasonably be deferred.  This is the time to make a virtue of necessity and use the session as an opportunity to prove to your doubting mind that you really are capable of pushing through pain.  In fact quite often it is helpful to reframe the word ‘pain’ in such circumstance, because what our mind might tend to interpret as pain during a threshold session on a stressful day should more accurately be described as a level of effort that we are not confident that we can sustain for more than another few minutes.  Almost invariably we can sustain this level of effort for longer.  Demonstrating this provides evidence to buttress the self-talk we might require in a subsequent occasion in a hard race.

In my view, even more important than the development of mental strength to deal with hard races is the opportunity that threshold training offers to facilitate the ability to get into that almost magical state known as the zone.  When we are in the zone running seems almost effortless.  We feel exhilarated, in control, and above all, confident.  The zone is a state of consciousness, but it is not a state that we can easily adopt consciously.  When it occurs it can feel like a state of grace endowed upon us by something outside of ourselves.  Nonetheless we can facilitate it.  Threshold running can provide great opportunities for developing the ability to facilitate it.

In my younger days, for several years I lived in a house facing the beach in Brighton, a sea-side suburb of my home town, Adelaide.  My favourite Sunday morning run took me from sea level to the summit of Mount Lofty, the highest point in the Adelaide Hills.  I ran up the gorge of Sturt Creek and through Belair National Part to the summit.  My return journey started with a steep descent of Waterfall Gully, followed by an almost level run on pavement via the eastern and southern suburbs of the city, back to my sea-side home. The total journey was around 25 miles.  It was my version of the run that Lydiard’s athletes did regularly on Sunday morning in the Waitakere Hills above Auckland, though perhaps a little more demanding in both terrain and distance.   My ascent of more than 2000 feet was often quite a slog, but the descent though Waterfall Gully was exciting.


Waterfall Gully (photo:

Nowadays there is a well-made walking path from the lowest waterfall to the summit, but in those days, almost fifty years ago, the gully was wild.  In many places the most feasible route involved hopping from rock to rock in the bed of the stream itself.   On a good day, when my legs felt strong and sure as I leapt nimbly from rock to rock, I emerged onto the road below the lowest waterfall thoroughly exhilarated.  On such days, I ran a large portion of the remaining distance at a fast tempo, around 10K race pace, aided by the slight descent with average slope of about 1% to sea level.  Even now, decades later, I have a clear memory of the sense of power and confidence as I ran.   Around that time I was able to recreate the same sensation of power and confidence during several races. Those races are among the most cherished memories of my running career.

Even in a polarised training program that places the main emphasis on a high volume of relatively  low intensity training with a small amount of high intensity training, there is a place for threshold training, perhaps around 10% of total training.    Those sessions have a crucial role to play in training the body to integrate the diverse physiological capacities required for distance running, and in particular, provide a valuable opportunity for training the brain to achieve integration of mind and body.

Cross Training

June 19, 2016

There is little doubt that if you wish to run well, a large part of your training should involve running.  Running requires a specialised pattern of muscle activity that must be practised.  It also subjects the body to unique stresses to which the body must adapt.  Gradual build-up of running itself is almost certainly an imporant part of acquiring the skill and adapting to the unique stresses.   In other words, training should be specific.  However, the principle of specificity has important limitations.  You do not become a good marathon runner merely by running marathons at your best race pace repeatedly.   This will merely lead to exhaustion.  The principle of specificity does not extend to exclusive training at race pace over the relevant distance.  We need to build up a variety of strengths and abilities and training should be adapted in a manner that allows the development of each of these strengths and abilities to the full extent without exhausting the body.  This leads to the question of whether it is more effective to include some cross-training activities other than running, in order to build specific strengths with minimal stress, and if so, what proportion of training should be cross-training.

The first point to make is that the answer almost certainly  depends on the individual.  Some individuals have achieved superlative performances with little or no cross training.   Among these is Ed Whitlock, undoubtedly the most successful elderly distance runner the world has seen; holder of more than 45 age-group world records, spanning distances from 1500m to marathon, in age groups ranging from  65-69 to 85-89. His training consists of low-intensity running for several hours each day, together with fairly frequent races at shorter distances.  He does no cross training at all.

However, if one examines Ed’s training in more detail, it is clear that he has crafted it carefully in a way that scrupulously avoids the stress of extensive amounts of running at or near race pace.  He describes his training pace a glacial.  He shuffles along with a short stride, scarcely becoming airborne, for the explicit purpose of minimising impact stresses on his legs.  Despite the fact that all of his explicit training is actually running, it is running in manner so different from his race pace and gait that one might almost be tempted to call it cross-training.  Nonetheless, it does involve the essential elements of running, albeit with one of running’s defining features, getting airborne, almost entirely removed.

At the other extreme is Dean Karnazes, ultra-distance runner famed for prodigious feats of endurance such as the Badwater Ultramarathon, which he won in 2004.  In his own words, he is very eager to try any form of cross training that presents itself.  At various times he has advocated the elliptigo, an elliptical cross-trainer on wheels designed to mimic the movements of running but with no impact forces, and more recently, the Zero Runner, in which the mounting rods of the platforms that you stand on are hinged at the level of foot and knee.  The leg action even more closely resembles that of running, yet impact forces are abolished.  Karnazes also emphasizes the importance of whole body training, including a wide range of strength exercises

There are few noteworthy examples of elite runners who have been forced to rely almost entirely on cross training.   Three months out from the Beijing Olympics, Paula Radcliffe suffered a stress fracture of her femur and was forced to rely heavily on elliptical cross training and pool running.  She did complete the race in 23rd place, in a creditable but intensely disappointing time of 2:32:38.  The images of her struggling after the first 19 miles of the race are almost as pitiful as the pictures of her sitting beside the road in Athens 4 years previously when she dropped out of a race that many expected would be the crowning glory of a phenomenal few years in which she had taken ownership of the women’s marathon.    The fact that in Beijing Paula was able to keep up with the leading pack for the first 19 miles indicates that her cross training produced impressive aerobic fitness, but the cross-training was inadequate to condition her legs to withstand the repeated trauma of impact.  In her words: ‘My calf stiffened up and the pain went all the way up my leg.  By the end, I was running on one leg’.


It is clear that different athletes have incorporated cross training into their training routines for various reasons and to a varying extent, with varying levels of success.  In my recent series of articles on strategies for enhancing longevity as a runner, I had concluded that the evidence suggested that cross training has an important role to play.  I will finish this article with an overview of the aspects of a runner’s physiology that might be developed effectively by cross-training, and in subsequent articles, will examine the virtues and limitations of a range of different forms of cross training, including resistance exercises and plyometrics; elliptical cross training, cycling, walking and swimming.


The heart’s capability to pump a large volume of oxygenated blood via arteries to muscles, together with the ability to sustain high cardiac output over prolonged periods, are key components of aerobic fitness.  Virtually all forms of cross training enhance the pumping capacity of the heart.  The various forms of low-impact aerobic exercise, especially cycling, elliptical cross training, aqua jogging and swimming offer the possibility of maintaining a high cardiac output for sustained periods with minimal trauma to the musculo-skeletal system. They contribute to the development of cardiac endurance by mechanisms such as increasing the capacity of heart muscle to utilise fats, while also enhancing capillaries within cardiac muscle itself that are essential for delivering oxygen to the heart muscle fibres.    Low-impact aerobic training can also be incorporated in high intensity interval training, providing a time-efficient way of increasing cardiac output, largely by increasing stroke volume.

Skeletal muscle

As in the case of heart muscle,  long duration aerobic cross-training develops the ability of skeletal muscle to metabolise fat and also enhance the capillary supply to the muscle fibres  Resistance training can be used to develop skeletal muscle strength and power in an efficient manner by employing loads that exceed those involved in running. Plyometric training is a very efficient way of enhancing power of eccentric contraction and developing resistance to damage from eccentric contraction, but unlike low-impact forms of cross training, plyometric exercises carry a serious risk of trauma to muscles, tendons and ligaments.  Hence plyometrics should be incorporated in a training program cautiously, gradually build-up of the intensity of the eccentric contractions.  However provided build-up is gradual it is possible to apply far greater forces than occur during running itself.  This generates reserve capacity to manage eccentric contraction, resulting in a more powerful running action together solid protection against injury

Systemic metabolism and hormones

Both long duration low intensity aerobic cross training and short duration high intensity cross training promote many of the metabolic and hormonal responses that are crucial for endurance running and for the repair of tissues. For example, low impact cross training in the mid to upper aerobic zone is potentially an effective way to enhance the capacity of the lactate shuttle that transports lactate to liver where it is converted back to glucose and stored as glycogen.  High intensity cross–training  can enhance the capacity to transport potassium that is released from muscle during contraction, back into muscle, thereby making the muscles more resistant to fatigue.   Both aerobic exercise and resistance training can promote growth hormone release, though in general résistance training is more effective for stimulating growth hormones and other anabolic hormones.

