The Longevity of the Long-distance Runner V : Whole Body Factors

April 16, 2016

In recent posts I have examined various the ways in which the body changes with age, with the aim of drawing some practical conclusions about lifestyle and training to maximize the chance of continuing to run well in old age.   After starting with anecdotal evidence drawn for the experiences and  the training of several of the world’s best elderly marathoners, and then examining some of the basic science, in the third and fourth articles in the series I addressed the effects of aging on heart muscle and on skeletal muscle.

However, the body functions as an integrated whole, due to the coordinating action of the nervous system and messenger molecules, such as hormones and cytokines, that circulate in the blood stream.  In this final article in the series I plan to examine ‘whole body’ factors that play a crucial role in how well we age.


Hormones: achieving a balance between catabolism and anabolism

Catabolic hormones, such as cortisol, promote the break down of tissues and the combustion of fuel to generate energy.  Anabolic hormones, including growth hormone and androgens promote the building up of tissues.

During distance running, cortisol plays an vital role in mobilising the glucose required to fuel muscle contraction, and  also to supply other crucial organs, especially the brain. However, the stress of regular training tends to create sustained elevation of cortisol thereby promoting a chronic catabolic state that favours the break down body tissues and might also impair immune defences.   A study by Skoluda and colleagues confirms that endurance athletes tend to have persistently high levels of cortisol. The increase is greater in those with higher training volume. Thus the regulation of cortisol is potentially of great importance, not only for ensuring that an athlete obtains benefits from training, but also for long term health

The balance between the beneficial role of short term increase in cortisol and the damaging influence of chronic elevation is illustrated in a study of distance runners by Balsalobre-Fernandez and colleagues. They measured salivary cortisol levels, neuromuscular effectiveness as indicated by counter-move jump height (CMJ) and various other measures throughout a 39 week running season..  As had been observed in previous studies, in this study CMJ was a predictor of an individual’s running performance, being highest before the season’s best and low before the season’ worst performance.  On a week by week basis, high cortisol correlated positively with CMJ height, but averaged across the entire season, there was a negative correlation between cortisol and CMJ height. In the short term, high cortisol is associated with good performance but in contrast chronic cortisol elevation is likely to impair performance.

Exercise, especially resistance exercise, also stimulates the release of anabolic hormones thereby promoting repair and compensatory strengthening of damages tissues, and helping restore a healthy balance between anabolism and catabolism.  With increasing age, the body becomes less responsive to anabolic stimuli and there is tendency for the balance to shift towards catabolism. Thus, for the elderly distance runner, avoiding excessive catabolism while promoting anabolism becomes important.

As illustrated in a study of older adults by Melov and colleagues, 6 months of resistance training can partially reverse muscle weakness, in parallel with a substantial reversal of the disadvantageous pattern of gene transcription and muscle protein synthesis associated with aging.

However it would be too simplistic to assume that artificially increasing the action of a specific anabolic hormone would lead to either longer life or greater longevity as a runner.  In fact there is only inconsistent evidence that levels of any one anabolic hormone are predictive of life-span.    The inconsistency of the evidence is probably due to the fact that hormones are subject feed-back control that moderates the effect of increase in level of a hormone, and furthermore there are complex interactions between hormones.  Nonetheless, the importance of addressing the tendency towards diminished anabolism with age is confirmed by the evidence that an overall decrease in anabolic effects due to a decrease of multiple anabolic hormones leads to shorter life expectancy and greater frailty.  For example, Maggio and colleagues found that low levels of multiple anabolic hormones are associated with increased and 6-year mortality in older men, while Cappola and colleagues  demonstrated that multiple deficiencies in anabolic hormones were associated with increased frailty in older women.

Growth Hormone

The inadequacy of augmenting a single anabolic hormone is illustrated well by the effects of altering levels of growth hormone.  Growth hormone is released by the anterior pituitary gland and acts on many tissues of the body to stimulate growth and cell regeneration.  It stimulates the liver to produce a messenger molecule, IGF-1 (Insulin-Like Growth Factor, type 1) that promotes hypertrophy while decreasing the formation of harmful free radicals and inhibiting cell death and slowing the atrophy of both skeletal and heart muscle (as illustrated in the figure).   It also raises the concentration of glucose and free fatty acids.  These multiple apparently beneficial effects initially led to enthusiasm for growth hormone supplementation as an anti-aging treatment.


Figure: The brain integrates information from the body and the external world, and when required sends signals to the pituitary gland at the base of the brain. The pituitary releases growth hormone which has multiple effects including stimulating the liver to produce IGF-1, which in turn stimulates repair and regeneration in muscle, bone and other tissues.

However despite some evidence of apparently beneficial changes, such as increased lean body mass and bone mineral density in elderly men reported by Rudman and colleagues, several meta-analyses that assembled the overall evidence from many studies failed to find clear-cut evidence of benefit.

Further light is cast on this paradox by evidence that in several species of animals ranging from nematode worms to mice, disruption of IGF signalling actually promotes increased life-span, by increasing the activity of several genes that promote longevity.   There is some evidence of similar effects in humans, especially among those reaching advanced old-age.  In a study of nonagenarians, Milman and colleagues demonstrated that low IGF levels were associated with increased survival in females.  Furthermore, in both males and females with a history of cancer, lower IGF-1 levels predicted longer survival.  It is possible that the observed beneficial effect of low IGF-1 levels on survival in humans is at least in part due to diminished cell production in individuals susceptible to malignant proliferation.

The paradoxical benefical consequences of diminished IGF-1 provide a strong warning against a simplistic approach based on supplementation of a single anabolic hormone.   Any such approach runs the risk of upsetting the balance in a finely tuned system of interacting hormone and messenger molecules.  However there are many ways in which we can promote the development of a beneficial balance between anabolism and catabolism by engaging the body’s more nuanced responses.  Exercise (especially resistance exercise); diet (rich in variety and with adequate protein); sleep (which promotes growth hormone release) and stress reduction (which reduces the sustained release of catabolic hormone) all shift the balance towards anabolism.


Damage produced by chronic inflammation

Inflammation is the cardinal mechanism by which the body repairs itself following injury.  It is also the mechanism by which many of the beneficial effects of training are achieved.  The stress of training induces microscopic trauma that triggers an inflammatory response that repairs and strengthens the body.  But chronic inflammation is harmful and plays a role in many of the diseases that that become more prevalent with increasing age, including diabetes, heart disease, stroke, cancer and Alzheimer’s  disease (reviewed in a readable article in U.S. News Health).

Within this series on the longevity of the long distance runner, we have already discussed the  adverse effects of chronic inflammation in the heart and in skeletal muscle.  While  many of the manifestations of inflammation are localised in a particular tissue, inflammation is mediated by messenger molecules that circulate throughout the blood stream and thus inflammation is a ’whole body’ issue.   Inadequate recovery from demanding exercise is likely to lead to circulating pro-inflammatory messenger molecules.   Although it is not proven, it is plausible that circulating pro-inflammatory messengers play a role in several of the harmful conditions that occur with increased prevalence in endurance athletes, such as asthma, cardiac rhythm disturbances, and more controversially, the increased atherosclerosis observed in elderly men who have competed in multiple marathon (discussed in my previous post in 2010),.

Diet can play an important role in increasing or decreasing the risk of chronic inflammation.  For example, omega-3 fatty acids tend to by anti-inflammatory while omega-6 fatty acids are pro-inflammatory. It is nonetheless important to re-iterate that inflammation has both beneficial and harmful effects, and in general, a healthy diet is a balanced diet.

As discussed in a more detail in a blog post in 2014, the three key things we can do to minimise the risk of damage are:

1)      Allow adequate recovery after heavy training and racing. Studies in animals and humans demonstrate that much of the fibrosis arising from chronic inflammation, resolves during an adequate recovery period.

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

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


Protecting our DNA

While variation in genetic endowment only contributes a minor fraction to the variation in longevity between individuals, our genes  nonetheless play a crucial in the functioning of the cells of our body throughout our lives.  The translation and transcription of the DNA strands that carry  the genetic code  generates  the RNA template required for building the proteins that are needed to sustain and repair bodily tissues.    Furthermore, the regeneration of cells via the process of cell division requires the duplication of the DNA so that each ‘daughter’ cell has the necessary complement of DNA. Thus the protection of the integrity of our DNA throughout our life-span is essential for repair and replacement of cells.

There are three main ways in which the integrity DNA can be compromised

  • Mutations, produced by radiation, environmental toxins or chance errors in duplication during cell division. Mutation change the sequence of the DNA base-pairs (A-T and G-C) thereby changing the code itself.  Mutations in sperm or eggs affect subsequent generations.  Mutation within other bodily cells are unlikely to have a widespread defect on the body, except in the situation where the mechanism that regulates cell division is damaged causing the affected cell becomes malignant.   A healthy immune system scavenges rogue cells that threaten to become malignant.  Moderate exercise and a well-balanced diet that promote a healthy balance between catabolism and anabolism help maintain a healthy immune system.


