Listening to the brain

March 27, 2021

Yesterday, Stephen Seiler, the sports scientist who had first coined the term ‘polarised training’ a few years ago, presented an interesting lecture (virtually) at the 2021 Spring Meeting of the American College of Sports Medicine-Northland Regional Chapter, entitled: ‘From Polarized to Individually Optimized Endurance Training….. in 5 steps.’

One of the themes of his lecture was that optimising training requires measurement of the ‘strain’ (i.e. the degree of ‘bending of our bodies under load’) arising from our training.

This takes me back to the time, a few years ago, when I employed daily measurement of resting heart rate and heart rate variability (HRV) to assess the accumulation of strain.  I found that to get a reliable assessment I had to combine these cardiac measurements with an estimate of subjective well-being – energy levels, fatigue, mood and enthusiasm for training.   These experiences can be quantified systematically using in the Profile of Mood States (POMS), though I did not use POMS regularly. I was nonetheless intrigued to note that in Seiler’s summary slide (at around 46 min in the recording) he listed POMS change at the top of his set of measures of strain. 

I remain convinced that despite the technology made available by modern sports watches and laboratory measurements, our own brains remain the most sensitive devices we have for assessing the strain of training.

This was recently reinforced for me by my own experience.  These days I am happy to describe myself as a casual fell-jogger rather than a competitive athlete. Nonetheless, since my late 60’s I have been aware of a gradual decrease in stride length, almost certainly attributable to a loss of power of the triple extension of hips, knees and ankles that is crucial for effective lift-off from stance when running.  A few months ago I decided that I would introduce some Olympic lifting into my training with the goal of arresting the decline of power. Unlike the so called ‘power-lifts’ (squats, deadlift, bench press) which mainly develop strength a rather than power, Olympic lifts develop power: that is, the ability to exert force rapidly.  The Olympic lifts involve a rapid triple extension to accelerate the weight upwards.  

However, powerful triple extension is a bit risky if your connective tissues are not well conditioned to withstand the stress.   In the past eighteen months I had not done much lifting because I did not have access to my weights for a period of several months following a house-move.  I decided that I should recover at least some of my former strength with squats and deadlift before starting Olympic lifting. 

My lifetime best for the squat was 5x105Kg achieved as one of the challenges in my informal 70th birthday ‘heptathlon five years ago. I had achieved that following several months of systematic preparation.   Most people can lift a heavier load with a deadlift than a squat, but I have not previously focussed on the deadlift in a systematic manner. My life-time best for the deadlift was only 5×102.5 Kg achieved eight years ago.  Because the deadlift entails engaging latissimus and trapezius in addtion to the spinal erectors, it is perhaps an even better foundation than the squat for Olympic lifts.   I therefore decided that for my 75th birthday challenge I would aim to achieve a life-time best deadlift.

At the start of the programme, I had 12 weeks until my birthday. I decided to follow the 5×5 Strong Lifts programme (×5/ ).  This programme actually includes more set of squats than deadlifts, and also adds some auxiliary lifts such as overhead press and barbell rows.  I thought that such a programme would be safer than focussing mainly on deadlifts, as heavy deadlifts are very stressful.  Although generally less stressful than deadlifts, squats nonetheless provide a good workout for the hip and knee extensors and hence contribute to the strength required for the deadlift.

I planned to start with modest loads and increment steadily to achieve at least 100Kg for both the squats and deadlift before my birthday. I was aware that was an ambitious goal and I built-in enough flexibility to allow a decrease the rate of incrementing the loads if necessary.  I planned to use resting HR as a guide to the strain, but was also aware that I would have to listen carefully to the messages my brain might send me.

In the first few weeks all went well. However, the first sign of undue stress emerged as I approached my previous limits for the auxiliary lifts, especially the overhead press, which I had rarely performed in the past.  I was aware of growing fatigue. I therefore decreased the rate of incrementing the squats and deadlifts and gradually phased out the auxiliary exercises. In the final few weeks, I was able to keep my overall fatigue an acceptable level by decreasing the total number of sets in each session and cutting the increments to only 1.25 Kg per session. I had to make a pair of wooden plates weighing only 0.625 Kg each to allow such small increments.

My subjective recovery after each session was still OK, until two weeks before my birthday. With a little over a week to go, I achieved 5×100 Kg for both squats and deadlift. These were maximum-effort sets and left me feeling drained.  If I was going to achieve 5 reps at any load greater than 100Kg on my birthday it was clear that I would need to taper the load for a week to allow full repair of damaged muscles fibres, while nonetheless maintaining adequate secretion of anabolic hormones to facilitate muscle repair.  In the final week I did two sessions: in the first I did a warm up and a single set of 5x90Kg deadlifts; in the other session, the warm-up was followed by 5x90Kg squats. Those session were invigorating but not stressful.

On my 75th birthday, it was apparent during my warm-up that I had recovered fairly well.  I was hopeful that muscle repair during the taper might have produced a small increase in my strength. Nonetheless, it was clear that increasing beyond 100Kg would be challenging. I decided to start with a deadlift 102.5 Kg and see if I could at least equal my previous lifetime best of 5×102.5 Kg.  The 5th repetition was challenging but I was not at my utter limit.  I braced myself for a 6th rep. The ascent was agonisingly slow and when I locked-out at the top of the lift I was totally spent.   I still felt wobbly two hours later. Nonetheless. I had achieved a life-time best for the deadlift, though only by a hairs’ breadth.