Enhanced recovery

A moderate body of evidence indicates that low intensity activity following strenuous training promotes potentially beneficial physiological changes, such as a decrease in blood levels of reactive proteins  that are marker for inflammation.  However the evidence that such changes actually enhance subsequent performance is sparse.   Perhaps the most convincing evidence comes from the study led by Peter Peeling at University of Western Australia,  in which nine triathletes performed an intense running interval session on two separate  occasions followed 10 hours later by either a swim recovery session (consisting of 20 × 100 m at 90 % of 1 km swimming time-trial speed), or a passive recovery session of similar duration.  On each occasion, on the day following the interval session, they performed a high-intensity treadmill run to fatigue to assess the degree of recovery of running performance.  The athletes were able to run for an average of 13 minutes, 50 seconds after swimming  recovery compared to only 12 minutes, 8 seconds after lying still for recovery.  Furthermore, the swimming  recovery was associated with significantly lower levels of c-reactive protein 24 hours after the interval run. Thus the swimming recovery was not only associated with reduction in a protein marker of inflammation but also with enhanced performance in the treadmill running test, 24 hours later.  Peeling and colleagues speculated that the non-weight bearing character of the swimming recovery was likely to be an important factor in the benefit



Overall, the various different forms of cross training can enhance the capacity of many of the physiological functions that are essential for distance running, while minimising the damage from impact at foot fall that is inevitable during running itself.   The diversity of different benefits from different forms of cross training make it possible to target specific weaknesses where  necessary.  Alternatively, incorporating a diverse range of cross training activities in your training program can deliver benefits in a wide range of physiological functions while minimising the accumulation of stress on the body.

The experience of Paula Radcliffe in Beijing suggests that a distance runner must nonetheless do a substantial amount of actual running.  On the other hand, a broader perspective on her career raises a more challenging question. Despite standing head and shoulders above all female marathon runners in history, her career was blighted by injury.  Would a more judicious balance between running and cross-training throughout her career have allowed her not only to set an astounding world record far beyond the reach of all others in the current era, but perhaps she might also have won an Olympic medal.

The longevity of the long distance runner, part IV: preserving muscle

March 7, 2016

I am afraid it has been a long time since my last blog post. I have been busy at work, though I have also made some progress in recovering fitness following my bicycle accident last summer.   Before the accident I had been planning a ’heptathlon’ of events, including running, jumping, swimming, cycling, lifting, and balancing, for the week of my seventieth birthday in late March of this year. Following the accident it appeared that the goals I had set were totally out of reach. In light of my rather slow recovery in the latter part of 2015, at the beginning of 2016 I had reset my targets for each event. However, although the torn ligaments in my left knee are still only partially healed, I have made substantial progress in the past 2 months and am now hopeful I will achieve my original targets in at least several of the events. I have had fun teaching myself the Fosbury Flop – despite having to adjust to taking-off from my non-preferred leg because of the damage to my left knee. Even when taking-off from the right leg I need to be very careful about foot placement during the run-up.   I have also taken the opportunity to learn the rudiments of a proper front-crawl swimming technique. But I will defer a more detailed account of my birthday heptathlon for a future post.

Now it is time to return to the issue of longevity of long distance runners. In previous posts I had addressed some of the basic science and had also examined the evidence regarding cardiac outcomes. In this post I will address the issue of deterioration of skeletal muscle, and what can be done to minimise it.


When a muscle is not used, signalling molecules within the muscle fibre initiate a sequence of events resulting in cessation of protein synthesis and increase in protein degradation.  In a world where cars and other mechanical devices have greatly reduced the need to use muscles vigorously, disuse is a major contributor to the loss of muscle and function with age, a condition known as sarcopenia.   However, even among those who continue to use their muscles, sarcopenia can only be held at bay, perhaps for decades, but eventually age extracts its remorseless toll.   For the general population, there is a simple public health message: exercise, along with a diet that includes adequate intake of protein and other nutrients, can slow the progression of sarcopenia.

However for the dedicated athlete the message is a little more complex.   Running itself can damage muscle both by direct mechanical trauma and also my biochemical trauma.   The question of what type and amount of exercise is most effective for ensuring longevity as a runner is challenging.   We should start by examining the mechanisms by which running itself might actually damage muscle.

Mechanical damage in skeletal muscle

The eccentric contraction of leg muscles at footfall results in stresses that pull muscle fibres asunder, especially at points where the contractile actin molecules attach to the structural framework of the muscle fibre.   This damage leads to an inflammatory response, in which fluid accumulates in the muscle, bringing with it the cells and nutrients required for repair and subsequent scavenging of debris. In the short term (over a time scale of hours) there is often a measurable increase in muscle size. As the repair proceeds a supportive mesh of collagen fibres are laid down. Initially this mesh is likely to prove a minor obstruction to smooth movement of the fibres.

Restricted movement leads to the accumulation of more fibre. Here is a quite intriguing short video by Gil Hedley about the fuzz that accumulates around muscle fibres that have become immobilised (illustrated in a cadaver, so do not watch it is you are squeamish). It is crucial to ensure tissues are mobilised during the recovery from a hard training session. While the most certain way to build up restrictive fibrous fuzz between muscles surfaces leading to restricted mobility in old age is a very sedentary lifestyle, but it is likely that years of training sessions which produce micro-trauma, without appropriate fuzz-clearing recovery is not much better.   It makes sense to me that a systematic strategy for mobilisation during recovery – be it massage, stretching or gentle movement – is crucial for longevity as an athlete. I have ready access to an elliptical cross trainer and my own preference is a relaxed elliptical session to maintain mobility of the fibres within my muscles. In addition I apply cross fibre friction massage (usually using my thumb) at focal sites of tenderness on tendons and other connective tissues to disrupt the formation of fuzz.

Biochemical trauma

Perhaps more insidiously, the very process that generates energy to fuel muscle contraction produces damage. Muscles generate energy by burning fuel, mainly glucose or fats, to generate the energy rich molecule, adenosine triphosphate (ATP). The energy contained in the phosphate bonds of ATP is the immediate source of energy the drives the ratchetting of actin over myosin molecules to produce muscle contraction.  A modest amount of ATP is produced during the early steps in metabolism of glucose via anaerobic glycolysis. Glycolysis converts glucose to pyruvate which is then converted to acetyl CoA provided oxygen is available. The early steps of fat metabolism also generate acetylCoA. In the presence of oxygen, acetylCoA is oxidised in mitochondria, via the Krebs (citric acid) cycle producing carbon dioxide and various molecules (such as NADH) that can act as electron donors. The most bountiful production of ATP during process of energy metabolism arises during the final stage: the electron transport chain.

In this final stage, electrons are transported along a chain of molecules embedded in the inner membrane of the mitochondria. In association with this transport of electrons, the charged protons that remain when an electron is removed from hydrogen, are transported into the space between the inner and outer membranes of the mitochondrion, setting up a voltage gradient, as depicted in figure 1.     This voltage gradient drives the protons back into the inner compartment of the mitochondrion via an ion channel though the enzyme, ATP synthase, embedded in the inner membrane, delivering the energy required to produce ATP.   However, this energetic process is almost literally playing with fire. In the process, electrons are stripped off oxygen atoms producing highly reactive positively charged oxygen ions that can leak out of the mitochondria and avidly bind to other molecules, producing irreversible oxidative damage.



Figure 1 The mitochondrial electron transport chain (by Fvasconcellos 22:35, 9 September 2007 (UTC) [Public domain], via Wikimedia Commons ) The oxidation of acetyl CoA via the Citric Acid Cycle generates electron donors such as NADH. The electrons pass along a chain of molecules embedded in the inner membrane of the mitochondria, tranferring hydrogen ions to the inter-membrane space. These ions are driven back to the matrix of the mitochondrion by the resulting electrical gradient, via a channel in the enzyme ATP synthase, thereby generating ATP.

Mitochondria become damaged; they typically have a half-life in the range 3 to 10 days. They must be replaced and the debris removed. Healthy aging requires the maintenance of efficient replacement, which is turn is dependent on the expression of the relevant genes as described in my recent post, and effective scavenging of debris. Damaged mitochondrial membranes are leakier, and are therefore more prone to release reactive oxygen ions and create greater damage within cells. In the elderly, mitochondria tend to be leakier.

There are also other metabolic mechanisms that result in exercise induced muscle damage. Although the details of the mechanism are debatable, exercising to the point where muscle glycogen store is seriously depleted also has the potential for damage. It is possible that glycogen depletion leads to serious depletion of ATP which is essential for most energy demanding intra-cellular processes, including the pumping of calcium. Calcium is released during muscle contraction and accumulates to damaging levels unless removed by ATP-fuelled pumping across the sarcolemma, the membrane that encloses each muscle cell membrane.   It is plausible that this is a major mechanism of muscle damage during the later stages of a marathon.


Minimizing damage from mechanical trauma

Gradual build-up

Although the inflammation induced by micro-trauma is a part of the mechanism by which the muscle is repaired and strengthened, at least in the elderly and perhaps in all athletes, it is almost certainly desirable to avoid excessive micro-trauma and subsequent accumulation of residual fibrous tissue as a by-product of the repair process. A sudden increase in training volume or intensity leads to Delayed Onset Muscle Soreness (DOMS) whereas more gradual increase is associated with minimal DOMS indicates that the first. This is a manifestation of the repeated bout effect, a protective adaptation against “maximal” eccentric contractions that is induced by submaximal eccentric contractions or a relatively small number of eccentric contractions. Perhaps the most important strategy for minimising accumulation of muscle damage with age is ensuring a gradual increase in training volume and intensity.  In a recent review, Nosaka and Aoki concluded that the magnitude of muscle damage can be attenuated by the use of the repeated bout effect more efficiently than any other prophylactic interventions.