  • Certain locations on DNA are prone to undergo a chemical change known as methylation, in which a methyl group (-CH3) is attached to cytosine (the letter ‘C’ in the genetic code). Although this chemical change does not change the order of the DNA base-pairs and therefore does not change the genetic code itself, it can affect the readiness with which the DNA can be transcribed to produce protein when required. DNA methylation patterns change in a systematic way with aging.  Some of the variations are predictive of likelihood of dying within a given time-span.  So far there is no convincing evidence that change in specific DNA methylation patterns can extend lifespan.  Nonetheless, the rate of age-specific DNA methylation changes is dependent on a range of circumstances, including tissue inflammation; exposure to the stress hormone, cortisol; and nutrition. In a review of aging and DNA methylation, Jung and Pfeiffer conclude that intake of essential nutrients (including methionine, folic acid, and vitamin B12) involved in the metabolism of methyl groups, might be key factors in delaying the progressive deterioration of DNA methylation patterns, and hence may be important for healthy aging.


  • Each chromosome has a protective cap known as telomere at its end, but these telomeres become shortened as a result of repeated cell duplication. When the telomeres become very short, cell division can no longer occur and tissues can no longer be regenerated. However shortening of telomeres is not irreversible.  For example, Ramunos and colleagues report that RNA treatment of cultured human cells can produce lengthening of telomeres. Furthermore, Ornish and colleagues have reported  evidence indicates that telomeres can be lengthened by a balanced diet, exercise and stress reduction:


Overall, the evidence indicates that a balanced diet, exercise and stress reduction can help protect of DNA.  However the question of what constitutes a healthy diet remains controversial, The various different studies that have led to the conclusion that a healthy diet might protect DNA have differed in the details of the diet.  Nonetheless, the main features of a healthy diet are a modest amount of each of the major macronutrients (carbohydrates fats and protein) and a plentiful supply of diverse micronutrients (vitamins and trace elements).  In the elderly, utilization of dietary protein is less efficient the in the young, and a higher daily intake of protein is required


The Brain and its Mind

The forgoing discussion has emphasized the important of control of stress in promoting a healthy balance of anabolism and catabolism, minimization of chronic inflammation and protection our genes.   The central controller of stress is the brain and the mind it supports.

For the athlete, perhaps that most useful way to describe the role of the brain is in terms of the central governor.   The concept of the central governor was originally proposed by Tim Noakes to account for the observation that even when athletes exert themselves to their utmost, at the end-point there is still at least a small amount of energy in reserve.   This is illustrated by the fact than many marathoners can muster a sprint when the end is in sight despite being unable to increase pace when there is still a mile still to run.   It appears that the brain exerts a restraining influence to prevent us pushing ourselves into a dangerously stressed state.  This concept of the central governor as a controller that sets a limit on performance has been controversial.  An alternative view is that fatigue is determined by exhaustion of muscles rather than signals from the brain.  Whether or not all aspects of the concept as proposed by Tim Noakes are accurate, there is no doubt that the brain and its mind exert a strong influence not only over athletic performance, but over many aspects of how our bodies react to challenge.

It is almost certainly misleading to envisage the central governor as a small homunculus wearing a pilots cap and googles sitting in a cockpit located near the front of the brain with hand on the throttle to determine how fast we run.  In fact a network of circuits in the brain receive input from diverse regions of the body and from the external world, synthesize this mass of information and send messages not only to the muscles but to the endocrine glands that secret hormones and either directly via the nervous system or indirectly via hormones, to all organs of the body that determine how our body responds to the challenges currently facing it.    The way in which the brain syntheses the sensory information is guided by past experiences and by beliefs and goals.   I find it helpful to regard this network of brain circuits that integrate sensory information, past experience, belief and goals to generate messages that determine how our body responds to challenge as the central governor.

Training teaches us what we are capable of, but our beliefs also have immense capacity to influence the decisions of our central governor.    The power of belief in athletic performance is well demonstrated by numerous anecdotes; not least by the way in which Roger Banister’s sub-4 minute mile opened the gate to a stream (though not a flood) of subsequent sub-4 minute miles.  Belief also influences the way in which our bodies respond to training.   Crum and Langer informed a group of hotel cleaners that the work they did would make them fitter. Four weeks later they had lower blood pressure, less body fat and other signs of improved fitness compared with a matched group of colleagues who had done the same work but had not been advised about the health benefits of that work.   In medical practice, the placebo effect is one of the most powerful tools in the hands of a physician.

In the domain of aging, it is common to hear ‘you are only as old as you feel’.   This is a truism that might ring a little hollow in the minds of aging runners who observe the almost inexorable deterioration of their performances with the passing years.    However, despite the overall validity of the expectation that the passing years bring deterioration, we risk sabotaging our own prospects by accepting that year-on-year decline is an absolute certainty.  I find it helpful to hold in mind the fact that Ed Whitlock failed to break 3 hours for the marathon at age 70 but achieved the time of 2:54:48 at age 73.

With regards to the effect of age on general health, the evidence from the MIDUS study (a large study of Midlife Development in the U.S.) that higher perceived control over one’s life affects the expression of genes that modulate physical health.    Furthermore there appears to be a reciprocal relationship between mental and physical factors insofar as vigorous exercise promotes a sense of control over one’s life.  It is plausible that the reciprocal relationship between mental and physical adaptation to aging arises from the reciprocal relationship between adaptation to stress and metabolic efficiency mediated by nervous and endocrine systems.

Despite the strong evidence that the mind can exert an influence over matter, it is a challenge to find effective ways of enhancing our ability to harness this powerful influence.     My own experience has taught me that one effective approach is avoiding jumping to premature conclusions about the effects of aging, but instead examining the evidence, both scientific and anecdotal, and putting my predictions based on this evidence to the test in practice, bearing in mind that average outcome predicted for the entire population does not dictate the fate of the individual.


If we wish to maintain health in old age, and in a particular, extend our longevity as distance runners, we need to achieve an optimum balance between catabolism and anabolism; derive benefit from the repair and strengthening mediated by acute inflammation while avoiding the damage of chronic inflammation; and maintain our DNA in good condition.   A balanced diet; gradual build-up of training and good recovery after intense exercise; avoidance of undue stress; and maintaining confidence that we have control over our own fate all play a role in achieving these goals.

In previous articles in this series on longevity of the long distance runner, I have identified practical things that can be done to maintain the function of skeletal muscles and heart. In my next post I will provide a summary of the series, with a list of 12 recommendations for maximising longevity as a runner.

Longevity of a long-distance runner? Personal experiences

April 2, 2016

Before posting the final article in the series on the longevity of the long-distance runner, I will insert an account of my own recent experiences.  For the past year I had been planning a ‘heptathlon’ of activities for the week following my 70th birthday, in March this year.   It was a whimsical idea that had grown out of discussion on one of the social threads on the Fetcheveryone web-site for runners.  I did not intend to take it too seriously, but nonetheless, I did consider it a good opportunity to develop some new skills and broaden my range of cross-training activities, as part of an overall long-term goal to keep fit and active for as many years as possible.

I planned seven activities intended to test strength, power, balance, technical skill and endurance, with one activity each day, spread over the week. I set myself performance targets for the various events.  These were not intended to be extraordinary individual achievements for each event, but rather an overall test of my ability to achieve a modest level in a wide range of activities.

However my plans were seriously disrupted by a bicycle accident last July that left me with torn lateral ligaments in my left knee.   For several months I could not run at all.  The physio estimated recovery would take about a year and advised very gradual increase in activities.  During the final months of 2015 progress was very slow.  Nonetheless, I did establish that provided I ran slowly with a very short stride length to minimise impact forces, my knee could cope.  By the end of the year I built up to a level where I could run 10 Km slowly with few complaints from my knee.

At the end of December, I reviewed my heptathlon plan.  I decided it was feasible to attempt the heptathlon, but there was little prospect of achieving my former performance targets.  I therefore set some less demanding ‘B standard’ targets for the various activities.   The only activity that I had to change completely was the planned 100 metre sprint.  There was a serious risk that any attempt to sprint would jeopardise the recovery of the torn ligaments.  Therefore I replaced the planned sprint with a sprint on the elliptical cross-trainer.

My partially healed ligaments coped fairly well as I built up the volume of training for the various activities in January and February.  Surprisingly, cycling was the activity that caused the most pain in my knee, and I was forced to limit the amount of cycling.  Provided I continued to run with a very short stride length, running produced only occasional transient stabs of pain.   When I had set my B standard targets at the end of 2015, I had selected 20 Km as the target for the planned off-road run, as it appeared that this would be as much as I could reasonably expect my knee to cope with by March. In fact, by early February I was able to run 20Km without upsetting my knee, and by the end of February, I had done one long run of 39 Km.

I had also made good progress with most of the other events, and it appeared possible that I might be able to achieve the A standard targets  that I had originally set before the accident, in at least some of the activities.  Unfortunately, in early March my knee became a little more troublesome, making it necessary to cut back the volume of training to ensure that I would at least able to get the start of my planned heptathlon at the end of the month.  In particular I was unable to do any more longish training runs, and it appeared likely that lack of endurance would be an issue during the heptathlon.