Three days later, I felt recovered. It was time for a squat session. Again during the warm-up it was clear that going beyond 100Kg would be challenging. I started at 102.5 Kg, and managed to complete 6 reps. I was not quite as spent as I had been after deadlifting 6×102.5 Kg, but I was sufficiently near my limit that I could not have done a 7th. In fact I nearly failed to get the bar back onto the rack. It was the nearest I have ever come to having to drop the bar onto the safety rails.

Overall it was a successful campaign.  Although I achieved my lifetime best deadlift at age 75, the campaign had been much more challenging than the build up to my 70th birthday heptathlon had been.  It is clear that I have lost an appreciable amount of intrinsic strength and resilience in the past 5 years.   There is little doubt that It was only by virtue of listening carefully to the subtle but definite messages from my brain that I managed to make the required steady increments up to 100Kg and then taper successfully . 

I wonder what might be possible if I were allow a full recovery during the next few weeks and then start incrementing again.  Perhaps I could achieve more than 5x105Kg. However, I do not see much point in that.  For a runner, power is more important than strength.    It is time to start a beginner’s programme for Olympic lifts.  Even more importantly, I want to continue enjoying being a casual fell jogger for the next few years.  If all goes well, it might then it will be time to consider taking up the marathon again. That would be a fitting 80th birthday challenge!    


February 27, 2021

In my previous post I proposed that optimal function of our mind and body requires the coordinated action of a multitude of control mechanisms that each individually regulate a specific aspect of bodily function.   In a comment on my post, ‘Febrile seizures’ (Tim) pointed out that the net outcome of the action of a distributed set of linked systems leads to chaos unless there is some architect who specifies an overall architecture.  In essence I agree with Tim though I think the image of an architect as the governor might not be the best image.   It is reminiscent of Tim Noakes concept of a central governor that ultimately sets the limits on our performance. Rather than a central governor, I think the evidence indicates that the actions of our mind and body are coordinated by a ‘distributed governor’.  Different control mechanisms can wield the baton in different circumstances.  The multiple components of this distributed governor nonetheless must act in accord with some constraining principles if we are to avoid chaos. 

In the brain, there are multiple distinct neural circuits, each focussed on a specialised aspect of brain function.  These various different circuits employ feedback loops to regulate their specialised aspect of brain function. Much of this processing is carried out automatically; that is, unconsciously.  However, if we are to avoid chaos in our brains, the diverse circuits must be constrained in some manner.  The renowned neuroscientist, Karl Friston, proposed that the overall system is governed by a principle that he has designated the Free Energy principle.  To achieve equilibrium with its environment a system acts in a manner that minimises it Free Energy

(See ).  

At any particular moment, depending on circumstances, among the babble of messages being communicated within the multitude of distinguishable but nonetheless linked, circuits in the brain, a particular pattern of brain activity achieves a pre-eminence and enters into awareness. In other words, the information represented by that pattern of brain activity enters consciousness.  The content of consciousness is not necessarily directed towards important goals. However, we are more likely to be successful in achieving our goals if we able to direct the content of consciousness towards our goals, while avoiding distraction and negative self-talk.  It is noteworthy that many neuroscientists consider that Karl Friston’s Free Energy Principle provides the best framework yet proposed for understanding consciousness.  (See for example Rayberon and Finkle, )

I do not want to get too deeply into a discussion of the abstract concepts embedded in the Free Energy Principle in this post; it is a topic that has evoked much debate in the neuroscience community.  I hope to return to that intriguing debate at a later date after I have spent some more time thinking about how to present the Free Energy principle in everyday terms that make sense to an athlete.  

In my recent post, I described how my best running performances have occurred when I was in that transcendent state commonly known as ‘flow’ or ‘the zone’.   ‘Flow’ is not supernatural, but it is remarkably elusive. At best, we can create circumstances in which flow is likely to emerge.  As mentioned in that post, mental framing of effort and focus on rhythmic breathing can help. 

In this post I want to address an even more mundane everyday experience.  How we can enhance our ability to get to sleep?  Sleep itself plays a cardinal part in the repair and recovery that is as important as the active work-out sessions in a fitness programme.   Although more mundane that ‘flow’, for individuals who are tormented by inability to sleep, sleep can seem like an elusive grace withheld by teasing sprites. But as with ‘flow’, awareness of rhythmic breathing can help unlock this state of grace.    

It would be melodramatic to describe my own experiences as torment. I have nonetheless has a life-long difficulty in sleeping. When I was a very young child my mother would usually come into the bedroom I shared with my brothers before she went to bed to check that we were OK.  I was usually awake and she would sometimes exclaim; ‘You must have killed a Chinaman’.  At that young age I had little reason to be wracked by guilt, and I was oblivious to any unintended racial overtones implied in my mother’s expression.  In my 5 year old mind there was a more obvious reason for my sleeplessness. I could hear the sound of an axeman chopping down trees outside our house and I was afraid that after he was finished with the trees he would come for me.  Years later, I discovered that the rhythmic chopping sound was the sound of blood pulsing through the carotid artery where it passes through the temporal bone, adjacent to the inner ear. 70 years later I can still hear that pulsation in the dead of night but my imagination no longer runs wild. I usually take little notice of it as I can sense my heart beat more strongly from the pulsations in my chest.  Nonetheless those early experiences of ‘listening to my body’ did eventually set me on the path of trying to find ways of getting to sleep.   