Adequate recovery

While acute inflammation is largely a beneficial process that is essential for repair of tissues, if inflammation is sustained it becomes chronic, leading to long-lasting and perhaps permanent impairment of function. Therefore, adequate recovery after demanding training sessions and races is crucial.   Recovery does not necessarily demand absolute rest, as mobilization of tissues is important to minimise build of fibrous tissue – the fuzz described graphically in the video by Gil Hedley. The mobilization should be active enough to break down mis-oriented collagen fibres and to encourage blood flow, but not so vigorous as to cause new trauma. I favour low-impact cross training for this purpose.

Optimising cadence

For fast running, a strong push off from stance, mediated by an eccentric contraction is essential (as illustrated by Peter Weyand and colleagues). However, for a distance runner the goal must be to achieve peak efficiency in a manner that does as little damage to muscle s as possible.   In general, increasing cadence reduced impact forces, and for many recreational athletes, an increase in cadence actually improves efficiency. As I have discussed elsewhere, there is a limit to the benefits of increasing cadence. Nonetheless, for the elderly runner, during training it is probably advisable to aim for a short stride with relatively high cadence during long runs. This is a key feature of the training of Ed Whitlock.

Protein and amino acids

Repair requires amino acids which are the building blocks of the proteins that required to rebuild the components of muscle fibres.   The presence of amino acids in the blood stream acts as a stimulus to protein synthesis. Furthermore certain amino acids are critical, especially branched chain amino acids, which are essential in the sense that they cannot be synthesized within the body and therefore must be ingested. Howatson and colleagues demonstrated that following a session in which muscles were damaged by eccentric contraction during drop-jumps, 12 days of supplementation with branched chain amino acids produced significantly greater reduction muscle soreness and in levels of creatinine kinase in the blood (a measure of muscle damage) and significantly greater recovery of muscle strength than observed in a control group who received placebo.

Low-impact cross-training

Another useful strategy for minimising muscle trauma is low-impact cross training. I personally do about 30% of my training on the elliptical cross trainer.   Some of these sessions are recovery sessions, but I also do many of my high intensity sessions on the cross trainer as this allows me to increase aerobic fitness with minimal muscle trauma.

Resistance training

It might be expected that resistance training would enhance the longevity of a distance runner by virtue of delaying sarcopenia and increasing resistance to mechanical trauma. However until recently the picture has been confusing. Skeletal muscles exhibit quite different changes in physiology and metabolism in response to resistance training compared with endurance training. Endurance training promotes a development of type 1 (slow twitch fibres) at the expense of type 2 (fast twitch) fibres, and increases the number of mitochondria, but does not produce muscle growth. In contrast, resistance training mainly stimulates muscle protein synthesis resulting in muscle growth, achieved by fusion of satellite cells (a type of stem cell found in muscle) with existing muscle fibres. These differences in response to different types of exercise reflect different signalling processes within the muscle cells.

In a seminal study of isolated rat muscle, Atherton and colleagues demonstrated that low frequency simulation switches on a signalling pathway known as the AMPK-PGC-1α signalling pathway, which promotes aerobic metabolism and leads to the changes typical of endurance training, whereas high frequency stimulation which mimics the effects of resistance training, selectively activates the PKB-TSC2-mTOR signalling cascade causing changes consistent with increased protein synthesis and muscle growth. mTOR is a cardinal growth regulator that is switched on by various nutritional and environmental cues.

While the observation of mTOR activation provides a plausible mechanism by which resistance training increases muscle growth, it was at first unclear whether or not this would promote increased or decreased longevity. mTOR has opposite effects to another regulator, myostatin, which switches off muscle growth. Early evidence indicated that myostatin acts to increase longevity. This evidence was consistent with the puzzling but robust evidence that calorie restriction promotes longevity in laboratory animals. However more recent studies have demonstrated that the effects of myostatin are more complex than initially believed.   In fact, there is growing evidence that activation of mTOR and associated muscle growth is associated with longevity.

For example, Melov and colleagues examined the effect of six months of regular resistance exercise in a group of elderly participants. At baseline the elderly participants were 59% weaker than a young adult control group, but after the six months of resistance exercise their strength increased significantly such that they were only 38% lower than the young adults. The investigators also examined the degree of expression of genes before and after the 6 months of resistance training. At baseline there were a large number of genes that showed different levels of expression in the elderly group, but following exercise training the expression of most of the relevant genes returned to the levels observed in the young adults. Thus, resistance training not only achieves quite different changes in muscles compared with the effects of endurance training, but these changes appear to reverse features of age-related degeneration.  In a recent review, Sakuma and Yamaguchi concluded that resistance training in combination with amino acid-containing nutrition appears to be the best candidate to attenuate, prevent, or ultimately reverse age-related muscle wasting and weakness.


Stretching and massage

Despite the popularity of stretching, the evidence of benefits is minimal. It is probable that static stretching of cold muscles does more harm than good. However, as mentioned above, it makes sense to me that a systematic strategy for mobilisation during recovery after racing and training is worthwhile. Furthermore, there is growing evidence that massage can be helpful. For example, a study by Crane and colleagues at McMaster University in Ontario demonstrated that massage therapy attenuates inflammatory signalling after exercise-induced muscle damage. Studies in rabbits, reviewed by Alex Hutchinson, indicate that massage promotes muscle repair, and blood vessel formation, possibly by a mechanism initiated by stretch-sensitive receptors in muscles .


Minimizing damage from biochemical trauma

There is little direct evidence of effective strategies for minimising biochemical trauma, but our current understanding of mechanisms suggests several plausible approaches.

In light of the fact that damaged mitochondria are prone to leak potentially damaging reactive oxygen ions generated as a by-product of the electron transport that generates copious ATP, maintaining mitochondria is good condition is crucial for minimising damage. The maintenance of a healthy stock of mitochondria depends on a balance between the genesis of new mitochondria (biogenesis) and the removal of old mitochondria (mitophagy). The complex set of intra-cellular signalling processes that regulate this balance is described in a review by Palikaras. The signalling molecule, PGC-1α, is the core regulator of mitochondrial biogenesis. Signalling via PGC-1α is promoted by aerobic exercise.   One of the key benefits of relatively low intensity aerobic exercise is the promotion of mitochondrial biogenesis with relatively little risk of further damage.

There are other potential benefits of low intensity training. The evidence that impaired ability to pump the calcium released during muscle contraction back into muscle cells when glycogen is seriously depleted indicates that sustained running in the upper aerobic zone is potentially harmful.   One way of minimising glycogen depletion is enhancing capacity for fat metabolism. Perhaps relatively large volume low intensity running is the safest way to achieve this.

It should however be noted that the first stage of metabolism of fats leading to the production of acetyl CoA (beta-oxidation) generates less ATP per molecule of acetyl CoA produced than the corresponding stage of glucose metabolism (glycolysis), more oxygen must be consumed to generate a given amount of energy from fat than from glucose. Thus, fat metabolism actually makes relatively greater demands on the citric acid cycle and the electron transport chain that glucose metabolism for a given rate of energy production. Thus, fat metabolism leads to less efficient use of oxygen and it remains unclear whether or not fat metabolism is less stressful for mitochondria overall. However, the contrast between the body’s limited store of glycogen yet abundant store of fat means that at moderate paces, ability to use a higher proportion of fat in the fuel mix would be expected to place less overall stress on the body during sustained running at such paces.

In light of the potential damage produced by excess release of calcium fron muscle cells, it is also potentially helpful to attempt to enhance the capacity for calcium ion transport back into cells.  Interestingly, high intensity training (HIT) has the capacity to achieve this. In contrast to the possibility of damage from sustained upper aerobic exercise, HIT would be expected to produce surges of calcium release during the bursts of high intensity activity with an opportunity for reuptake during the recovery epochs.

Although this is speculative, I think that a polarised training program characterised by a large volume of low intensity running and a small proportion of high intensity interval running is potentially the optimum strategy for optimising longevity as a runner.


The evidence reviewed above leads to several recommendations for promoting longevity as a runner.

  • Gradual increase in training volume
  • Optimising cadence
  • Thorough recovery after strenuous events
  • Stretching and mobilization; massage
  • Low impact cross training
  • Low intensity running to promote both mitochondrial biogenesis and fat metabolism
  • Enhancing calcium pumping by High Intensity Training
  • Adequate protein intake, including adequate sources of branched chain amino acids.


So far in this series we have focussed largely on local effects in cardiac muscle and in skeletal muscle. However, there are also important mechanisms mediated by hormones and other signalling molecules in the blood stream, that play a role in damage, repair and protection. In the final post in this series we will examine these mechanisms.

The longevity of the long distance runner, part 2: the basic science.

January 1, 2016

In my previous blog post I had posed the question: What determines the rate at which a runner’s performance declines with age?   As a prelude to addressing the scientific evidence, I had discussed anecdotal evidence gleaned from the family history, lifestyle and training of the two greatest veteran distance runners of all time: Derek Turnbull and Ed Whitlock. The anecdotal evidence suggested that genes, life-style and training all played a role. Especially in the case of Ed Whitlock, it is probable that having long-lived forebears; deferring very high volume training until after his retirement from work; and adopting a training program designed to minimise stress all contributed to his extraordinary longevity as a world-record breaking marathoner into his mid-eighties.   However, anecdotal evidence provides little basis for drawing general conclusions. What does science tell us?

At first sight, the answer appears to be that science provides a lot of obscure information that in practice offers us little guidance as to how we might adjust our life-style or training to maximise longevity, either as functioning living creatures or more particularly, as athletes. However, if we do not allow ourselves to be put-off by the apparent complexity of the story, it is possible to establish the basis for some simple speculations that might be useful in practice.