A further scheduling issue created an additional problem.  I was scheduled to attend a two day academic conference in York in late March. When the conference dates were confirmed, it turned out to coincide with the first two days of my planned heptathlon.  Despite the anticipated lack of endurance, distance running is nonetheless my primary activity.   For the final heptathlon event, I had planned a 50K off-road ultra-marathon and this had to be on Easter Monday, so I could not defer the start.

Fortunately, the least demanding of the events, a test of balance that involved maintaining the Tree Pose, standing on one leg with arms extended above my head for 2 minutes on each leg, could be performed with minimal time commitment and at any location. I had originally planned that this non-demanding activity would be in the middle of the heptathlon to provide a recovery day, but I simply had to sacrifice the planned recovery day by doing this activity on the first day.  The second activity was a test of strength: the target was 5x100Kg barbell squats and 100 consecutive push-ups. Fortunately, I was able to do the push-ups in my hotel room before the second day of the conference and the barbell squats after returning home to Nottingham in the evening.

Once the first two days were behind me, the subsequent 5 days went very well, though there was an unexpected challenge on the final day.  Storm Katie swept across England on Easter Monday bringing high winds, heavy rain, sleet and snow, and causing quite a lot of damage.  For most of the first 20 Km of the 50 Km ultra I was struggling against a storm-force head-wind.  A few hours later, when running on the opposite direction, the fury of the storm had subsided, depriving me of the benefit of a strong tail-wind.  On numerous occasions throughout the run, I was sloshing through ankle deep water and mud.   I was very grateful that my friend Helen and her husband James joined me for a substantial part of the second half of the run.


Running beside Zouch Lock on the River Soar, with Helen, at 30Km (photo by James)

By the end I was utterly exhausted, more exhausted than I have ever been before, but very happy that I had completed the heptathlon.  I achieved six A standard and one B standard performance.  The performance targets and my actual achievements are shown in the table.


I had included two of the activities, the high jump and the swim, mainly because I wanted to learn the required techniques. As a youngster at school my friends and I sometimes did high-jumping during the lunch hour, using high jump uprights and bar in a corner of the school sports field.  We did not have a mat, so it was only feasible to do the scissors.  I did not have any special talent for jumping and my best performance in those days was only 3 feet 6 inches (106.7 cm).

About 10 years later, Dick Fosbury amazed the world by winning gold at the 1968 Olympics in Mexico City with his specular Flop technique.  The name ‘Flop’ is an appropriate description of the combined sideways and backwards somersault over the bar.  The thing that impressed me as a young physicist nearing the completion of my PhD was the fact that because the head and shoulders are already descending as the hips cross the bar, the centre of gravity is below the height of the bar at all times throughout the jump.   This appeared to be a magic trick.  However, by that stage of my life, I was a distance runner, so it did not occur to me to experiment with the technique myself at that time.

However, as I planned my 70th birthday heptathlon I recalled my previous fascination with the Flop and decided that I would learn the technique, with the aim of jumping higher that I had managed as a school boy about 57 years ago.   After the accident, the injury to my left knee forced me to change the take-off from my preferred left foot to the right. In addition, I had to restrict the run-up to a fairly slow approach of no more than 6 short steps to avoid stress on the left knee.  I was nonetheless delighted to clear 112 cm, a life-time personal best for the high jump by more than 5 cm.

Somewhat similarly in the case of swimming, despite learning to do the dog-paddle at age 6, in the subsequent 64 years I had only swum occasionally, usually for the purpose of enjoying being in the water, but I had not focused on technique.  I had no reason to learn how to coordinate breathing with my stroke, nor how to keep my legs from sinking.    Preparing for the heptathlon provided an opportunity to learn how to do the front crawl properly.

In fact swimming was the only activity in which I failed to reach my A standard, but I was nonetheless very pleased with the progress that I made with the technique.   I can now coordinate breathing-out while my head is under water and breathing in while the recovery of the arm on the breathing side passes close to my head, and I can keep my feet near the surface using a flutter kick from the hips.  At this stage, I feel I have mastered the rudiments of the technique.  The main thing I need to do in future is to make the action more automatic, allowing me to relax a little more, and swim comfortably for longer distances.

Overall, despite being a rather whimsical idea at first, the heptathlon has proven to be a very satisfying challenge.   Now, my most important goal is recovering my running speed, at least to the level near that I could achieve a year ago.  However, until my knee ligaments are strong, my stride length and pace will be severely limited.  I will have to be patient.  At least I have an interesting range of cross-training activities to help me sustain overall fitness without undue stress on my legs.

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 3: Cardiac Outcomes

January 10, 2016

After examining the anecdotal evidence provided by elderly marathoners and then grappling with some of the basic science underlying longevity in recent posts, it is time to attempt to draw some practical conclusions about what can be done to optimise longevity as a runner.   While the unfolding science of the molecular mechanisms by which our bodies respond to wear and tear offers intriguing prospects of identifying strategies for promoting heathy aging, there are at this stage more questions than answers. However we each live only once and if we want to optimise our chances of running fluently in old age, we must make the most of the evidence that is currently available. Despite the uncertainties, the evolving science provides a framework for weighing up the value of the lessons that might be drawn from the anecdotes.

But it is necessary to be aware of the pitfalls if we are too simplistic in our interpretation of the science. For example, at first sight the fact that catabolic hormones such as cortisol promote the break-down of body tissues to provide fuel for energy generation in stressful situations, suggests that avoiding sustained elevation of cortisol is likely to promote longevity. Indeed this conclusion might be valid in some circumstances, but it is not a universal rule. The strategy that is most successful for promoting longevity in animals is a calorie restricted diet. This works for creatures as diverse as worms, fish, rodents and dogs, and there is some evidence for health benefits in primates. The mechanisms by which it achieves its benefits include an increase in resistance to oxidative damage to tissues by virtue of more resilient mitochondrial membranes. However calorie restriction is stressful and promotes long term elevation of cortisol. It appears that animals actually need at a least a moderate level of ongoing stress to encourage heathy adaptation. The goal is achieving balance between stressful stimuli and adaptive responses.   The balance point depends on individual circumstances, and is likely to shift as we grow older.

The nature of training

The basic principle of athletic training is stressing the body in order to encourage it to grow stronger. One of the key mechanisms by which this is achieved is inflammation, a process by which damage to tissues generates a cascade of responses mediated by chemical messenger molecules that circulate in the blood stream, triggering repair and strengthening but also leaving a trail of debris.

There is abundant evidence that running increases life expectancy. In a 21 year follow-up study of elderly runners Chakravarty and colleagues at Stanford University found that continuing to run into the seventh and eighth decades has continuing benefits for both life expectancy and reduction of disability. Death rates were less in runners than in controls not only for cardiovascular causes, but also other causes, including cancer, neurological disorders and infections. Nonetheless, unsurprisingly, Chakravarty reported that although the increase in disability with age was substantially less in runners than in non-runners, the runners did nonetheless suffer increasing disability over the follow-up period. This is of course what would be expected if the processes by which training strengthens the body also leave a trail of debris.

If our goal is to increase not only life expectancy but also to achieve healthy aging and longevity as runners, we need to look more closely at the mechanisms by which running damages tissues. Ensuring longevity as a runner requires training in a manner that ensures that the accumulation of debris is minimised.

Healthy aging is a process affecting all parts of the body. Nonetheless, for the runner, the cardiovascular system, musculoskeletal system, nervous systems and endocrine systems are of special importance. There is a large body of evidence about how these systems age and about both the beneficial and the damaging effects of running on these systems.   I will examine the evidence regarding cardiovascular system in this post, and draw some tentative conclusions about how we might train to achieve healthy aging of the heart. In my next post I will examine the evidence regarding the musculo skeletal system, for which much more detailed information about cellular mechanism is available due to the feasibility of tissue biopsy. This will allow us to extend and consolidate the conclusions regarding optimal training for maximizing longevity as a runner.    In the final posts in this series I will turn my attention to the nervous and endocrine systems, and speculate about the way in which optimal training might impact upon health aging of those crucial systems.

Cardiovascular changes

Running produces both short term and long term changes in the cardiovascular system, some beneficial, some potentially harmful. I have discussed many of these changes in several previous blog posts (e.g. ‘The athletes heart’; ‘Inflammation, heart-rhythms, training-effects and overtraining’; ‘Endurance training and heart health, revisited’) and will present a brief overview here.

In the medium term (over time scale of weeks) regular training leads to an increase in blood volume. This increases venous return to the heart. The stretching of the heart muscle leads to more forceful contraction and a greater stroke volume. The cardiac output for a given heart rate is increased. Resting heart rate decreases and the heart rate required to run at a particular sub-maximal pace decreases.

In the longer term, the heart muscle is remodelled, with an increase in overall volume and in thickness of the ventricular walls. This condition is known as ‘athletes heart’. The mechanism is mediated by the intra-cellular signalling pathway that engages an enzyme known as Akt, which promotes growth of both muscle cells and capillaries. This is usually regarded as a benign physiological adaptation. The enlargement of the heart that accompanies pathological conditions such as high blood pressure or obstruction of the heart valves is also mediated by the Akt signalling pathway, but in contrast to the benign enlargement of the athlete’s heart, the Akt signalling is accompanied by inhibition of a growth factor required for the development of capillaries. Thus, in the athlete’s heart the enlargement is accompanied by adequate development of a blood supply to the heart muscle, whereas in pathological conditions the blood supply is usually inadequate.