As a child I had little reason to think sleep was important.   Even in my under-graduate days, trying to fit a marathon training programme around the edges of a demanding academic course, I was often forced to sacrifice sleep for the sake of a training run in early hours of the morning. It would have been better for my health and for my marathon performances if I had slept more.  I have no regrets about cramming as much as I could into the hours available, but as more information has emerged about the role of sleep in optimum training, I have come to realise that it would have been better if I had put sleep higher in my list of priorities. Now, when I am focussed on the best way of maintaining my longevity as a runner, I regard adequate sleep as crucial.  

Sleep is a cardinal component of the rest and recovery phase of a training programme.  During the early hours of sleep, the rate of release of anabolic hormones, especially growth hormone increases, promoting repair and growth of muscles.  During that early phase of sleep, release of the stress hormone, cortisol, diminishes. Then toward morning, the cortisol levels rise, as part of a diurnal pattern that leads to the highest level of cortisol in mid-morning.  The increase of cortisol promotes glucose metabolism and prepares us to cope with the demands of the waking day. 

The diurnal variation in cortisol is matched by a diurnal pattern of variation in the autonomic nervous system, the nervous system that governs our internal organs.  In the early phase of sleep, the parasympathetic division of the autonomic system tends to be dominant.  The parasympathetic innervation of the heart and gut slows the heart and promotes digestion, while the parasympathetic innervation of the liver promotes the synthesis of glycogen.  Towards morning, as cortisol rises, so too does the activity of the sympathetic nervous system: the fight and flight system acts together with cortisol to prepare us for the demands of the day.  

The activities of the parasympathetic and sympathetic nervous systems also play a role in the regulation of inflammation and the function of the immune system.  In general the parasympathetic system has anti-inflammatory effects. The multiple branches of the vagus nerve carry a large proportion of the parasympathetic messages dealing with the thoracic and abdominal viscera to and from the brain.   The vagus senses peripheral inflammation and transmits messages to the brain stem mobilising the brain centres involved in regulating the immune system  

While a large body of evidence demonstrates that the sympathetic and parasympathetic divisions of the autonomic nervous system play key roles in coordinating neuro-immune interactions, it is overly simplistic to describe the roles of these two divisions as opposing roles.  There are complex and dynamic interactions between these two divisions. Nonetheless, in most respects the simplistic description in terms of opposing roles is a useful approximation to reality. 


Overall, sleep is a state in which a sequence of inter-related hormonal, immune and neuronal processes occur.  These processes are crucial for the repair, maintenance and protection of all of the tissues of our bodies.  Because the timing of these processes should fit with the diurnal variation of body rhythms over the entire 24 hour day, it is highly desirable not only to get enough sleep, but to establish a regular schedule that is stable from day to day.

Does this understanding of the physiology of sleep provide practical guidance as to how we can get to sleep?  The problem I have faced since childhood has been hugely exacerbated in old age.  I now wake several times each night; always at least twice and often three times.   In recent years I have often found it challenging to get back to sleep after waking in the early hours of the morning.  Ironically, I usually found that after several wakeful hours, once daylight arrived, I would fall deeply asleep.  It was clearly necessary to find a successful strategy for getting to sleep.

Folk-lore recommends counting imaginary sheep.  This makes some sense insofar as the mind cannot get drawn into interesting or worrying trains of thought when occupied by something repetitive but boring. Clearing the mind of either interesting or worrying thoughts is almost certainly the first requisite of getting to sleep.  However, I could not abide the boredom of counting sheep.  

A technique recommended by many psychologists is Jacobson’s progressive muscular relaxation. This entails a conscious focus on tightening and then releasing the tension in a sequence of muscle groups, one by one. With a few weeks practice, this can be a good way to decrease sympathetic nervous system activity.  Heart rate decreases and blood pressure falls.  However I find the degree of focussed attention required for a full sequence of progressive muscular relation engages consciousness too strongly.  Therefore in my present routine, I start with relaxing my jaw and then trunk and limbs so that I am aware of the weight of my body sinking into the mattress, but do not follow Jacobson’s full recommended sequence.

The US military recommends a similarly abbreviated form of progressive muscular relaxation, followed by a mind-clearing technique such as focussing on a relaxing situation (for example, imaging relaxing in a hammock or lying in a canoe in an idyllic setting).  I found this approach helpful.  The image of the relaxing situation captures the limited space on the summit of awareness from other intrusive thoughts clamouring for attention.  It is self-defeating to treat this as a mental battle.  You need to acquire the knack of simply observing the intrusive thoughts but not engaging with them. 

Sleep entails releasing oneself from the control of consciousness, in a manner that entails a shift from dominance of the sympathetic ‘fight and flight’ state to the parasympathetic ‘rest and digest’ state.  Imagining a relaxing scene tends to evoke the parasympathetic state.   However, there are more direct ways of achieving this. 