Although my primary focus is on longevity as a runner, longevity as a runner is very closely linked to healthy aging.   Healthy aging is not merely freedom from identified illnesses, though many illnesses are common in the elderly and unhealthy elderly people are often afflicted by multiple illnesses.  In fact it is probably more appropriate to consider that healthy aging is a state characterised continued good functioning of all systems of the body, that creates a low vulnerability to illness and is also a requirement for longevity as a runner.

Are there genes for longevity?

There have been several large studies of genes associated with longevity in the general population. These indicate that many genes contribute a small amount to longevity but few contribute an appreciable amount. In fact only one gene has emerged as a significant predictor of longevity in genome-wide association studies: the gene for apolipoprotein E (APOE).   Apolipoprotein E is a protein involved in the transport and metabolism of cholesterol and in several other metabolic functions. The E4 variant of the gene for APOE is associated with substantially increased risk of Alzheimer’s disease and also of heart disease and of increased rate of shortening of telomeres – the protective caps on the ends of chromosome that protect them from damage. Rapid shortening of telomeres is associated with decreased longevity.

We have two copies of each gene (apart from genes on the sex chromosomes), one copy inherited from each parent. In individuals in whom both copies of the APOE gene are the E4 variant, the risk of Alzheimer’s disease is around 15 times greater than in individuals who have two copies of the ‘neutral’ E3 variant, but fortunately very few individuals carry two copies of the E4 variant. However, almost 14% of the population carry one E4 variant. An individual with one copy of E4 together with a copy of E3 has a risk of Alzheimer’s that is about 3 times greater than that of a person with two copies of E3.   Similarly, carrying the unfavourable E4 variant of the gene for APOE does have an apprecibale effect on life expectancy, but even this ‘unfavourable’ gene accounts for only small amount of the variation in longevity in the population. It should also be noted that in contrast, the unfavourable E4 variant is associated with potentially beneficial higher levels of vitamin D which might explain why the gene has persisted in the population despite its unfavourable effects.

But the gene for APOE is the exception. Other genes that appear to contribute to variation in longevity in the population account for a much smaller proportion of the variation than the APOE gene. One other gene that warrants a passing acknowledgement is a gene with the whimsical name, FOXO3. It is a gene that plays a role in regulating gene transcription: the process by which the genetic code specified in our DNA is transcribed onto a temporary RNA copy in preparation for translation into the structure of the proteins that are the building blocks of our bodies. FOXO3 influences the process by which cells die naturally and also plays a role in defence against oxidative damage – a topic we shall return to later.   Its function suggests that FOXO3 is a candidate for an important role in determining longevity, but in fact its influence is not large enough to be discernible above the noise in the data obtained in large (‘genome wide’) studies of the association between genes and longevity.

Genetic variants with small effect

Most of the variants of the many genes that are associated with small alterations in longevity occur commonly in the population. Individually these genetic variants produce a slight perturbation of the structure or function of the body. The very fact that these variants are common demonstrates that individually they cannot have a devastating effect on structure or function, as variants with devastating effects are unlikely to get handed down through many generations.

At this stage it is worth pausing to look briefly at the nature of genetic variation and the mechanism by which it can affect the body’s structure or function. The genetic code is specified by the sequence of the molecular units that a strung together to form the double helical chains of DNA. There are only four of these elementary molecular units, which are assigned the labels A, T, G and C. (These labels are the first letters of the names of the purine and pyrimidine molecules that from part of these units.) DNA consists of a pair of intertwined chains, linked by the bonds that form between A and T or between G and C, at corresponding locations on the two chains Thus each element in the code is either an A-T pair or a G-C pair.  During the preparation for translation, the twinned DNA strands get copied as a single-stranded RNA molecule where each A,T,G, or C unit in one of the DNA chains is copied as a U,A,C or G.   Note that the elementary unit labelled as T (representing the pyrimidine, thymine) in DNA has been replaced by a slightly different molecular unit labelled U (representing the pyrimidine, uracil) in RNA. The crucial thing is that each possible triplet of three sequential units in an RNA chain is the code for a particular amino acid. Amino acids are the basic units that are assembled to form proteins. Proteins are the basic building blocks of the body, serving many specific purposes. Many are enzymes that catalyse the various metabolic processes in the body. Others, such as collagen, are structural elements. The contractile proteins, actin and myosin, enable muscles to do work.

The mechanism by which the genetic code gets transcribed and translated into protein is known as gene expression.  It is gene expression that shapes the structure and function of the body.  As we shall discuss later, many things can influence gene expression.


Figure 1: schematic illustration of gene expression. An extra-cellular signalling molecule (eg an inflammatory cytokine) binds to a specific receptor embedded in the membrane of the cell , triggering a cascade of signalling within the cell. This cascade involves messenger molecules such as cAMP and various effector proteins, including kinase enzymes which activate other proteins by attaching a phosphate group (‘phosphorylation’). When the CREB protein is activated it initiates transcription of DNA, producing an RNA molecule in which the order of the A, U, C & G units is the code for a specific protein. Each triplet of A, U, C & G units represents a particular amino acid. The code specified by the RNA template is translated into the sequence of amino acids that are assembled to make the specified protein. The process of assembling the protein is performed by a molecular construction device called a ribosome.



During the rough and tumble process of cell duplication that occurs regularly in living tissues, one letter of the code might get changed (‘mutated’). This is known as a point mutation, and the resulting variation is known as a Single Nucleotide Polymorphism (SNP). The mutation might be triggered by irradiation by radioactive materials, chemical assault by disruptive chemicals in the environment or the diet, or merely by random jiggling of units making up DNA as it is duplicated during cell division.   As a result of the change in one of the letters, a particular triplet in the code is likely to specify a different amino acid. When the mutant DNA is transcribed into RNA and subsequently translated into a protein, one amino acid will be replaced by another. Just as when a particular footballer is substituted during a football match, the substitution might have a dramatic effect, for better or worse, or alternatively, the team might continue to function with little overall change in effectiveness, in the case of amino acid substitution, there might be either a dramatic change in function of the protein if the substituted amino acid plays a cardinal role or merely a slight change in effectiveness of the protein. Because the sequence of amino acids in proteins has been shaped though many generations, most proteins in the body are well honed to fit their particular role. In the absence of major environmental change, mutations that substantially enhance the fitness of the body for its survival are extremely rare.   On the other hand, mutations that result in serious disruption of the function of the protein diminish fitness for survival, and therefore disappear from the population. The mutations that survive to become common in the population usually have only small effects on the function of the specified protein. In addition to the point mutations that generate SNPs, other types of variation are possible, but these are beyond the scope of this discussion

In summary, the commonly occurring variations in the genes that code for particular proteins usually have only minor effects on the function of those proteins. These functional effects might be helpful or helpful depending on circumstance. But the crucial thing is that it is likely that in most instances various other circumstances including life-style factors might over-ride the relatively minor effect of a specific genetic variant on the structure or function of the body. For most of us, our fate is not pre-ordained by these genes.

One might expect to find that that among the minority of exceptional individuals who live to a great age, the co-existence of many favourable genes each contributing a little, might make an appreciable contribution to their extraordinary longevity. While twin studies demonstrate that the genes contribute only about 25% to the probability of survival to age 85, studies of extremely elderly individuals, such as the study of 801 centenarians (with median age at death of 104 years) by Sebastian and colleagues,, demonstrate that genes play a substantially greater role in the longevity of these exceptional individuals. Similarly, for individuals who exhibit extraordinary longevity as athletes, it is probable that the co-existence of many favourable genes plays an appreciable role. When a large number of small nudges all push in the same direction, their combined effect is appreciable. However for the majority of us, who carry a mixed selection of mildly favourable and unfavourable genetic variants, it is plausible that if we could adopt a range of life-style choices (including appropriate training) that tend to enhance longevity in a consistent manner, we could engineer our fate in a way that swamps the potpourri of random minor influences arising from our genetic endowment.

Gene expression does matter

While the selection of minor genetic variants we happen to have been born with plays only a small part in life-expectancy for most of us, the manner in which our genes are expressed nonetheless plays a crucial role in determining how long we live and how well we continue to function in old age. Unlike an inanimate machine, such as a bicycle with parts that become abraded or degraded by friction and/or corrosion as it grows old, living creatures have inbuilt mechanisms for repair and for correcting internal imbalances that threaten their well-being. A bicycle eventually ceases to function because the abrasion or degradation causes a component to break or jam unless maintained and repaired by an external agency.   However, when a human is subject to wear and tear an elaborate self-repair mechanism is mobilised. The occurrence of damage triggers the release of signalling molecules, which travel via the blood stream to remote regions of the body to mobilise defences. The signalling molecules bind to specific receptors on the surface of the target cell, initiating a series of steps leading to the transcription and translation of DNA to produce proteins that replace or augment the existing proteins as required to repair or even enhance the functions of the body.

After the arrival at the cell surface of a signalling molecule indicating the need for repair or some other response to the external environment, the next step is a cascade of internal signalling within the cell which initiates the transcription of the DNA code onto a temporary RNA template (as discussed above in the review of the process by which the genetic code is expressed, and illustrated in figure 1).

There is a unique RNA template for each protein that is to be constructed. Therefore at any time, the profile of RNA in the cells of a particular tissue indicates which particular proteins are under construction at that time.   The RNA profile of a particular tissue at a particular time is in effect a snap-shot of the multiple building, repair and maintenance processes underway in that tissue at that time.