However, in some athletes the enlargement might have adverse effects. There is compelling evidence that endurance runners with a long history of substantial training have an increased risk of disturbances of heart rhythm, including both ‘supra-ventricular’ disturbances such as atrial fibrillation, and potentially more lethal ventricular disturbances. The cause of these rhythm disturbances is not fully established but it is probable that the re-modelling of the heart muscle in a way that alters electrical conduction pathways plays a role.  It is likely that residual fibrosis at sites where damaged muscle has been repaired also plays a role by producing local irritability of the cardiac muscle cells leading them to fire spontaneously.

During intense prolonged exercise the strength of ventricular contraction, especially that of the right ventricle, is diminished, a condition known as Exercise-Induced Right Ventricular Dysfunction. If the exercise is sufficiently intense and prolonged, cardiac enzymes can be detected in the bloodstream, indicating a least temporary structural damage to heart muscle.

In a study of forty highly trained athletes competing in events ranging from marathon to iron-man triathlon, LaGerche and colleagues from Melbourne found transient weakening of the right ventricle immediately after the event. This was more severe the longer the duration of the event. The transient weakness returned near to normal within a week. However in 5 of the athletes, there was evidence of long term fibrosis of the ventricular septum, indicating chronic damage. Those with evidence suggesting long term damage had an average age of 43 and had been competing for an average of 20 years. Those without evidence of chronic damage had an average age of 35 and had been competing for an average of 8 years.   The evidence suggests that duration of endurance competition is a strong predictor of chronic damage.

Although an enlarged athlete’s heart usually has a much better blood supply than the enlarged heart associated with high blood pressure or obstruction of the heart valves, there is disconcerting but controversial evidence of excessive calcification of the arteries in at least some athletes, especially in males in who run marathons over period of many years. The mechanism is uncertain, though sustained inflammation is a plausible mechanism.

Effects of the amount and type of training

Although an overwhelming mass of evidence demonstrates that runners have a longer life expectancy and in particular, a lower risk of death from heart attack or heart failure than sedentary individuals, several large epidemiological studies raise the possibility that adverse health effects (especially cardiac events) tend to be a little more frequent in those who engage in a large amount of exercise than in those who exercise moderately. The US Aerobic Longitudinal Study examined the associations of running with all-cause and cardiovascular mortality risks in 55,137 adults, aged 18 to 100 years (mean age 44 years) over an average period of 15 years and found a marked decreased in both cardiac and all-cause mortality in runners compared with non-runners, but the reduction in mortality was a little less in those training 6 or more times per week compared with those training 1-5 times per week. The Copenhagen City Heart Study followed 1,098 healthy joggers and 3,950 healthy non-joggers for a period of 12 years and found that 1 to 2.4 hours of jogging per week was associated with the lowest mortality. These ‘moderate’ joggers had a mortality hazard ratio of 0.29 compared with sedentary non-joggers.

But closer look at the evidence reveals a potentially informative detail. In a study of heart health of over a million women, Miranda Armstrong and her co-investigators from Oxford  found that among obese women, those who did a large amount of exercise suffered more heart problems than those who did a moderate amount. However, in contrast, among the women who had a Body Mass Index less than 25, those doing a large amount of exercise had fewer heart problems than those doing a moderate amount of exercise.   This suggests that if there is a risk in doing a large amount of exercise, it is mainly confined to those for whom the exercise is excessively stressful due to other risk factors that shift the balance towards harm rather than benefit.

Although the evidence from the large epidemiological studies remains a topic of debate because of issues such as possible bias in participant selection and the relatively small numbers of individuals in the category who take a very large amount of exercise, I think the balance of evidence does indicate that at least some individuals who take a large amount of exercise do have an increased risk of death, including death form cardiac events, within a given time period.   In my opinion, the important question is what determines which individuals will be harmed by a large amount of exercise, and whether there are ways in which we can minimise the risk of harm.

There is evidence that adequate prior training can protect against damage.   Neilan and colleagues studied non-elite marathoners runners completing the Boston Marathon and reported that right ventricle weakness was more pronounced in those who had trained less than 35 miles per week compared with those who had trained more than 45 miles per week.   The logical conclusion from studies such as the Oxford study of obese female runners and Neilan’s study of marathoners is that running in a manner that exceeds the individual’s current ability to cope with the stress increases the risk of damage.   This in turn suggests that building up gradually in a manner that ensures that training sessions are never excessively stressful is likely to be the safest approach.

Furthermore, it is likely that lack of adequate prior training or obesity are not the only factors that impair the ability to cope with the stress of demanding training and racing. Following a very demanding marathon or ultra-marathon, the evidence of damage remains detectable for a period of weeks. It is plausible that demanding training when the heart is in a weakened state will compound the damage. It is widely accepted in practice that recovery following intense racing or heavy training is crucial, but unfortunately there is relatively little scientific evidence addressing the question of whether or not the adverse cardiac effects of intense exercise resolve during a recovery period, or conversely, whether the adverse effects are compounded by repeated bouts of exercise.   We must therefore turn to evidence from studies of rats.

Benito and colleagues exercised rats on a treadmill for 60 minutes at a quite vigorous pace of 60 cm/s (achieved after 2 weeks of progressive training) 5 days per week for a total of 4 weeks, 8 weeks or 16 weeks. For a rat, 16 weeks of life is roughly equivalent to 10 years for a human. During the first 8 weeks there was relatively little evidence of damage, but prominent signs of damage emerged between 8 and 16 weeks. After the 16 weeks of exercise, the rats exhibited hypertrophy of the left ventricle and also the reduced function of the right ventricle, similar to the findings reported in humans. Furthermore the rats had marked deposits of collagen in the right ventricle, and messenger RNA and protein expression characteristic of fibrosis in both atria and the right ventricle. The exercised rats had an increased susceptibility to induction of ventricular arrhythmias. A sub-group of the rats were examined after an 8 week recovery period following the 16 weeks of exercise. Although the increased weight of the heart had not fully returned to normal level, all of the fibrotic changes that had been observed after 16 weeks of exercise had returned to the normal level observed in sedentary control rats. Thus, at least in rats, the adverse potentially arrhythmigenic changes produced by intense exercise over a 16 week period appear to be reversible after an adequate recovery period.    Thus the best available scientific evidence does support the accepted principle that recovery following intense racing or heavy training is crucial.


Proposed cardiac outcomes of long-term training. The size of the ellipses indicates cardiac fitness at each stage; colour indicates balance between recovery (blue) and stress (red)

In summary, the evidence regarding the cardiovascular effects of running suggests the following guidelines for healthy aging and longevity as a runner:

  • Continuing to run regularly, at least into the seventh and eight decades decreases risk of death and disability.
  • Training volume should be built up gradually.
  • Adequate recovery after demanding events, such as a marathon (or indeed, even after heavy training sessions) is likely to be crucial.

My next post will examine the evidence regarding the effects of training on the musculoskeletal system, and will both consolidate and extend these conclusions.

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.

Emulating Ed Whitlock’s training: a follow-up

November 29, 2015

Over the past two years I have written on several occasions about the training of Ed Whitlock, without doubt the greatest elderly distance runner the world has ever seen; the first and only 70 year old to run a marathon in less than 3 hours and holder of the age-group world marathon  records for ages M70-74, M75-79 and M80-84, together with the M80-84 world records for  1500m, 3000m, 5Km, 10Km, 15Km and half-marathon,  and numerous other records.  While may factors, including genes for longevity and intense training in early middle age probably contribute to this phenomenal ability, the striking feature that sets him apart from all others is his approach to training: he runs for up to 3 hours per day at a slow pace, many days a week, and in addition, races fairly regularly over distances ranging for 3000m to 10,000m. His overall training program can be regarded as the ultimate in polarised training.

Whitlock himself makes no special claims for his training, other than noting that it works for him.  Apart from having an uncle who lived to age 107, there little that is remarkable about his background or his physiology that might explain his phenomenal distance running ability.  When assessed at age 70 he had a VO2 max that was high for a man of his age, but consistent with his running performance.    A high VO2 max might be a consequence of training and/or genes.

The fact that he won the M45 world masters 1500m championship in 4:09 at age 48 makes it likely that his VO2max was already relatively high very early in middle-age.  At that stage his training included a substantial number of intense track sessions.  It is therefore unlikely that his VO2max at age 70 can be attributed entirely to the nature of the training and racing that he has done since his late 60’s.

He has maintained this polarised pattern for more than 15 years, apart from several instances in which misadventure or injury have demanded quite long periods of recovery, during which he has re-built training volume slowly.   Whatever the contributions of his genes and the training earlier in his career, the long duration of his current pattern of training and racing does indicate that this current pattern has succeeded in maintaining his extremely high level of performance into his mid-eighties.  It is therefore potentially worthwhile for other elderly distance runners to explore the possibility that it might work for them.