In my experience, the most effective way is regular, slow deep breathing.  The reduction of pressure within the chest during inspiration promotes return of blood to the heart, distending the right atrium. As in skeletal muscle, stretching promotes a stronger subsequent contraction. The stronger pulse acts on the pressure receptors in the large arteries in the neck. The vagus nerve carries messages directly from these pressure receptors to the parasympathetic nuclei in the brain stem and thence to higher brain centres involved in control of the autonomic system, promoting a shift from sympathetic to parasympathetic balance.  Within each breathing cycle heart rate falls during expiration and increases during inspiration. Over the course of a few respiratory cycles, heart rate falls while healthy beat-to-beat variability in heart rate increases.  

My Garmin VA3 watch monitors this change in heart rate variability and generates an estimate of stress, ranging for 0 to 100. I find that over the course of a few minute I can typically reduce stress level from around 65% (medium stress) to 15% (rested).  Figure 1 shows heart rate and stress level assessed using my VA3 during 12 minutes of relaxed deep breathing starting from a moderately high stress level of 76 % (mid-morning on an active day) and reducing to a level of 9 % (well rested) while HR decreased from 90 to 61. When going to sleep I would generally start at a medium to low level of stress (typically 35%) and decrease to a rested level (perhaps 5% with HR around 50 b/min.)

Figure 1: Decrease in heart rate and level of stress (quantified by measuring heart rate variabillity over 3 minute segments) during 12 minutes of relaxed breathing, starting from a moderately stressed state. Stress level below 25% (denoted by blue colour) indicates a resting state, domination of parasympathetic over sympathetic nervous activity.

However it would be counter-productive to focus on your watch while trying to get to sleep; you need to disengage conscious focus on complex perceptions arriving via the five external senses, and allow internal body sensations to impinge passively on your awareness.   Do not strain to attend to the messages from your body; simply ‘listen’ passively.  At first I am aware of the weight of my body sinking into the mattress through my shoulder blades, glutes and the back of my legs. These external somatic sensations give way to sensations from within my body.  Over the course of half a minute I become aware of my abdominal wall gently rising and falling with each breath, and then, the pulsation of my heart beat, usually five beats on each inspiration and five beats on each expiration.  Rather than counting imaginary sheep I passively attend to a soothing internal rhythm.   

Often, I drift into sleep within a few minutes, and I only become aware of the success of the procedure when I awaken many hours later.  But if sleep does not carry me away within a few minutes, it is crucial that I avoid a judgmental evaluation of the situation.  I simply appreciate the sense of quiet relaxation.  In fact my body by this stage is already in a restful state that is promoting recovery for the wear and tear of the preceding day. A person who has acquired the art of observing intrusive thoughts but not engaging with them, eventually drifts into sleep. This usually happens to me.

In summary, the sequence is:

  1. Allow your jaw, trunk and limbs to relax so that you become aware of your body sinking into the mattress.
  2. Breathe regularly, allowing an increasing awareness of the gentle rise and fall of your abdomen.
  3. Allow awareness of the regular rhythm of your heart beating in your chest to combine with the awareness of the rhythm of breathing.
  4. If you have not fallen asleep with a few minutes, simply appreciate the sense of quiet relaxation.   If thoughts intrude, observe them but avoid engaging with them. 

Here are two recent outputs from my VA3 presenting the stages of sleep.

Figure 2A: Stages of sleep. Note two short periods of deep sleep within the first two hours and increasing amounts of REM sleep as the night progresses. There were three awakenings. I succeeded in getting back to sleep quickly after the first two, but did not make a deliberate attempt to get back to sleep during the dreamy, drowsey period after 7AM

Fig 2B: Sleep stages. Again note the period of deep sleep early in the night and the increasing amounts of REM as the night progresses. Again I succeeded in getting back to sleep quickly after the two awakenings.

These show the normal feature of deep sleep within the first few hours after falling asleep followed by longer periods of light sleep interspersed with increasing amounts of Rapid Eye Movement (REM) sleep. There are several features that might be described as abnormal, but are in fact typical of older people, especially males.  Ever since my late sixties, I almost always awaken two or three times during the night.  However the pleasing feature now is that in contrast to the situation a few years ago when I often lay awake for more than an hour, I usually get back to sleep with a few minutes.  The second noteworthy fact is that I rarely get more than 30-40 minutes of deep sleep, and sometimes none at all.  I suspect this is associated with lesser secretion of growth hormone and with less effective recovery in old age than is typical in healthy younger people.   I may have to accept that this is a consequence of aging that is inevitable. I do not think the answer is to engage in more demanding activity during the day, but it might be that I can develop a more effective fitness programme.   Nonetheless, I think it is likely that that my sleep pattern now is the healthiest it has ever been 

I have addressed sleep in this post largely because of the important role of sleep in the recovery phase of a fitness programme.  However I consider that this topic illustrates the more general issue of training the proposed ‘distributed governor’ to optimise the regulation of mind and body.  In getting to sleep, it is necessary to escape the control of consciousness. In other circumstances, the crucial issue is optimising what we allow to enter into conscious to ensure that the most appropriate control system determines our behaviour.

I was never a serious sprinter, though I did aspire to represent my school as a sprinter long before I was old enough to enter longer events. But I was a notoriously bad starter.  Looking back, I think that my problem was allowing too many distracting thoughts to enter consciousness between the set and go commands.  In that brief period, you need to be responsive to only one thing: the crack of the starter’s pistol.    That sound should initiate a reflex mobilisation of your muscles, with minimal conscious interference.   The task of setting-up optimum posture should have been done in the interval between ‘on your marks’ and ‘get set’.