Environmental factors including life-style and training work in synergy with genes to maintain the body in good working order.   The expression of genes in muscle is not only of particular importance for athletes whose activities are depend on well-functioning muscles, but growing evidence indicates that the expression of genes in muscles is a marker for heathy aging throughout the body. Recent studies indicate that the RNA profile of muscle in late middle age might be a good predictor of the fitness not only of muscle but of other body tissues in subsequent decades.

For example, Sood and colleagues from Kings College, London, demonstrated that a particular RNA profile initially identified in muscle biopsies from a small sample of healthy individuals at age 65, could be used to predict subsequent health of kidneys and brain in several independent samples of elderly people. In one sample followed for 20 years, this profile proved to be a significant predictor of overall survival. Sood proposes that this RNA profile, initially identified in muscle, is a robust marker of healthy aging.

The finding that the state of gene expression in muscle at age 65 can be a good predictor of subsequent overall health is consistent with the observation that self-selected walking speed in late middle age is a strong predictor of survival, and is perhaps of special interest to dedicated runners, though we should not read too much into the fact that the investigators chose to examine muscle tissue. At this stage many question remain unanswered. Two key questions are: what does the set of proteins that are specified by the RNA profile identified by Sood tell us about the molecular processes that characterise healthy aging; and what are the factors that determine the RNA profile in muscle in middle age.

Examination of the list of proteins specified by the identified RNA profile provides few strong clues regarding the molecular processes that characterise healthy aging. Some of the proteins have a known role in cell survival. Perhaps disappointingly for anyone dedicated to running, none of the proteins are those known to be produced in response to vigorous exercise.   However, I am not greatly surprised by this. Although the sample of individual in who the RNA profile was initially identified were healthy and active, none were athletes.   Nonetheless even as a dedicated runner, I find it intriguing that there are features in the current internal state of muscle fibres, other than (or perhaps in addition to) the recognised consequences of vigorous exercise, that indicate current good health and predict future well-being. Vigorous exercise is not all that matters.

Furthermore, the identified RNA profile does not include diminished amounts of the RNA associated with the known risks for diabetes and cardiovascular disease, suggesting that there are aspects s of healthy aging that are not specifically associated with low risk of heart disease. This implies that current guidelines for a healthy lifestyle, which focus largely on known factors associated with cardiovascular health, might fail to include other important aspects of healthy aging.

Perhaps the most important practical issue is whether we can do anything to promote the development of a healthy RNA profile. In general, RNA profile is determined by a combination of genetic and environmental factors.   The fact that genes themselves are not a strong predictor of longevity (except in the small group of exceptional individuals who reach extreme old age) makes it plausible that environmental factors play a large role in promoting the identified healthy RNA profile in middle age. At this stage there is little reason to propose that these factors are uniquely related to muscle. It is possible that influences from elsewhere in the body, such as neural regulation by the brain, the action of hormones or effects produced by other signalling molecules circulating in the blood stream, might shape the RNA profile in muscle.

It is likely that the challenge of remaining a healthy athlete into old age is a ‘whole body’ challenge, and I therefore look forward to future studies that might indicate what can be done to promote the development of a healthy RNA profile in muscle in middle age, irrespective of whether the direct site of action is in muscle or elsewhere in the body.

What can we do now?

Studies such as that of Sood and colleagues provide a fascinating pointer towards future investigations that might enable us to improve our chances of aging in a healthy manner, but it is reasonable to ask what guidance science provides now. In fact there is a substantial body of existing evidence about the mechanisms of cellular repair, protection and maintenance that allows us to make intelligent guesses about what might be helpful.

At the heart of this self-repair mechanism is the process of inflammation. This mechanism is not only responsible for repair of overt damage, but is also the mechanism by which training makes an athlete stronger and fitter. But the mechanism for self-repair does not confer immortality for two reasons. First, inflammation itself can leave a trail of debris in the tissues of the body. The debris is at least partially removed by the crucial scavenging process known as autophagy, but ultimately the residual junk gums up the works. Secondly, it appears that there is a limit to the number of times that the cells of the body can divide to generate new cells to replace those that are worn out. The gradual shortening of the protective telomeres on the ends of chromosomes is a crucial factor in limiting the number of times that cells can divide.

Cardinal among the processes that regulate the maintenance of living tissues are processes mediated by hormones. In particular achieving a balance between catabolic hormones that promote the break-down of tissues, including the process of autophagy, and anabolic hormones that promote the building of tissues, is crucial.

Finally, in light of the fact that gene expression matters throughout life, the cellular mechanism for protecting and repairing DNA itself, are likely to play an important role in life-expectancy and in our longevity as runners.


Figure 2: Schematic illustration of the mechanisms involved in cellular repair. These mechanisms are central to the response to training and also to the responses various other types of cellular damage that are crucial for healthy aging.

Although there is still much to learn about all of these processes, there are things that we can do now that help harness inflammation constructively, achieve a good balance between catabolism and anabolism and perhaps even promote the protection and repair of DNA. But this post has already grown long. I will address these issues in greater detail in future posts

The longevity of the long distance runner

December 7, 2015

What determines the rate at which a runner’s performance declines with age? Is it genes, training, life-style, or a combination of all three?  There is no clear answer to this complex question, but there are intriguing clues. I will set the scene in this post with some anecdotal evidence gleaned for a comparison of the two greatest veteran distance runners of all time: Derek Turnbull and Ed Whitlock. In my next post, I will examine some of the relevant scientific evidence.

Youthful talent

Both Turnbull and Whitlock were talented athletes in their youth, though in those early years neither reached the world-class level that they went on to achieve in later years.

Derek Turnbull was a New Zealander born in 1926. During his student days, he had a personal best for the mile of 4:23 on a grass track and achieved fourth place in national three- and six-miles championships. He was awarded a University Blue for these performances. After leaving Massey University with a diploma in farming, he travelled for several years before settling down to continue the family tradition of sheep farming. He eventually recommenced running largely as the whim took him across the fields and through woodland in his neighbourhood.

Ed Whitlock was born in London in 1931. As a schoolboy he achieved his greatest successes in cross-country events. During his university days, studying mining engineering at the Royal School of Mines at Imperial College, he won the University of London cross country championship and was also the University’s 3 mile champion on the track. One of his noteworthy achievements was a cross county victory over Gordon Pirie. Pirie went on to set a world record for 5,000m when he beat the formidable Russian, Vladimir Kuts in an epic ace in Bergen, Norway, in June 1956. Meanwhile Whitlock completed a university degree and emigrated to Canada where he took a job in mining engineering in a relatively remote region where there was no opportunity to continue as a competitive athlete.  After moving to Quebec, he recommenced running at age 41, almost by accident after his wife had volunteered him to do some coaching at a local school. Fortuitously, his return to running coincided with the birth of competitive masters athletics.


World Masters 1500m championships, 1977 and 1979

Both Turnbull and Whitlock came to international prominence at the 2nd World Veterans Championships in Gothenburg, Sweden, in 1977. Turnbull won gold in the M50-54 1500m in a time of 4:23.5. Whitlock took silver in the M45-49 1500m in 4:06.1. Two years later, in the 3rd World Veterans Championships in Hannover, Germany, Turnbull again won gold in the M50-54 1500m in a time of 4:17.0 and Whitlock won gold in the M45-49 1500m in 4:09.6.


Marathon performances

Derek Turnbull

In 1987, Turnbull became the first 60 year old to break 2:40:00 for the marathon with a time of 2:38:46, in my home town, Adelaide.  Four years later Luciano Acquarone shaved 31 seconds off Turnbull’s record, and then in 2009, Yosihisa Hosaka reduced the record to 2:36:30. Nonetheless, Turnbull’s time remains the fourth fastest ever recorded in the age category M60-64. Turnbull went on from his record breaking performance in Adelaide to a golden period of record breaking. In a two month period prior to the London marathon in 1992 he set M65-69 world records in 800m, mile, 3000m, 5000m, and 10000m; all of which, apart from the 800m record, still stand. In the marathon itself he set a new M65-69 marathon world record of 2:41:57.  That record still stands 23 years later. These performances mark him as the greatest middle-aged long distance runner the world has ever seen.

Although Turnbull remained capable of world class performances at age 70, there had been a marked decline in his late 60’s, as illustrated in figure 1. The deterioration in the 800m and 1500m was discernible even before his phenomenal performances at age 65 in in 1992, whereas there was only minor deterioration in 5000m, 10,000m and marathon between 60 and 65. In fact the minimal deterioration in the longer events between 60 and 65 is remarkable. However after his amazing performances at age 65, there was acceleration of decline across all distances with the greatest rate of deterioration in the longer distances. His marathon time of 3:15:59 recorded at the World Masters Athletics championships in Durban, South Africa at age 70 places him 28th on the world all-time list for the M70-75 category.


fig 1: Derek Turnbull; change in performance with age, expressed as the proportional change in time compared with time recorded at age 60

Unfortunately, he suffered a stroke in 2001. Although he continued to compete in track, road and trail races after that stroke, sadly he died in 2006 at age 79.

Ed Whitlock

Whitlock exhibits a markedly different pattern of decline with age. He had achieved his life-time personal best of 2:31:25 for the marathon at age 48, although he was not focused on the marathon at that stage. In his late 60’s after retirement from work he turned his attention to the marathon. He developed his unique training program characterised by frequent long slow runs. By age 68 he was running three of more runs of at least 2 hours each week. That year, he set a time of 2:51:02 in the marathon in Columbus Ohio, and the following year returned to Columbus to record a time of 2:52:50. He had his eyes on becoming the first 70 year old to break the 3 hour mark. The following year, 2001, in London, Ontario, he just missed out on that target with a time of 3:00:23, which was nonetheless a M70-74 world record at the time.