About 18 months ago, I set out to emulate the major features of his training program, aiming for at least three long slow runs each week, gradually increasing the duration from 60 minutes to 120 minutes over a period of 3 months.  As I still work and have limited time available, I was obliged to do two of my long runs on the week-end and therefore had little opportunity for the intense racing that was part of Ed’s program.  I was also aware of the need to avoid placing undue stress on my left knee that had bene damaged in an episode of acute arthritis a few years ago.  I therefore replaced Ed’s intense racing with intense sessions of 30-50 minutes duration on the elliptical cross trainer.

Over a three month period I was able to build up the duration of long runs with no difficulty. I enjoyed not only a clear increase in endurance but also developed a substantial capacity to metabolise fat, most noticeable from my ketotic breath at the end of long training runs.  However the improvement of my aerobic capacity, assessed by calculating beats/Km recorded over similar terrain, was only modest.  I was a little disappointed by this modest gain, and also a little disconcerted by early signs of accumulating fatigue in December.  Nonetheless, I considered that progress at that stage was satisfactory, and was looking forward to a spring marathon.

However a problem that I should have foreseen developed over the winter.  I have long standing asthma that is usually relatively mild, though it is exacerbate by cold air.  I also tend to suffer from various side effects of my asthma medication, and have had little success form changing to different medications.  I therefore need to limit the dose.  Inhaling cold winter air for periods of several hours during my long runs triggered marked constriction of my airways.  To add to this, beginning in mid-December, I suffered a series of quite severe upper respiratory tract infections that exacerbated my breathing difficulties.  I was forced to defer my Whitlock style training until the spring.  By March my fitness had deteriorated quite markedly.  Once again I began the gradual build-up  of long run duration.  Progress was slow, but nonetheless, I set my sights on an autumn marathon.

During a long run with my marathon running sister-in-law, Mary, in the Border District of Scotland in April

During a long run in the Borders District of Scotland in April with my marathon running sister-in-law, Mary, who took the photos


Like Ed Whitlock in training, I adopted a short stride and high cadence to minimise impact damage to my legs.

Like Ed Whitlock in training, I adopted a short stride and high cadence to minimise impact damage to my legs.

Then in July disaster struck.  I suffered quite a nasty fall from my bicycle when the front wheel got stuck in tram–tracks that I need to cross at an oblique angle on my daily commute to work. I hit the ground very hard, producing spectacular bruising at every protruding point on the right hand side of by body from knee to forehead.  For several weeks, one side of my face was stained, at first purple and then yellow, along the path where a broad tide of blood had tracked beneath the skin.  The initial concern of the two nurses who rushed to my aid at the scene of the fall had been the possibility of serious head injury, but in the longer term, after the bruises had faded, it turned out that the most troublesome injuries were to my left knee and right elbow.     I had torn lateral ligaments of my left knee, and also damaged the attachment of tendons at my right elbow.  Even now, five months later, both of these injuries limit my movements.  The physio anticipates it will be a year before the knee has recovered.

For several months I could not run at all, but over the past two months I have been cautiously rebuilding once again. In recent weeks I have increased the length of my ‘longish’ runs up to 10Km.  The most dismaying feature is that I cannot cope with paces any faster than 10 minutes/mile.  While the crucial limitation is the knee, I am also appalled by how unfit I have become.    I remind  myself that Ed Whitlock has on several occasions taken almost year to get back to fitness after an injury.   In fact Ed has scarcely raced at all this year, subsequent to an upper thigh/ groin injury that he suffered last year.   For two successive years he has missed the Toronto Waterfront Marathon – an event in which he had set a single age world record on six occasions during the preceding decade. However, despite failing to be on the starting line for this year’s marathon, he did set an M84 single age 10K World Record of 49:08 in the Longboat Island Race in September.

I have no expectation of setting any records, but I fear that even after making generous allowance for the expected slow recovery from my illness last winter and my injury in the summer, I am suffering an alarming deterioration in my overall physical condition.  I suspect that I do not have good genes for longevity. In my next post I will examine the evidence regarding genes for healthy aging.

But whatever my prospects for the longer term future, I am now focused on rebuilding my endurance.  Despite the limited evidence that a Whitlock style program is the best way for me to build aerobic fitness, my experience so far does indicate that it is a good way to build endurance.  As this is my immediate goal, I am again using a modest version of a Whitlock style program.   At present, three runs per week, each of an hour in duration, is about all my body can cope with.  Promoting recovery of my knee ligaments and also vigilant deployment of my inhaler to minimise the constriction of my airways during winter training runs will be equally high priorities. I will not set any marathon target for the near future.   I am playing with the idea of setting targets for a ’heptathlon’ of physical activities, including not only running but also some other challenges to be completed in the week of my seventieth birthday in March.   I will defer specifying the specific targets until I establish how my recovery progresses in December.

The dream of capturing the force of gravity for forward propulsion: re-incarnations of Pose

November 15, 2015

The beguiling dream of capturing the force of gravity to assist forward motion when running has re-emerged in recent months.  There have been two recent re-incarnations of the dream.  Both attempt to overcome the problems of the Pose technique that had attracted enthusiastic followers but also critical analysis in the past decade.   I discussed the benefits and problems of Pose in some detail on this site five years ago.   The more recent versions avoid the unrealistic claim implicit in the Pose mantra ‘Pose, Fall, Pull’ that the Centre of Mass (COM) actually falls between mid-stance and lift-off from stance.  This claim is simply contrary the evidence that the COM rises after mid-stance.  This rise can easily be observed in video recordings of elite and recreational runners.   Both of the recent versions of the theory accept this.

Nonetheless in common with Pose, the recent versions are both based on the argument  that when the COM is ahead of the point of support in late stance, there is a torque acting on the body that tends to produce head-forwards and downwards  rotation.  Unfortunately neither of the new versions adequately addresses the fact than an oppositely direct torque acts prior to mid-stance, and both under-estimate the importance of the push that is required to overcome the braking that occurred during early stance and to get airborne.

Although both theories are flawed and neither provides grounds for claiming that gravity provides energy for forward propulsion, both provide a pointer to  cues that might perhaps help a runner improve efficiency and decrease risk of injury.   It is therefore potentially worthwhile to examine them in greater detail. However, if you are more interested in the practical conclusions than the detail, you can skip to the final section

Kanstad’s Model

Svein Kanstad a Norwegian coach has teamed up with an academic physiologist, Aulikki Kononoff, from University of Kuitpo in Finland to test and publish a creative new version of the hypothesis that gravitational torque acting after mid- stance can drive horizontal motion.  As in the theory of Pose, they argue that due to the forward inclination of the body after mid-stance, there is a component of gravity that drives a head forward and down rotation, as illustrated in Figure 1.

Figure 1. Forces acting after Mid-Stance. GRF = Ground Reaction Force. Force C1 directed along the line of action of GRF propels the body forward and upward. Force C2, at right angle to GRF produces a torque which promotes head-forwards rotation around the point of support

Figure 1. Forces acting after Mid-Stance. vGRF = vertical Ground Reaction Force; hGRF= horizontal Ground Reaction Force.  Force C1 directed along the line of action of total GRF propels the body forward and upward. Force C2, at right angle to GRF produces a torque which promotes head-forwards rotation around the point of support.  Illustrative numerical values are based on the model I presented on this site in 2012

Kanstad’s theory is somewhat more sophisticated than Pose theory, insofar as he recognises that the leg extends during late stance so that there is no net fall of the centre of mass after mid-stance. Because of the leg extension, the situation is a little more complex than portrayed in figure 2 of their paper, which depicts a body rotating about a fixed point of support, with fixed length from point of support to COM.  In reality, the distance from point of support to COM increases as the leg extends, thereby changing the moment of inertias (i.e. the body’s resistance to rotation) and furthermore, the point of support moves forwards in late stance.  Nonetheless as discussed in the extensive comments section of my article ‘Running: a Dance with the Devil’, computation based on a reasonably realistic model confirms that angular rotation in a head-forwards direction does occur after mid-stance.

Kanstad and Kononoff accept that both energy and angular momentum must be conserved, in accord with the laws of physics.  They argue that the angular momentum imparted in late stance is preserved during the airborne phase and then converted to forward linear motion at the next footfall, analogous to the manner in top-spin imparted to a tennis ball causes the ball to accelerate forwards as it rebounds off the ground.

In other words, instead of simply claiming that gravitational energy is captured by falling after mid-stance, they argue that gravity generates angular momentum as the body rises, and the associated head-forwards rotation of the body is converted to forward linear motion at the next footfall.

There are two flaws in their argument.   First of all, while they state that the rotational motion imparted after mid-stance might provide propulsive power at the next footfall, they do not address the question of where the energy associated with this rotation comes from.  It has certainly not been provided by gravity because the body actually rises after mid-stance.  Gravity extracts kinetic energy from the body during this phase. When averaged over the entire gait cycle, the net contribution from gravity is zero.