For most of my life, I have been more interested in distance running, both for the sake of competition and for sheer enjoyment.  While maintaining a constant pace, the goal is avoiding intrusive self-defeating thoughts about discomfort or fear of inability to sustain the pace.  Awareness is best focussed on the rhythms of running: the rhythm of respiration and the rhythmic movement of your limbs. These sensations are framed as effort rather than pain.  The overall sensation is exhilaration. 

Acquiring the knack of getting to sleep might improve your running not only by enhancing recovery but also by enhancing your ability to engage the most appropriate control system when you are actually running.  

The distributed governor

February 14, 2021

Once again, almost a year has passed since I have posted.  The year has been dominated by Covid-19. For many people it has been a very distressing and traumatic year. So far, I have been fortunate. I can work from home, maintaining contact with colleagues and students via MS Teams and with family via Zoom.  I live in a small village with easy access to nearby wonderful countryside.  I have remained well apart from a frustrating flare-up of the arthritis in my knee.

I have had intermittent episodes of inflammatory arthritis for over forty years and the knee is now showing signs of enduring damage. However, the recent acute episode is settling and I am once again running, though only slowly, and mindful of the need to protect my knee. Mainly I run on the local fells.   

I live in the southern part of the UK Lake District. Our village nestles on the slope of a fell that is modest in height but rich in detail. I walk or run each day on ill-defined paths that are largely maintained by animals: fell ponies; sheep and deer, and I scramble up the rocky edges.  The upper slopes offer wonderful views across to the higher Cumbrian Fells. At present, the skyline differentiates the every changing winter cloud-scape from a spectacular snow-scape that extends from the peaks at the head of Ribbledale in to east, sweeping past the richly indented Howgill Fells, and northwards to Helvelyn.  In this time of Covid, when it is especially important to minimise risk of an emergency call out of the Cumbrian Search and Mountain Rescue team, I am very happy to view the more challenging mountains from the local terrain that I know well.  I am at present content to describe myself as a casual fell jogger. These runs are mostly pure delight.

I began running to and from school at age 4. I did it because I like to run.  A theme that has intrigued me over the subsequent seven decades is the apparent conflict between the joy of running and the human inclination to sit down whenever possible.  Brief consideration of the evolution of our species provides a partial explanation.  As creatures who were both predator and prey, our ancestors needed to be fleet of foot.  Children who ran playfully were more likely to contribute to the gene pool.  Honing those running skills in adulthood even beyond child-bearing years, contributed to the wellbeing of their tribe.  On the other hand, our ancestors faced not only the challenge of being both predator and prey, but also needed to conserve the energy gleaned from hard-won food and protect themselves from perilous exhaustion.  Of necessity, our evolving brains developed a sophisticated mechanism for regulating activity, a system that Tim Noakes has dubbed ‘the central governor’. 

However this governor is not a detached dictatorial figure that issues commands from a localised seat of government within the brain. It is not even confined to the brain.  The seat of government is an intricate network of body tissues that communicate via nerves and a profusion of chemical messengers: hormones and cytokines.  Cytokines are small proteins, peptides or glycoproteins secreted by cells of the immune system; the endothelial cells that line blood vessels; and by muscles.  The messages that they carry mobilise or inhibit tissues throughout the body ensuring an integrated response that throughout human history has tended to promote our survival.   Rather than being a central governor, it is a distributed governor.   The action of the governor: monitoring the state of the body and making appropriate adjustments, is performed by an intricate but integrated system.

There are multiple control systems in the brain and body. These engage feedback loops to adjust the level of activity in that system. They include the autonomic nervous system (the sympathetic branch mobilises ‘fight or flight’; the parasympathetic branch promotes ‘rest and digest’); the hypothalamo-pituitary-adrenal axis’ that regulates several hormones, most notably the hormone cortisol which plays a key role in mobilising the body to deal with various types of stress;  the salience network, a brain network that plays a cardinal role in the deployment of the brain’s resources to deal with current circumstances; the cortico-striato-thalamo-cortical loops in the brain that facilitate the role of the modulatory neurotransmitter dopamine in setting the tone of brain activity; the myokine signalling system that employs peptide molecules released by muscle fibres to carry messages from muscle to other organs in the body facilitating muscle proliferation, differentiation, and regeneration.  These are a few among many control systems.  How are all of these control systems integrated to achieve overall harmony?

The brain plays a crucial role. It receives messages from all parts of the body and it feeds back instructions via nerves and hormones.  And in the case of the human brain, there is a remarkable feature that shapes the brain’s responses: consciousness.  Although the origin and nature of consciousness is still a topic of extensive debate, perhaps the most plausible account describes it is a spontaneously emergent property of a vastly complex integrated system.  Among all of the diverse patterns of ongoing communication between the myriad component parts, there is a ‘winner-takes all’ mechanism that allows a particular pattern of communication to reach a dominant level that we experience as conscious awareness.   This gives us the ability to mould our activity according not only to current circumstances but also past experiences and future goals.