The following year was blighted by arthritis, but then in 2003, at age 72, he achieved his goal of breaking 3 hours with a time of 2:59:09. But the best was still to come. He further increased the duration of his long training runs typically doing 3 or more runs of 3 hours duration each week. In the 2004 Toronto Waterfront Marathon he achieved the utterly astounding time of 2:54:48, arguably one of the greatest marathons of all time.

He was a frequent winner of his age category in the Waterfront marathon in the ten years from 2004 to 2013, often setting a single-age world record time. In addition to the M70-74 world record set in 2004, he also set the M75-79 and M80-84 records, with times of 3:04:53 at 76 and 3:15:53 at 80. In 2013 he set the single-age world record for an 82 year with a time of 3:41:57, giving him a total of 11 single age world records for the marathon spanning the age range 68 to 82, and demonstrating his near total domination of the marathon over this age span.

He missed the Waterfront marathon in 2014 due to an injury to his upper thigh. He attempted to rebuild his fitness in 2015. However he was dogged by a series of troublesome injuries that prevented him from building training volume consistently for more than a few months at a time. He did achieve a M84 single age world record in the Longboat Island 10,000m in September. However he was unable to build his training to the level required for a marathon, and did not start in this year’s Waterfront Marathon.


Genes, life-style and training

Derek Turnbull

Apart from the knowledge that he was from a family that had farmed in New Zealand for several generations, I know little of Derek Turnbull’s family background. However he himself lived a robust life as a sheep farmer: mending fences; heaving ewes into pens; shearing.

He cultivated a self-deprecatory attitude when describing his racing and training. Roger Robinson reports that he would say “I don’t train. I just run — when I feel, where I feel, how I feel.”   By all accounts his training was spontaneous. Much of it was over rugged terrain on his farm or nearby; and much was fairly demanding: either long runs over hilly routes or fast shorter runs. According to Robinson’s account, Turnbull’s spontaneity produced a well-balanced program of long runs, tempo, and fast work.

By most standards, Derek Turnbull would be rightly considered to have lived a remarkably healthy life. His ability to work hard and train hard though his sixties is a testimony to his extraordinarily robust constitution. Despite the stroke at age 74, he continued to run and to work on his farm, shearing sheep up to the year of his death at age 79.   However, the decline from his superlative marathon performance at age 65 to a performance that is merely 28th on the world all-time list at age 70 raises the question of how long it is possible for a distance runner to remain at the pinnacle of international competition.

Ed Whitlock

I have described Whitlock’s background and training in detail in a previous post.   With regard to the present topic, a potentially key issue is the fact that he comes from a long-lived family, with an uncle who lived to age 107.

After taking up running again in his early 40’s, at first he merely jogged, but after he joined a club and became involved in competitive masters athletics, his training was largely track based and included demanding interval sessions. After his gold medal in the 1500m at age 48 in the World Veterans Championships in Hannover, he continued to train for track events though his 50’s and 60’s. In the 1995 World Masters championships in Buffalo, NY at age 64 he came 7th in the 5000m.  It is nonetheless noteworthy that a time of 4:46 for a 1500m in Toronto at age 66 confirmed that he still had quite impressive speed in his legs. But in his mid-sixties, after retiring from work, he turned his attention to the marathon.

As outlined above, for the majority of the past 16 years the central feature of his training has been multiple slow runs each week, typically building-up to 3 hours per session for at least 3 days per week . These long, slow sessions are complemented by quite frequent races over distances from 3000m to 10Km. This markedly polarised program has kept him at the pinnacle of veteran marathoning throughout that 16 year period, apart from the four years in which his training has been blighted by arthritis or injury.

He has generously shared a great deal of information about his training in his comments on multiple threads on the Lets Run forum over the years. A striking feature of his training is the care he takes to minimise stress.   Most importantly he maintains what he describes as a ‘glacial’ pace. He runs with a short stride, scarcely getting airborne, in order to minimise the impact at footfall. He trains in the Milton Evergreen Cemetery only a few blocks from his house so that he will be near to home should an injury develop.   He keeps to the level paths and in particular avoids the only short incline in the cemetery. He tolerates the monotony of repeated short loops around the paths of the cemetery in exchange for the advantage of avoiding protracted battles against headwinds.

Whenever he has had a break from training due to misadventure or injury he builds up very slowly, starting with runs as short as 15 minutes and building at a rate sufficiently gradual to avoid accumulation of fatigue from day to day. As a general rule, his only rest days are the days after a race, although he is not obsessional about training every day, if some other event intervenes.   It typically takes him many months, even as along as a year or more, to build up run duration to 3 hours

Similarities and Contrasts

Both Whitlock and Turnbull had taken a break for regular training after their student days and then in mid-adult life resumed regular training. Although Whitlock’s approach to track sessions were probably more systematic than Turnbull’s rather spontaneous approach, it appears that both benefitted from a substantial amount of quite intense training, leading to gold medals in veterans world championship in the 1500m; Whitlock in his late forties and Turnbull in his early fifties.

The marked contrasts emerged in their 60’s. Turnbull had his golden period in his early and mid sixties, setting world records across the full range of middle and long distance events. In those years he continued to work as a sheep farmer. He combined days of strenuous farm work with demanding training sessions. The remarkable lack of deterioration in his performances over 5000m, 10000m and marathon in the period from age 60 to 65 suggests that after his record breaking run in the Adelaide marathon at age 60 he had increased the volume of his training to a new level, with a greater focus on longer training runs, though I do not have any direct evidence for this.  Perhaps his relaxed spontaneous approach to training protected him from over-training during this golden period. By age 70 he was still competing creditably in international events, though no longer setting world marathon records.

In contrast, although Whitlock competed in his early and mid-sixties, he recorded few exceptional performances in those years. It was only after retiring from work and developing his training program based on multiple long slow runs each week that he blossomed as a marathon runner. He showed signs of things to come with his world single age record in Columbus, Ohio at age 68, but his greatest performance was his M70-74 world record time of 2:54:48. at age 73. He has continued to set world records into his eighties, not only in the marathon but in a variety of shorter events.  This year, at age of 84 he is struggling to achieve sustained training for a period of more than a few months, but nonetheless set a M84 single age world record in the 10,000m in September

There are few general conclusions that can be drawn from anecdotal evidence regarding two unique champions, though the similarities and differences do prompt some interesting speculations. However, before engaging in these speculations, it is informative to examine briefly the career of another marathoner who until recently appeared to have the potential to challenge the records of Turnbull and Whitlock: Yoshihisa Hosaka.

Yoshihisa Hosaka

I have described Hosaka’s training in some detail in a previous blog post. Like Turnbull and Whitlock, he had been a champion at regional level in his student days, but gave up running to pursue his talent for surfing in his twenties and returned to running in his thirties, initially in relatively short road races and then, from his mid-forties, in the marathon. At age 60, he set a new M60-64 world record of 2:36:30 in Beppu Oita, taking nearly 2 minutes off the record that had belonged to Derek Turnbull a few years previously.

The key feature of Hosaka’s training in those days was an unvarying daily schedule of two sessions, each of which included intervals at a pace which would be only moderately demanding in isolation, but in the context of a daily total of 32Km of running, contributed to a formidable weekly total volume and intensity. He fitted his twice daily sessions around an 8.5 hour working day as a businessman.     He included regular strength training to increase his defence against injury, and he argued that his unvarying daily schedule allowed him to monitor how well his body was coping with the training much more effectively than a program that alternates hard and easy days.

In 2013, four years after setting the M60-64 record, he ran 2:46:14 at the Gold Coast Airport Marathon in July, and then in November was frustrated by tightening of his leg muscles in the mid-stages of the Toronto Waterfront marathon, finishing in 2:50:44. Although it is unwise to read too much into two performances, these times were perhaps the first glimmering of evidence of accelerating deterioration as he approached his mid-60’s. Nonetheless, he planned an assault on Turnbull’s M65+ record in 2014. He won the M65-69 age group at the Gold Coast marathon but his time of 2:52:13 was well outside Turnbull’s record of 2:41:57, and he did not start in the Toronto Waterfront Marathon that year.


Figure 2: The decline in marathon performance of Whitlock, Turnbull and Hosaka. Apart from a minor ‘stutter’ at age 70, Whitlock did not exhibit marked decline until age 80; Turnbull exhibited a similarly marked decline in his late 60’s ; Hosaka shows a trend towards an even earlier decline. The data point at age 64 represents his time in the 2013 Gold Coast marathon.


This anecdotal evidence from the careers of Derek Turnbull and Ed Whitlock,and also that of Yoshihisa Hosaka, is consistent with the claim that it is very difficult to remain at the pinnacle of international performance as a distance runner for many decades.

In their student days, all three demonstrated that they were endowed with substantial talent, but it was only after they again took-up intense training a decade or more later that they came to prominence on the international scene. For all three, there were aspects of their life-style and training that probably provided some protection against injury and burn-out, allowing them to achieve great performances in their 60’s.