The energy associated with the rotation imparted during late stance comes largely from a redistribution of the kinetic energy existing at mid-stance.   A small fraction of the energy associated with forward motion of the body is transferred to the rotation.   Rotation acts as a temporary store of energy derived from an energy source other than gravity.

With regard to determining the energy requirement of running, the re-redistribution of energy within the three interchangeable energy pools (kinetic, gravitational and elastic) does not result in any net increase in total energy over the gait cycle.  There is however a loss of energy from these three pools due to several processes that dissipate energy.  There is loss due to friction within the tissues of the body; loss due to air resistance; loss to due to failure to capture all of impact energy at footfall and loss of energy due to the braking that occurs during early stance.   When running at constant speed, these losses are made-up by active contraction of muscles that consumes metabolic energy.  Any suggestion that rotational energy derived from gravity might be a source of propulsive power is false.   Muscle contraction must meet the costs, and the key issue in maximizing efficiency of running is minimising the losses.

Kanstad and Kononoff recommend that the runner should land with the foot as nearly under the COM as possible.  They point out that this would decrease the amount of head-backwards rotation that might otherwise detract from the proposed (but illusionary) advantage of head forwards rotation.   However, the second flaw in their argument is a serious under-estimate of the amount by which foot must be ahead of the COM at footfall.

The laws of physics demand that the foot must be placed appreciably ahead of the COM.  Apart from the instant when the COM is directly above the point of support at mid-stance, the COM must be either before or behind the point of support throughout stance.  The line from COM to point of support is angled either  forwards when COM is behind the support producing a braking effect, or backwards when the COM is ahead of the point of support, producing forward and upwards acceleration (as shown in Figure 1).  If there is no net change in pace over the gait cycle, the forward acceleration generated by the push when the COM is ahead of the point of support must be equal to the deceleration due to braking (if we ignore the effect of air resistance).

It would only be possible to abolish braking while landing with the foot under the COM if the duration on stance was zero, but this would require an infinite vertical ground reaction force. If there is to be no net generation of momentum in an vertical direction averaged over the gait cycle, the upwards impulse generated by upwards ground reaction force (GRF)  during stance must equal the body weight which acts downwards over the entire gait cycle.   Thus the average value of vertical GRF is body weight divided by proportion of the gait cycle on stance and this approaches infinity as duration on stance approaches zero.  Therefore the foot must be on stance for an appreciable time.  While on stance there must be appreciable but equal amounts of acceleration and deceleration.  The deceleration occurs when the point of support is ahead of  the COM between footfall and mid-stance.  Therefore, the foot must land an appreciable distance in front of the COM.

Where should the foot land?

Although the issue of rotation is of trivial importance, the question of where the foot lands is actually of vital importance because it determines braking costs.  It therefore warrants careful consideration.  While the forward acceleration generated when the COM is ahead of the point of support must equal the deceleration occurring when the COM is behind, the proportion of stance time spent with the COM ahead of the point of support is not necessarily equal to the proportion when COM is behind the point of support, because the cumulative effect of acceleration or deceleration are determined by both duration and magnitude of the force. The force tends to be greater in early stance because there is substantial tension in the leg at footfall to prevent the knee buckling.  Force plate data confirms the rapid rise in ground reaction force immediately after footfall.  As a result, the duration between footfall and mid-stance is less than that between mid-stance and lift off, even though the net transfer of linear momentum over the gait cycle is zero when running at a steady pace.

Observation confirms these theoretical predictions. For example Cavagna and colleagues reported measurements of the braking time and the acceleration time during stance in sample of 10 runners at various speeds.  At 10 Km/hour (2.8 m/sec) the average braking time was 0.125 sec and the acceleration time was .145 sec.  From these numbers it can easily be shown that on average the COM advanced 35 cm from footfall to mid-stance (i.e. the COM was approximately 35 cm  behind the point of support at footfall) and at lift-off it was  40 cm ahead of the point of support. (Note that to be precise we need to know how much the point of support moved forwards during stance but allowing a small movement of the point of support would make only a small change in these estimates of distance travelled during braking and acceleration.)

Cavagna  also reported that the difference between braking time and acceleration time diminished as speed increased.  This is almost certainly because at greater speed it is necessary to exert a stronger push against the ground after mid-stance, thereby reducing the difference between forces exerted during braking and acceleration phases.  Cavagna reported that braking time and acceleration time were equal at paces above 15Km/hour.    At 15Km/hour (4.15 m/sec) braking time and acceleration time were both 0.1sec. Thus the COM advanced by 41.5 cm in each half of the stance period.

However Cavagna provided no indication of the competence of these runners.    His runners did not necessarily achieve optimal placement of the foot. Would they have been more efficient if the foot had landed less far in front of the COM leading to a shorter time on stance and less braking?

The key question is: what is the optimum time on stance? It is necessary to bear in mind that while less time on stance decreases braking costs, the need for a relatively longer airborne time demands a more powerful push, creating not only greater stress on the legs but also greater loss of energy at impact, as only about 50% of impact energy can be captured as elastic energy, so an extremely short time on stance is likely to be inefficient.

In the study of Weyand, in which nine of the 10 runners studied were competitive athletes, all except one of the 10 spent appreciably less time on stance, at comparable paces, than the average runner in the study by Cavagna.  As they approached their top speed, all of Weyand’s runners decreased time on stance towards a limit of 0.1 sec (total for both acceleration and deceleration).   It is possible that 0.1 sec on stance is the optimum duration for efficient capture of impact energy as elastic energy.

The shorter stance times achieved by the runners studied by Weyand suggest that on average Cavagna’s runners spent too long on stance for optimum efficiency.  Possibly they simply lacked the power to get airborne, but it is also possible that a mental focus on landing with the foot more nearly under the body might have helped reduce stance time.  While the recommendation of Kanstad and Kononoff  (and many other coaches) to land with the foot as nearly under the COM as possible is advice to aim for something impossible, it is nonetheless is likely to be a useful cue for runners who tend to spend too long on stance.

The Virtual Pivot Point Model

The second these recent versions of the ‘gravitational torque’ theory  is the Virtual Pivot Point (VPP) model described by Mick Wilson in a post on 15th Oct 2015. on Lee Saxby’s  ‘Born To Run’ web- site.   Mick Wilson is a Senior Lecturer in the Department of Sport and Exercise Sciences at Northumbria University

A key feature of the VPP model is that the tension in the muscles of the trunk, especially the hip extensors and flexors is adjusted to ensure that the ground reaction force is directed along a line joining the point of contact of foot with the ground to a fixed point (the VPP) high in the runners torso (Figure 2).   During early stance, when the point of support is ahead of the VPP the direction of action of GRF is upwards and backward.  The torso is tilted forwards a little due to the momentum of the torso when the forward movement of the foot is arrested. The hip extensors act to prevent buckling at the hip.  By late stance the direction of action of GRF is upwards and forwards.  The torso now tends to incline backwards relative to the thigh and the hip flexors contract to resist this. The action of hip extensors in early stance and flexors in late stance stabilises the body, preventing it buckling at the hip, and keeping it upright.  It is reasonable to propose that these actions of hip extensors and flexors play a cardinal role in keeping the body upright.

Figure 2. The Virtual Pivot Point Model. The combination of gravity and GRF results in a force acting along the line of GRF and a component at right angles to GRF which exerts a rotational effect. VPP = Virtual pivot point; COM = Centre of Mass; GRF = Ground Reaction Force. In early stance, the force aligned with GRF arrests the descent of the body and also has a braking effect, while the ‘rotational’ component at right angles to GRF creates a head-backwards rotation. In late stance, the force aligned with GRF propels the body upwards and forwards, while the ‘rotational’ component at right angles to GRF creates a head-forwards rotation.

Figure 2. The Virtual Pivot Point Model. The combination of gravity and GRF results in a force acting along the line of GRF and a component at right angles to GRF which exerts a rotational effect. VPP = Virtual pivot point; COM = Centre of Mass; GRF = Ground Reaction Force.
In early stance, the force aligned with GRF arrests the descent of the body and also has a braking effect, while the ‘rotational’ component at right angles to GRF creates a head-backwards rotation.
In late stance, the force aligned with GRF propels the body upwards and forwards, while the ‘rotational’ component at right angles to GRF creates a head-forwards rotation.

Furthermore, the variation of inclination of torso relative to hips from a slight forward lean in early stances results in the direction of action of GRF passing forwards of the COM to pass through the VPP, in early stance, while it passes behind the COM in late stance to the same pivot point in upper torso in late stance.  Although in the VPP model the line of action of GRF does not pass through the COM (as was assumed by Kanstad and Kononoff), the direction of action of GRF is nonetheless upwards and forwards in late stance.  As in the Kanstad model (and also in the Pose model) there is a torque that tends to produce acceleration in ahead forward and down direction during later stance.  Similarly, an oppositely directed rotation will be generated when the COM is behind the points of support in early stance. The main difference between the models is that at any particular point in time after mid-stance, the inclination of GRF is a little less forwards that would be the case in the Kanstad and Pose models.