For the runner, consciousness can be both a boon and a curse.  By facilitating planning and engaging motivation, it enables us to pursue our goals with determination. It can also be an enemy when we allow the signals that indicate stress on the body to prompt negative self-talk that undermines our self-confidence.  We can deploy our consciousness in a determined manner that can override the negative self-talk.   It is commonplace to assume that exceptional performance in endurance events entails victory of determination over negative self-talk.  However, in my own experience, this is not always the case. It has not been the case during the performances that I look back on my best performances.  During these best performances, I have experienced the state that is sometimes called ‘flow’ or ‘being in the zone’.

Flow is a transcendental state; a level of consciousness in which awareness transcends the stream of irrelevant or negative messages that attempt to break in.   It is a state of calmly focussed attention.  For the runner, there is a sense of harmonious motion of the limbs and confidence in achieving the goal.   It is not a mystical or supernatural state.  It arises via the natural agency of the distributed governor.  Nonetheless, it is not easy to invoke this state; indeed despite my long-standing fascination with this transcendental state, I am far from certain about how to invoke it.  However, I do have some ideas about how to set the scene within which it can emerge.

The first step is reframing the sensations associated with effort.  While our body sends messages that provide early warning of possible peril or the early phases of exhaustion, we can consciously reframe the implications of these messages. They are a sign that we are indeed exerting effort to achieve our goals.  This is a positive situation. We need to ensure that we do not mistake the sensation of effort for pain.  In most circumstances, running is not painful but it is effortful.  We need to reframe the sensation of effort as a positive sensation.  There are automatic biochemical processes in the brain, including the release of dopamine, endorphins and endogenous cannabinoids that promote this positive reframing. However, by virtue of consciousness we are not hapless victims of uncontrolled biochemistry.  Awareness of our goals and the self-confidence that comes of practice allows us to take charge of this reframing process.

There are other physiological mechanisms for enhancing control at our disposal.  Central to these is breathing.  Eastern mysticism places emphasis on the importance of the life-giving breath that infuses a spiritual awareness lifting us above mundane distractions.  I believe that Eastern mysticism is founded on centuries of astute observation of the human condition, but I do not believe it is necessary to regard the experience of the transcendental power of breathing as a divine grace.

I am a scientist. I regard scientific explanations of our experiences as no less wonderful than explanations based on the intervention of supernatural powers.  As a biomedical scientist engaged in research into ways of improving treatment for mental disorders, one aspect of my research is an investigation into the way in which conscious awareness of breathing affects our mind and brain.  I use brain imaging techniques to investigate what happens in our brains when we engage is consciously controlled deep breathing.  It is clear that conscious awareness of deep breathing does produce coherent patterns of electrical oscillations in the brain that might support a focussed mental state.  However, our work is not yet sufficiently advanced to justify confident conclusions regarding the best way of producing a calm, focussed mental state.

As a runner who has one life in which to draw the best conclusions as I can from personal experience, I am not bound by the requirements of a biomedical scientist who seeks to draw conclusions that can be generalised to the human population.  It is reasonable for me to draw conclusions from my own experiences.  I do not claim that what works for me will work for anyone else.  On the other hand, it is reasonable to share my experience and let you reach your own conclusion about what works for you.

I find that conscious awareness of my breathing provides not only a useful guide to the effort that I am exerting, but by deliberately increasing depth and rate of breathing I can consciously ‘shift-up a gear’ when I wish to increase speed.  At a steady pace, awareness of my rhythmic breathing helps me get in state of that approaches ‘flow’. 

I will blog somewhat more regularly in the near future, further exploring the nature of the distributed governor, and the strategies that enhance the likelihood of flow.  In present circumstances I am largely focussed on strategies for enhancing my longevity as a runner, though perhaps at some future time, I will be once again focus on racing.

Exercise in the era of covid-19: what should we do?

March 18, 2020

It is many months since I last posted.  I had been unable to run for many months in 2019 on account of debilitating illness.  As a result, my attention was taken up by other things and blogging was not a priority.  Fortunately, I was able to recommence running again at the end of December, and have been running regularly since then.  I am recovering fitness slowly.

I ended my post in June 2019 with the statement that my next post would examine the issue of what a distance runner might do to enhance their longevity as a runner.  I still intend to address that question in the future.  My recent experience of the slow process of regaining my former fitness has increased my determination to understand more about the optimum ways to maintain longevity as a runner.  But meanwhile, a more urgent issue has emerged.  Corona virus is sweeping though most countries on earth.  The risk of serious illness or death, especially for the elderly, and the threat that health services will be overwhelmed, is now a pressing issue facing us all.  Running no longer appears so important.

At least in the UK, where the Corona death toll has just passed 100, the situation is not yet anywhere near as devastating as it has been in Wuhan or in Italy.  It is a time when governments and individuals are trying to identify the best course of action, yet there are so many things that are unknown.  If the pandemic persists for many months, we need to take seriously what we can do to maintain our health in the longer term, when many aspects of our lives are likely to be seriously disrupted.

At least for the present time, the UK government recognises the importance of exercise for the elderly. Exercise is also important for the young. Whatever our age, we share a responsibility to do what we can to minimise the probability that we will become clinical cases, infecting others and perhaps even needing admission to an over-stretched hospital.  Good hygiene and social distancing are the essential requirements.  Nonetheless, exercise too has a role to play in minimising the risk that we will become ill.