Perhaps it was Derek Turnbull’s relaxed spontaneous approach to training, together with the robustness engendered by his farming life-style that protected him in middle-age, though combining strenuous farm work with intense running on a whim creates a risk of excessive stress in the long term. In contrast, Hosaka’s disciplined and consistent training made it possible for him to judge accurately how well his body was coping, while his resistance sessions probably helped strengthen the connective tissues of his body. However, as with Turnbull, a life-style and training schedule as demanding as that of Hosaka carries a risk of eventual burn-out

Whitlock stands out on account of his longevity at the top. His family history of longevity makes it likely that genes played a crucial role.   But genes alone rarely shape outcome; it is highly probable that aspects of his life-style and training have also played a crucial role.   He has designed a program of training and racing that places a strong focus on avoiding stress as much as possible despite the very high volume of his training. The notable features are making the most of his retirement from work to devote his energies almost exclusively to running; a markedly polarised program with a very large volume of very low intensity running, augmented by regular intense racing; a very gradual build-up of training volume with a degree of day to day consistency facilitating a sensitive assessment of progress; and a training gait designed to minimise impact forces on his legs.

In my next post I will examine some of the scientific evidence about the role of genes, life-style and training, and the possible interactions between them in determining longevity as a distance runner.

What is the best way to increase lactate threshold?

September 20, 2014

There are five physiological variables that need to be trained in preparation for a good marathon:

  • VO2max – this measures the maximum rate at which oxygen can be delivered to tissues and hence the maximum rate at which muscles can generate energy.
  • Speed at VO2max.
  • Pace at lactate threshold as a proportion of pace at VO2max. For a well-trained marathoner, race pace is near to lactate threshold.
  • Ability to conserve glycogen so that glucose supply is not exhausted before 26.2 miles.
  • Resilience of leg muscles to sustain pounding for the duration of the marathon with only minimal loss of power.

These five variables are all trainable to at least some extent, though the first two are largely determined by genetic factors. These two variables set the ultimate limit on performance. The other three can be trained to the level where they no longer impose the limit. But nonetheless, the way in which any of them is trained is likely to affect the others, and hence the choice of training schedule must take account of all of the requirements.

As discussed in my previous post about the physiology of Paula Radcliffe, once you have dealt with any remediable defects of strength or form that impede your speed, if you want to push to the very edge of the limitations that your genes and/or the aging process have placed on VO2max and speed at VO2 max, the main focus of training should be on increasing pace at lactate threshold. Therefore in this post, I will address the question of how best to increase pace at lactate threshold, while minimising risk of injury and taking into account the need to ensure that none of the other four requirements are undermined.

Threshold training

The most obvious way to increase pace at lactate threshold is to do a lot of running near lactate threshold. This will encourage the development of the mechanism for transporting lactate out of muscles and for metabolising lactate in other tissues such as liver and heart, thereby not only conserving fuel but also minimising the accumulation of acidity. Thus lactate threshold will be pushed upwards to a faster pace. This is the approach that was employed by Paula Radcliffe, with striking success. I think it is highly likely that this is the approach can work well for many runners, at least in the short term, but there are dangers in this approach that limit its value.

The greatest of these dangers is undue accumulation of stress. This is likely to lead to sustained high levels of cortisol that damage tissues. Such damage not only decreases the ability to generate the power essential for achieving optimum speed at VO2max,but also decreases the resilience of muscles and increases risk of injury.   Furthermore, the impact forces at foot strike increase greatly with speed, so the direct physical trauma imposed on the legs is substantially greater during threshold training than low intensity training.  As shown in figure 1 (showing data reported by Peter Weyand and colleagues) the impulse transmitted through the leg (the product of average force  x time on stance) rises very rapidly as speed increases from low speed reaching a peak at typical tempo speeds and then actually decreases a little a higher speed due to decreased time on stance.  Since energy is consumed while force is sustained and muscle failure will occur when the required force can no longer be sustained, I suspect that impulse might be a better predictor of likelihood of damage than the magnitude of the force.  If so, tempo speeds are likely to be especially damaging.

Figure 1. Upper panel: the average vertical force (expressed relative to body weight) during stance as a function of running speed.  Lower panel: the vertical impulse (average force x duration of stance) transmitted through the leg during stance as a function of running speed.

Figure 1. Upper panel: the average vertical force (expressed relative to body weight) during stance as a function of running speed. Lower panel: the vertical impulse (average force x duration of stance) transmitted through the leg during stance as a function of running speed.

I believe that Paula Radcilffe achieved her phenomenal marathon record of 2:15:25 in 2003 not only because she did a lot of training at a pace near lactate threshold but also because she employed a strengthening program that minimised loss of power and provided some protection against injury. However, I also think that it is likely that in Paula’s case, her strategy did ultimately lead to injury that frustrated her hopes of Olympic gold. The question of whether or not she could have achieved her phenomenal run in London in 2003 without putting herself at risk of injury in the longer term remains unanswered and perhaps will remain unanswered until someone else breaks her record via a less stressful training program.

Low intensity training.

The alterative to relying on highly developed enzymes for metabolising lactate is minimising production of lactate. Lactate is produced when glucose is metabolised in the absence of a copious supply of oxygen. Fat metabolism generates energy via aerobic metabolism and hence is not able to meet needs when oxygen supply is seriously limited. However, provided there is some oxygen available, fat metabolism generates energy without the production of lactic acid because the pathway of fat metabolism leads directly into the Krebs cycle (as illustrated in my post of 5th Dec 2013). The rate at which energy is produced by fat metabolism is relatively slow, and therefore, for most athletes, fat metabolism is inadequate to meet the requirements in the upper aerobic zone. However, the capacity to generate energy by fat metabolism can be increased. Such an increase will not only help conserve glucose, but also minimise production of lactic acid when running in the upper aerobic zone.   Thus, increased ability to metabolise fat would be expected to raise lactate threshold such that a faster pace can be achieved at threshold. One way to promote the capacity to metabolise fat is to do a lot of running at slow speeds. This mobilises slow twitch fibres that preferentially utilise fat.

A large amount of slow running will also help develop the muscle resilience to cope with a long duration of running, though perhaps not the resilience required to maintain marathon pace for a long period. A schedule that consists entirely of slow running is unlikely to develop the neuromuscular coordination required to achieve a high speed at VO2 max, nor the coordination required to protect the muscles against damage at marathon pace. Furthermore, merely minimising the generation of lactate is not adequate for optimum performance, since once pace increases to the level where lactate does begin to accumulate, the accumulation will be rapid unless the ability to metabolise lactate is also well developed.. In addition, a large amount of slow running would also be expected to lead to sustained high cortisol levels unless the body is well adapted to long slow runs. So low intensity training alone is unlikely to be the answer.

Polarised training

We are faced with several competing demands: the need to raise lactate threshold without undue accumulation of stress, while also maintaining the neuromuscular coordination and power required to run fast. This suggests that some higher intensity training is required. The key question is whether it is possible to combine low intensity and high intensity training in a manner that achieves the advantages of both without each damaging the benefits produced by the other.

High intensity training (above lactate threshold) does actually enhance fat metabolism while increasing aerobic enzymes. Therefore, in itself high intensity training, at least in moderation, would not be expected to harm the benefits derived from low intensity training. High intensity training also enhances ability to metabolise lactate. In addition, high intensity training promotes release of anabolic hormones. However, the risk is rapid accumulation of stress. The greater impact forces at higher speeds increase the risk of physical trauma to muscles. Thus, high intensity training is potentially dangerous unless done judiciously.

On the other hand, excessive low intensity training might harm neuromuscular coordination required for faster running, but the contrast between the pictures of Ed Whitlock training in the Evergreen Cemetery and racing suggests that only a small proportion of higher intensity running is required to maintain the required neuromuscular coordination.

Thus, there is little reason for believing that a judicious combination low and high intensity training will be mutually antagonistic. The major issue to be addressed is avoidance of accumulated stress from both types of training. The accumulation of stress is probably best dealt with by gradual build up.

The question of how much high intensity training is required to develop adequate ability to metabolise lactate, or alternatively, whether at least some threshold training is required remains unanswered. The evidence from the training of elite athletes suggests that at least some threshold training should be included in the mix.

Cruise intervals

There is an alternative strategy for enhancing capacity to metabolise lactate: cruise intervals in which periods of running at or perhaps a little faster than lactate threshold pace alternate with recovery periods during which the lactate is cleared from the system. Jack Daniels advocated moderately long periods at tempo pace with short recovery to enable tempo pace to be maintained longer. It is likely that Zatopek’s legendary interval sessions were a variant of cruise intervals with the faster epochs appreciably faster than lactate threshold pace, as Ewen pointed out in his comments on my post about Zatopek in 2009. I find that I recover well from cruise intervals with moderately short effort epochs (e.g 6 minutes) a little above lactate threshold.


On balance, the evidence indicates that polarised training is best if one wants to achieve year on year development, or to slow the deterioration with age. But it remains unclear whether a strategy that produces year on year development will ultimately lead to one’s best possible performance. Alternatively, if one’s goal is to produce one’s best possible marathon without concern for longevity, might a large amount of threshold training be best? Is it better to flash with the brilliance of Paula Radcliffe in 2003 but burn like a meteorite, or is it best to glow with the unassuming brightness of Ed Whitlock, like Sirius in the night sky?

Perhaps Yoshihisa Hosaka will break Ed’s M70-75 record in a few years’ time providing evidence suggesting that Whitlock might have done better with more intense training. Perhaps some yet unknown female marathoner will eclipse Paula Radcliffe’s record after less stressful training. The future will answer these questions. But at least for the time being, my own evaluation of the evidence favours the polarised approach: a large amount of low intensity running to enhance fat metabolism thereby minimising the production of lactate in the upper aerobic zone, together with a small proportion of high intensity training and a similar proportion of threshold training, perhaps in the form of cruise intervals, to enhance lactate metabolism.