Unlike Kanstad, Wilson makes no attempt to explain how this rotation might be converted to forward motion.  Furthermore, Wilson does not specifically claim that the head forward rotation induced after mid-stances exceeds the head-backward rotation induced before mid-stance.   However these limitations do not matter, because, as in the Kanstad model, gravity can provide no additional energy while the COM rises after mid-stance.  The energy associated with any rotation generated by gravitational torque after mid-stance is largely derived by redistribution of the energy in the pool of kinetic and elastic energy existing at mid-stance.  There is one slight difference.   In the VPP model, the direction of action of GRF is long a line that passes behind the COM.  If this is in fact the case, the active contraction of muscles responsible for generating GRF will contribute directly to the energy associated with rotation.     But gravity does not contribute.

Another misleading feature of Wilson’s account of the VPP model is his claim that the forwards and upwards GRF is generated purely by elastic recoil, so that an active push is not necessary.  This could only be the case if the kinetic energy associated with downward movement at footfall could be captured as elastic energy and subsequently released with 100% efficiency.  In fact, only about 50% of the kinetic energy of downwards motion at footfall can be recovered.  Although Wilson acknowledges the fact that the COM rises after mid-stance, he actually appears to deny that any active muscle contraction is required to generate GRF.  Thus he very seriously underestimates the work that must be done when running.  But could this under-estimate be a virtue? This question leads us to the issue of what useful lessons might be learned from these two recent versions of the gravitational torque theory.

What useful practical lessons might be learned?

Why does the claim that gravity provides forward propulsion continue to attract attention?  Many recreational athletes appear to benefit from the mental image created by the notion that gravity provides forward propulsion.  As mentioned in my discussion of the theory of Kanstad and Knononoff, at least part of the benefit comes from the encouragement to land as nearly under the COM as possible.  Although impossible to achieve, this advice discourages over-striding and tends to promote a short time on stance.   However, the advice to land nearly under the COM is not specific to theories claiming that gravity provides forward propulsion.

In a more subtle way, the illusion that gravity might provide propulsive power tends to discourage a conscious focus on pushing against the ground.   A short time on stance is only possible if there is a strong push, but perhaps paradoxically, for most athletes, conscious focus on the push is counter-productive.   It is likely to lead to delay on stance – the opposite of what is required.  Effective push-off from stance requires precise timing.   For most runners, this precision is best achieved automatically.   A cue that minimises potentially harmful conscious interference with the precision of  timing is likely to be beneficial.

While a cue that promotes an automatic rapid lift off from stance is likely to be beneficial, I would prefer to employ a cue that is based on sound science rather than one based on illusionary theory.   One consequence of spending a short time on stance is a relatively long airborne time associated with a relatively large amount of flexion and hip and knee of the swinging leg.   I find that conscious focus on the swing rather than the push can be the most effective way to minimise harmful conscious interference with the precision of timing of the push.

The focus on an upward and forward swing of the thigh should be combined with a focus on a sharp swing of the arm in a downwards and backward direction.  Our brains are wired to produce coordinated oppositely directed movements of the leg and arm.  Because the brain can apply more finely tuned control of our arms and hands than to our legs and feet, more precise control can be achieved by placing the main focus on the arm swing.  Precision in timing of the flexion of the hip is necessary to ensure that the swing does not lead to over-striding .

The required mental image of the swing is cultivated by the swing drill. However the swing drill does not involve getting airborne and hence does not help develop the association of a conscious swing with a forceful non-conscious push of the stance leg.   For this, I find the Pose Change of Support (CoS) drill is effective.   This drill entails alternating shift of stance from one leg to the other without forward motion.  The mental focus is on a precise flexion of knee and hip of the ‘swing’ leg as it lifts off from stance; not on driving the other leg downwards.

Although CoS is a Pose drill, you do not have to invest faith in the claim that gravity provides forward propulsion to benefit from it. In fact CoS is similar to the major form of the ‘Hundred Up’ drill developed by WG George, the world’s fastest miler in the nineteenth century.   While similar to Pose CoS, the ‘Hundred Up’ places emphasis on flexion of the hip to bring the knee to the level of the hip. This makes the drill quite effortful, but I do not think it is essential to lift the knee to hip height.  The greatest focus should be on precise timing.  George did place emphasis on the well-controlled swing of the arms, which helps promote precise timing.  I recommend raising the arm somewhat higher and closer to the chest during the forward arm swing than is depicted in George’s model (Figure 3) as I believe bringing the arm close to the chest promotes better control of the swinging leg and minimises risk of over-striding.

Figure 3: Illustration from

Figure 3: By courtesy of

In conclusion, in my opinion Pose and its more recent re-incarnations encourage a helpful focus on an effective swing without over-striding, while minimising the risk of harmful conscious interference in the essential push.  I do not consider that it is necessary to invest faith in an illusory horizontal propulsive effect of gravity in order to achieve this helpful focus on the swing.

How much does this matter during every day running? For an athlete who suffers repeated injury, careful analysis of running form to identify possible errors is crucial and conscious focus on cues promoting good style is an essential part of correcting errors.   Even when not dealing with injury, I think it is worthwhile to consciously attend to form during at least a small portion of each training session.  During long races, conscious focus on a precise and firm downwards and backwards swing of the arm at lift-off from stance can play an important part in preventing a loss of power when tiredness builds up. I recommend including a short period of the CoS drill, together with conscious attention to arm action, in the warm-up to all training sessions.

Cadence, stride length and Mo Farah’s finishing kick

September 5, 2015

To run faster you need to increase cadence, stride length or both.  The question of which it is best to increase is not easy to answer. In particular, the question of the optimum cadence has long been an issue of discussion among runners and coaches.

On the basis of observations of athletes racing distances ranging from 800 m to marathon at the Los  Angeles  Olympics in 1984, Jack Daniels suggested that across various distances, cadence should be at least 180 steps per minute.  The figure 180 became enshrined in folklore.  There have been two niggling concerns about this. First, many recreational athletes tend to adopt a slower cadence.  Secondly, it is clear that among both recreational runners and elites, cadence tends to increase with pace.  For example, observation of a video recordings of 5000 m races reveals that many elite athletes increase cadence to 200 steps/min or more in the final lap.

Consideration of  the effect of increasing cadence on the peak height of the centre of gravity during the airborne phase illustrates why a fairly high cadence is beneficial from the point of view of both efficiency and minimizing risk of injury.

First, we need to consider the question of what proportion of the gait cycle should be spent airborne. Much empirical evidence indicates as speed increases, a shorter time is spent of stance.  For example in his study of the factors influencing running speed, Peter Weyand found that the proportion of gait cycle spent on stance typically decreased by around 40% as speed increased from 3 m/sec to 8 m/sec.  This is understandable as the shorter the time on stance, the less the braking.  To minimize braking at high speed, at least half of the gait cycle should spent airborne.

However when airborne, after mid-flight, the  body inevitably accelerates downwards under the influence of gravity.  The total vertical distance fallen in one long hop is greater than the fall in a series of short hops of equal total duration because the body accelerates to a greater average speed in a longer fall.  As a result, the total gain in height and the energy that must be spent on getting airborne increases with increases of step duration.  In addition, the impact forces are greater the longer the step duration.  Conversely higher cadence and shorter step duration result in lesser expenditure of energy on getting airborne and lesser impact forces.

However, the saving in cost of getting airborne must be set against the increased cost in repositioning the legs, The swing leg must overtake the torso before footfall, and the cost of accelerating the swing leg increases in proportion to the product of cadence and speed (see calculations in the side bar).  The need to avoid large repositioning costs sets an upper limit to cadence. The most efficient cadence is that which minimizes the total cost of getting airborne; overcoming braking; and repositioning the legs.

However, self-selected cadence differs  greatly between individuals. Recreational runners tend to have relatively low cadence, often less than the 180 recommended by folk-lore.  A study of recreational runners  by Heiderscheit and colleagues  demonstrated that a typical recreational runner might decrease both airborne costs and braking costs by increasing the self-selected cadence by up to 10% .  Heiderscheit reported that at a pace around 3 m/sec, a 10% increase in step rate from a self-selected mean step rate of around 170 resulted in a reduction of approximately  20%  in energy absorbed at hip, knee and ankle joints., It is likely than many recreational runners would  benefit by increasing cadence.

Elite 5000 m runners

Even elites differ greatly, with typical cadence during the mid-stages of a 5000 m ranging from 180 to over 200 steps/min.  Why is there such a large range of cadence among elites? I suspect it is largely determined by the efficiency with which the athlete can capture the energy of impact at footfall as elastic energy and use it to help get airborne again.  An athlete who can achieve a greater saving through elastic recoil will require less energy to get airborne and therefore can afford a lower cadence and longer stride at a given pace.  If such an athlete can increase cadence while maintaining his/her long stride in the final lap of  a 5000m, he/she will have an awe-inspiring  powerful finishing kick.

The best illustration of this is provided by Mo Farah.  In a previous blog post, I discussed Mo’s cadence during the indoor meeting in Glasgow in 2009, when he set a British indoor 3000 m record.  In the middle stages of the race, his cadence was around 175.  For example, he covered the sixth lap of the 200 m track at a pace of 6.4 m/sec with a cadence of 175 steps / min and a step length of 2.18 m.    He made his decisive break from the field in 13th lap, by increasing pace to 6.6 m/sec. He achieved this by increasing his cadence to 185 steps / min while his step length remained virtually unchanged at 2.17 m.