There are many individual scientific studies that support this claim, though it is best not to place too much emphasis on a single study. In this review I will place emphasis on the consensus conclusions drawn by reputable experts from extensive review of the evidence. But bear in mind that even experts are sometimes influenced by the zeitgeist. I should also mention at this point that I am a medically qualified biomedical scientist, who, over a period of many decades, has practised as a medical doctor and also carried out research in diverse fields including biochemistry and physiology. I retired from clinical practice almost nine years ago. I am currently a neuroscientist working mainly in the field of mental health I will draw mainly on evidence regarding respiratory infections in general, though where possible I will make specific reference to covid-19, the illness produced by the corona virus.

The effects of exercise on resistance to infection depends on many factors including the fitness of the individual, the nature of the exercise and the timing in relation to exposure to the virus. An extensive review of many experimental studies of exercise in animals indicates that exercise or training before infection has either no effect or decreases morbidity and mortality from respiratory infections. Exercise during the incubation period of the infection appears to have either no effect or increases the severity of infection.

In humans it is less feasible to perform a well-controlled comparison of the period before infection with the period during incubation. However, the available evidence is consistent with the bi-phasic relationship observed in animals. A well regarded expert consensus statement (the BASES statement) concluded: Regular moderate exercise reduces the risk of infection compared with a sedentary lifestyle, but very prolonged bouts of exercise and periods of intensified training are associated with an increased risk of infection.

The simple message

A more recent consensus statement by a group of experts convened by the International Olympic Committee is consistent with the BASES consensus statement. They produced a simple pictorial summary of the evidence relating to risk of illness related to athletic training.


Illustration of the J-shaped relationship between training load and risk of illness (from Schwellnus et al, Br J Sports Med. 2016 Sep;50(17):1043-52


This is a simplified illustration. The risk for an individual depends on many factors including their natural resilience against illness, and many other variables including their current level of fitness; how well rested they are; general nutrition, how well fuelled they are during exercise, and many other life-style related factors. There is some evidence that elite athletes tend to have exceptional resilience and hence have an increased capacity for a high training load without increased risk of illness, illustrated by the dotted line.

In this blog I will do my best to assemble the science-based information about the many factors that influence the effect of exercise on the response to infection.

The incubation period

Covid-19 is now circulating in our community, and any of us might possibly be in the incubation period.

However, provided you feel well, the chance that you are incubating covid-19 is low, at least in the UK at present. Continuing moderate training is likely to strengthen your immune system. With many races cancelled in the near future, it is probable that few of us want to continue intense training in the near future. However, if you do, you should be cautious about the amount of heavy training. We will address this further below.

If you have respiratory symptoms you need to take careful stock of the situation. The usual rule of thumb among runners is that if you have respiratory symptoms above the neck, training is OK. The problem with covid-19 is the early symptoms are often above the neck; most notably cough. A recent onset cough is one of the key signs that you should be self-isolating. You should not be training. Light activity to maintain mobility is probably OK, but also ensure you get adequate rest.

If you have a sore throat without cough, a cold is more likely but covid-19 is possible. I would suggest that you take your temperature before training. Elevated temperature is the other key sign indicating that you should self-isolate. If you have an elevated temperature, ensuring adequate rest is a high priority

Nutritional status

The cells of the immune system are heavily dependent on adequate glucose to meet their energy requirements. Many studies suggest that the most effective nutritional strategies for athletes, include a substantial intake of carbohydrates Carbohydrate intake during prolonged and intense exercise is associated not only with higher glucose level in the blood but also lower stress hormones and lower levels of chemical messengers that promote inflammation.

Carbohydrate intake makes an important contribution to optimising immune defence during exercise. Various micronutrients (vitamins and minerals) also play a role. Therefore, if you are engaging in regular exercise while at risk of exposure to covid-19, it makes sense to consume an adequate amount of carbohydrates, within a diet that includes vegetables and other sources of vitamins and minerals.


Humans evolved to live on a planet that revolves on its axis generating a 24 hour cycle of day and night. Hormonal activity and immune function fluctuate with a 24 hour circadian rhythm that optimizes our readiness to forage or hunt in the daytime and recuperate during the night time. A surge of growth hormone that promotes body repair is released within the first 2 hours of going to sleep. In contrast, release of the stress hormone, cortisol, rises towards dawn and reaches a peak around waking time to mobilise glucose and provide fuel for a diverse range of bodily activities. Cortisol subsequently falls to a low level by evening.

Many of the messenger molecules that control the immune system fluctuate in synchrony with the daily fluctuation of cortisol. The relationship between cortisol and immune function is complex. While cortisol mobilises glucose and promotes energy metabolism, thereby supporting the function of the cells of the immune system, sustained elevation of cortisol suppresses the immune system. Good health depends on a well-regulated, coordinated daily variation of cortisol and the immune system. Chronic sleep deprivation, and also chronic excessive sleep are associated with diminished life-expectancy. For the typical person, between 7 and 9 hours sleep per day is optimal. Sleeping pattern potentially plays an important role in ensuring that moderate exercise enhances rather than harms immune function. I do not know of any specific data on sleep and resistance to covid-19, but it is almost certain that a healthy sleep pattern will help optimise defence.