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.

A race on New Years Day

January 1, 2009

I run mainly because I enjoy primitive low tech interaction with the natural world, and also because I enjoy the occasional fleeting experiences of powerful efficiency when I get into a good rhythm. I also quite like the extra spice provided by racing – the challenge of achieving a personal best and the psychological contest with the other runners – though the battle is mainly with one’s own psyche. Last year I ran only two races and I have decided that this year I will run a few more races.

Today I set out for an easy 18-20Km run to Attenborough. Shortly after joining the riverside path heading northeast towards Clifton Bridge I could see a family – dad, mum and two young girls – on bicycles about 500 metres ahead of me. What better day than New Years Day to implement my plan for more racing, so the race was on. I didn’t know how far we would be racing, and the family were starting with two advantages: they were already 500 metres ahead, and they were on bicycles. However I also had two secret weapons: While I didn’t know whether the race would be over 3 Km, 5 Km or 10 Km, they didn’t even know they were in a race. Secondly, I knew that about 2Km ahead was the gate to a field that was home to two friendly horses. Sure enough, I overtook them in time to hear the younger daughter saying ‘Goodbye horsey’ while dad was pushing onwards toward the up-ramp to Clifton Bridge with a demeanour that said: ‘We’ll all freeze to death if we hang around here patting horses’ I strode into the lead up the long incline to the bridge, but about 600m later, coming off the down-ramp, dad and elder daughter whizzed past me at a speed I could not have hoped to match. I turned southwards along the river bank towards Attenborough while the family continued onwards towards Nottingham. I was still ahead of mum and younger daughter. So my first ‘race’ for the year could be considered a drawn match.

With regard to more serious races, although my current level of aerobic fitness is not great, I will stick to my plan to build up my speed to a moderate level in the near future and run a few shorter races in late winter or early spring, before settling in for some longer distance training in the summer and a half-marathon race in the autumn, with a ‘gold standard’ target of 96 min and a ‘silver standard’ target of 99 min.


Running and stress on the knees

In his comment on my blog about adjustments to my running style to deal with my knee problem, Andrew wondered whether he had enough patience and knowledge to adjust his running style to eliminate his knee problem. The human body is complex and each individual has a unique history, so tackling any serious musculoskeletal problem must start with individual assessment by a qualified professional. However, there are also some general principles of running style that can help reduce the stress on the knee. Adjusting running style requires some patience, but the challenge of mastering a skill can be in itself rewarding. With regard to knowledge, there is a lot of information available in books or via the internet, but if possible it is best to get a well-informed coach. The big challenge is finding the right coach, and it is probably best to do some searching of internet sources beforehand so that you can ask the right questions of a potential coach.

I did quite a lot of searching when I decided to adjust my own running style. There are quite a lot of modern schools of running technique. Reassuringly, they almost all agree on some of the key features for high performance, such as short time on stance, but they differ in regard to features that influence the amount of stress on the knee.

For example the Dutch BK method ( advises against substantial flexion of knee and ankle at footfall but instead favours a relatively rigid leg to maximise rapid recoil and minimise time on stance. This might be optimal if speed is your highest priority, but I suspect that it places a lot of stress on muscles and joints, and in my search for a technique that is kind to the joints, I decided that it was not the method for me.

On the other hand there are several modern methods that do favour a softer landing. These include Stride Mechanics, Evolution Running, and Pose. In my opinion, Stride Mechanics is the most soundly based of these methods, and Pose the least. Because I have a background in both physics and physiology, I decide to try to incorporate what I regarded as the most sensible of the ideas from these schools of thought (together with the ideas of Gordon Pirie) into a coherent framework based on the principles of physics and physiology. The current version of my synthesis is described in the series of articles under the heading ‘Running: a dance with the devil’ in the side bar of this blog. I cannot yet claim that I have proven that these ideas have led to an improvement in my own running, though they appear to have alleviated my knee problem. Furthermore, I cannot offer the type of guidance and support that a commercially developed package can offer.

Therefore, if you want a comprehensive package, I suggest starting with the material on the Stride Mechanics website ( and consider buying the book.

The most fully developed commercial package is provided by Pose, developed by Nicholas Romanov ( I have spent a lot of time exploring Pose and doing my best to put the method into practice. I have been on a two day course run by Nicholas Romanov. In those two days I was fascinated but also somewhat appalled by what I perceived as psychological tricks designed to convert us into disciples. However, I was also very impressed by the intuitive grasp of running mechanics of one of the Pose coaches present (Dr Mark Hainsworth) and I learned a lot from him.

My conclusions about Pose, after much reading, thought and practice, are:

1) It does reduce stress on the knee. This was confirmed in the study by Arendse and colleagues from Tim Noakes laboratory in Capetown (Medicine and Science in Sports and exercise 36(2):272-7, 2004)

2) The recommendation to land on the forefoot increases risk of injury to the Achilles tendon and calf muscles. This was apparently also observed in the Capetown study, according to Ross Tucker, one of the scientists involved (see (, but those findings were apparently never submitted for publication in a peer-reviewed scientific journal. In the 2004 edition of ‘Pose Method of Running’ Romanov has decreased the emphasis on forefoot landing, but many illustrations in that edition still show an exaggerated forefoot landing that creates a high risk of Achilles or calf injury.

3) The Pose principle that gravity provides the energy for forward propulsion is misleading. It implies violation of the law of Conservation of Energy. However, despite being misleading from the theoretical point of view, it might well have the desirable effect of discouraging unnecessary muscle action and thereby reduce the risk of injury. On the other hand, it might also discourage beneficial muscle action and therefore result in less powerful performance – in comparison with approaches such as the more muscular BK method.)

4) The Pose principle of landing under the centre of gravity (COG) is actually impossible to achieve while remaining upright, except in the presence of a substantial head wind, because if the foot is only grounded when beneath or behind the COG, the body will acquire an increasing amount of angular momentum in a forwards and face-down direction on every stride and a face-down crash within a few strides is inevitable. Nonetheless, trying to achieve the impossible goal of landing under the COG might in practice be helpful as it does discourage over-striding (reaching forwards with leg immediately before footfall, which is undoubtedly inefficient and injurious).

5) The available evidence indicates that in the short and medium term, Pose results in a decrease in running efficiency; that is, it requires more energy to maintain a given speed (See Although many elite athletes have experimented with Pose, as far as I can establish very few have substantially improved their performance after taking up Pose. The British triathlete, Tim Don is sometimes quoted as an example of a Pose success because his running performances improved during Romanov’s limited tenure with the British Triathlon team, but apparently Don no longer persists with orthodox Pose technique. In contrast, Debbie Savage (Australian 800m runner) continues to be enthusiastic about Pose and is a Pose coach.

6) Nicholas Romanov’s claim that the same technique can be applied irrespective of pace is misleading. When sprinting (or for that matter when running a 10K in less than 27 minutes) it is probably best to land on the forefoot without grounding the heel, but for a moderate standard marathon runner who takes more than 32,000 steps while running a marathon in 3 hours, it might be better to allow the heel to touch ground during each step to avoid repetitive strain injury to the Achilles tendon.

So, on balance, I would only recommend Pose if you can find a coach who understands its positive points, but is also aware of its potential pitfalls. But best of all would be a coach with an intelligent grasp of the strengths and weaknesses of all of these approaches to efficient running.

He could pass for a 62…

December 29, 2008 the dusk with the light behind him (with apologies to Angelina from Gilbert and Sullivan’s Trial by Jury, for the minor adjustment of age and sex).

It has been a year in which I have become increasingly aware of my age. The minor infirmities that were a mild nuisance in my youth have emerged from the shadows like drab spoil-sport harpies clawing at me and attempting to either suffocate me or hobble me. I am grateful that I can still run and have even enjoyed a few sublime running moments during the year, but more often I have been struggling with my wheezy chest or the fragile aching connective tissues that barely hold my frame together. So I was quite amused by a trivial incident during my run this morning.

I had set out with no particular plan other than to run as the mood took me. The northerly air stream that has swept over Britain during the Christmas period had abated to a mild breeze and swung from north to east bringing air from Siberia rather than the North Pole. Nonetheless, it was still quite bracing, and despite my recent debilitating episode of flu, I felt reasonably frisky. After crossing to the opposite bank of the Trent and heading southwards to Beeston, I decided that I would continue onwards to Attenborough Nature Reserve, a gaggle of lakes formed from old gravel pits and laced with a network of delightful paths. The point where the riverside path enters the Reserve is about 8 Km from home, so I was committed to a run of around 20 Km even if I only did one of the shorter lakeside loops. I was still feeling quite lively as I approached a man of about my own age pushing a bicycle. I called out hello and he responded: ‘Great weather for a run, kid’. I am not sure whether the ‘kid’ was ironic, or merely an indication of his failing eyesight, but I decided to take it as a compliment, and continued on my way with renewed friskiness.


Here is a picture taken during the Hardrock Challenge a few months ago. It was taken about a kilometre from the finish; at the point where I had pushed myself into the anaerobic zone to break free from the pack with whom I had been running in the mid-stages of the race. It is unclear whether the etched lines on my face are the furrows of effort or merely the wrinkles of old age. That race was probably the high point of my running year. The challenge for next year will be to train hard enough to improve without injuring myself or becoming ill.