It was interesting to contrast his long-loping style with that of Galen Rupp as they ran together in the middle of the pack, with Galen about metre behind Mo, along the back-straight in eighth lap of the 5000 m in the London Olympics in 2012.  Mo’s cadence was 190 steps/min while Galen’s was 204 steps/min.  In the fiercely contested final lap Galen was dropped as Mo increased his cadence to 208 steps per minute while maintaining  a step length of 2.18 m to hold off six strong contenders.

In the World Championships in Beijing in 2015, again it was Mo’s ability to maintain his long stride while increasing cadence that carried him 8 metres clear of Caleb Ndiku in the home straight.   Mo’s cadence of 204 steps per minute was only  marginally faster than Ndiku’s 202 steps per minute, but the telling difference was Mo’s step length of 2.24,m  compared with Ndiku’s 2.08 m.

The secret of Mo’s powerful finishing kick is his ability to maintain his long stride as he increases cadence to match that of his opponents in the final lap.   It is most likely that this is based on very effective elastic recoil allowing him to re-use impact energy to get airborne.  It is noteworthy that he had this ability in 2009, before he joined Alberto Salazar’s training group in Oregon. It is probable that the discipline of Alberto’s coaching took him from the status of UK record holder to World Champion, but the foundation for his later achievement had clearly been laid before 2009.  It is an intriguing question to wonder how much of this reflects his genetic endowment and how much reflects the trainable features of his running style.

At footfall, his right foot splays outwards in an ungainly manner, but perhaps more relevant, to my eye, he typically exhibits about 10 degrees of dorsiflexion of his ankle immediately prior to foot-strike.  This is clearly illustrated by contrasting the orientation of Mo and Galen’s feet an instant before footfall as they run lock-step (though with Mo landing on the left while Galen is on the right) along the back straight at 9:05 in the 5000m at London, 2012, captured in  Michael Wilson’s slow motion video.   This small degree of dorsiflexion will pre-tension Mo’s Achilles and promote efficient capture of elastic energy.

Neuromuscular coordination for distance running

July 30, 2015

It is well established that countermove jump height (CMJ) is a good predictor of sprinting speed.  This is not surprising because CMJ performance depends on powerful type 2 muscle fibres and on the ability to coordinate the recruitment of these fibres.  In the CMJ, flexion of the hips and knees produces eccentric contraction of the corresponding extensors immediately prior to the explosive concentric contraction that propels the body upwards.  It is necessary to recruit the muscle fibres in a manner that harnesses the enhancement of power generated by the eccentric contraction.

The relationship between CMJ performance and distance running performance has been less thoroughly investigated.

In assessing endurance training, aerobic capacity and lactate threshold have been the main foci of attention, but other training-related variables also predict performance.  It is has been demonstrated that difference between elite athletes in volume of zone 1 training (comfortably below LT) predicts distance race performance (e.g. 10Km). In addition, it is fairly well established that a high values of the ‘stress hormone’ cortisol sustained across a period of months predicts poorer performance.

However, somewhat paradoxically, within an individual athlete, week to week variations in training volume and cortisol values make the opposite predictions.  In a study comparing seasons best and seasons worst performance in elite athletes, total training volume  was less but volume of zone 3 training  (appreciably above LT)  was greater in the week before the seasons best performance. Cortisol tended to be higher a week before the best performance, Countermove jump height was also higher in the week before the best performance.

This apparent paradox is consistent with the evidence that a taper should involve decrease volume but not a decrease in training intensity.  The fact that CMJ was higher before the season’s best performance suggest to me that zone 3 training in the week preceding the event promotes good neuromuscular coordination.

The importance of neuromuscular coordination is clearly illustrated by the clunkiness that triathletes experience during the bike to run transition.   The rapid gains in weight lifting performance  at the beginning of a lifting program are most likely due to improved recruitment of muscle fibres.  Conversely, fatigue impairs neuromuscular coordination, and measurement of postural sway has been proposed as a sensitive measure of impaired neuromuscular coordination arising from fatigue in footballers.

Overall, the evidence indicates that neuromuscular coordination is crucial for both athletic performance and injury minimization but it is rarely the focus of attention in endurance training.  While not a specific focus of attention, when we engage in routine warm up we do in fact achieve  short-term enhancement of neuromuscular coordination, and when we accumulate miles of training, we engage in long-term enhancement of neuromuscular coordination, but we rarely think of these activities as exercises in enhancing neuromuscular  coordination.  However, we are more likely to produce effective enhancement of  neuromuscular coordination if we plan our warm-up and training activities bearing neuromuscular coordination in mind.

The elements of coordination

Recruitment of the optimal number and type of muscle fibres:  because much of our training should be at an intensity less than racing intensity, we need pay attention to the need to ensure that we do retain the ability to recruit type 2 fibres as effectively as required at race pace.  Although the importance specificity in training is sometimes over-rated, at least some specificity is essential.  As discussed in my recent post on lactate shuttling, beneficial enhancement of the ability to handle the accumulation of the lactate can be achieved by a large volume of low intensity training.  However the danger of a program focussed too strongly on low intensity running is the development of a tendency to plod slowly under all circumstances.    It is therefore crucial to do at least some training at or near race pace, especially when fatigued as is likely to be the situation in the later stages of a race.  Progressive runs that achieve a pace at or even a little faster than race pace are likely to be beneficial

Recruitment of muscles in the optimal sequence:  The action of running entails a very complex combination of muscle contractions, requiring that the extensors and flexors at each of the major joints of the leg are recruited in a precisely timed sequence.

Speed of recruitment of muscle fibres:    With increasing age, deterioration in running speed is associated with loss of stride length; not cadence.    This is accompanied by a atrophy of muscles and loss of strength.  However as I found three years ago when engaged in  intense high-load weight lifting program for several months, I was able to increase my strength to the point where I could squat a heavier load than Mo Farah, but  my stride length did not increase appreciably, and my speed remained but a very pale shadow of Mo’s speed.    Speed depends on  power: the ability to exert force rapidly.  This requires effective, rapid recruitment of muscle fibres.  It is far harder to train power than speed, though there is some evidence that focussing on a rapid contraction during the concentric phase of a lift, at moderate load, can produce a worthwhile gain in power.

Implications for warming up For most of my training sessions, I employ a warm up procedure that includes 10 activities, beginning with simple movements designed to get all of the major joints  of the leg moving freely, and proceeds though a sequence in which  power output gradually increases.

Calf raises

Hip swings, (straight front to back; rotating from foot behind to opposite side in front.)

Body-weight  squats (aiming for hips below knees)

Single leg squats

Lunge, to front and side

High knees

High knees skipping

Hopping (fast, small hops)


Surges at race pace

Time for each is adjusted according to how my body is reacting, though typically each of the first 8 activities takes 20-60 seconds; the focus is on fluent action rather than effort.

Implications for injury minimization Recent studies, reviewed by Herman and colleagues, reveal  that in a variety of different sports, poor neurocognitive performance, either at baseline or in the aftermath of a concussion, is associated with elevated risk of musculoskeletal injury. It is probable that a thorough warm-up that  sharpens up neuromuscular coordination is a good way to minimise risk of injury.

Measuring neuromuscular coordination The CMJ is widely used  in various sports, especially team games such as football, to assess fitness.  However, it has three potential disadvantages as a measure of neuromuscular coordination for the distance runner: 1) it is not a ‘pure’ measure as performance depends on type 2 fibre strength in addition to coordination; 2) maximal performance is quite demanding and creates the risk of injury; 3) accurate measurement requires special equipment.

I have been experimenting with time taken to perform 20 line jumps as a test of coordination.  It does depend on other aspects of fitness such as muscle strength  to at least a small extent, but placing the emphasis on time rather than maximal power focuses attention on coordination rather than strength.  The risk of injury is small. At this stage, the utility of timed line-jump performance as a test remains speculative as I have not tested it systematically.  Typically, I find that my time for 20 line jumps decreases from 9.0 seconds after a few minutes of jogging to 7.5 seconds after the ‘neuromuscular’ warm up described above.  Time for 20 jumps increases dramatically after a long run.  Provided I can establish that the test yields consistent results when assessing deterioration in neuromuscular coordination associated with fatigue, I plan to use it to determine whether or not light weight shoes (Nike Free 3.0) result in greater deterioration in coordination during a long run, compared with more heavily padded shoes.

Conclusion It is almost certainly true that many of the activities that athletes and coaches have traditionally incorporated into warm-up and training achieve their benefit at least partly through enhancing neuromuscular coordination.  However by focussing on the more easily quantifiable physiological variables when planning and assessing training sessions, there is a risk that endurance athletes might fail to optimise training to achieve the required combination of aerobic capacity, strength and coordination.   Perhaps we should place more emphasis on a systematic approach to enhancing neuromuscular coordination during training, and on measuring it to assess the outcome of that training.