I was a junior hospital doctor in the years long before the European Union Working Time Directive came into force. In those days we worked very unhealthy long hours. There might be pressure on hospitals to relax working time restrictions for front-line staff in the coming months. For the good of all of us, I hope those pressures can be minimised. Meanwhile, those of us who are at home chaffing at the bit because our social activities are restricted should use this opportunity to improve our sleeping habits.


Dehydration increases the risk that exposure to the virus will result in infection. The upper airways are lined with hair-like cilia that sweep invading material, including viruses, wrapped in mucus, upwards and out of the system. If the airways become too dry the cilia get clogged and cannot sweep the viruses out, making it easier for the virus to invade the cells lining of the airways. The virus causing covid-19 prefers dry surfaces.

Life-style factors

Alcohol interferes with immune function in several different ways. Alcohol disrupts the function of the cilia in the upper airways, and impairs the function of immune cells. Excessive alcohol consumption increases susceptibility to pneumonia and in particular increases the likelihood of acute respiratory distress syndrome – one of the potentially lethal manifestations of covid-19.

Presumably few of us are smokers; smoking seriously degrades the ability of the lungs to mount an immune response. Smoking also damages cilia.

Indoors v outdoors

In the years before the discovery of antibiotics, one of the mainstays of treatment of respiratory infections was exposure to fresh air and sunlight. The mechanism was a mystery at the time and remains a matter of speculation. The potent antibacterial and antiviral effects of sunlight probably contributed.  Another likely contributing factor was the beneficial increase in synthesis of vitamin D due to sunlight falling on exposed skin.
Vitamin D not only keeps bones, teeth and muscles healthy, but also promotes healthy immune function. Vitamin D can be derived from dietary sources, but at least in the months April-September in the UK, an adequate amount can be derived from sunlight. The duration of exposure required depends on skin colour and amount of exposed skin. In summer, 15 minutes of exposure of arms, legs, abdomen and back to sun is generally adequate. When wearing a top, the duration of exposure must be increased by an amount proportional to the reduction in area of skin exposed.

For these reasons, outdoor exercise is likely to be preferable to indoor exercise, if it is feasible

Psychological stress

Many studies have reported that the combination of emotional stress with the physical stress of running increases the release of the stress hormone, cortisol, and hence is likely to add to the disruption of immune function produced by heavy exercise.

Cumulative heavy exercise

The potential decrease in immune function produced by heavy exercise is compounded by repeated bouts of heavy exercise. Most of us are aware of the need to avoid repeated demanding training sessions. There is a low probability that we will be drawn into such a pattern of training when the majority of major races have been cancelled or postponed. However if you are inclined to continue a strenuous training program, there is greater need than ever to monitor for signs of over-training at this time. Elevated resting heart rate is one sign, though in fact it is not a reliable sign. One of the most reliable signs of over-training is a deterioration in energy levels, mood and sleep.

I hope you all keep well!

Edit, 20 March 2020: Following the very helpful comment by David Dunbar (see below) I wish to add two points:

First, the data that strenuous exercise can reduce immunity in humans still a topic of debate. David provided the link to the paper by Campbell and Turner published last year. That paper provides a useful, up-to-date discussion of some of the evidence regarding exercise and the immune system.  I think the title of the paper which refers to debunking the myth of exercise-induced immune suppression is a little misleading.  Campbell and Turner discuss the positive effects of exercise on immunity. I agree with the points in their discussion. It also examines the studies that report increased respiratory illness following strenuous exercise and points out that several of these studies have weaknesses.  I also agree with most of that discussion. That is the reason why I started with the studies of controlled investigations of exercise and immunity in animals rather than the evidence from observational studies of athletes. Some of the animal studies do report that exercise during the incubation period increases the severity of the infection.   That is a major reason why I consider that we should be cautious in the era of covid-19, and in particular, we should monitor carefully for over-training if we wish to pursue a strenuous training program.

Secondly, with regard to the risk that strenuous training might reduce immunity in athletes, the majority of the evidence indicates that prolonged, demanding exercise is more likely to suppress immunity than short intense exercise. However, this evidence is still debateable. This is why I consider that monitoring for over-training in the most important thing.

The effects of training on longevity: what can we learn from Haile, Paula, Ed and Gene?

June 4, 2019

In my post in January, I discussed the ways in which genes might influence the career longevity of a long-distance runner. To provide context for that discussion I compared the possible ways in which genes might have contributed to the longevity of the two greatest elderly long distance runners ever, Ed Whitlock and Gene Dykes.  They are the only two people to have run a marathon in less than 3 hours in their 70’s. (As discussed in the comment section on my post in December, I consider it remains unproven whether or not Frank Mesa also achieved this; a recent examination of the evidence by Derek Murphy of Marathon Investigation provides a well-researched case casting doubt on Frank’s performance).

In this and the following post, I will examine the influence of training on longevity, focussing especially on the effects of training on the musculo-skeletal system.  Again the contrast of Ed Whitlock and Gene Dykes will contribute to the context for this discussion, but I will broaden the context by also examining the training of two of the greatest distance runners in the open age group in recent years: Haile Gebrselassie and Paula Radcliffe

Haile Gebreselassie

Haile Gebreselassie was born in  April 1973.  As a school boy, he ran 10 Km to and from school daily.  At age 19, he won the 5000m and 10,000m at the 1992 World Junior Championships in Seoul, and the following year won the men’s 10,000m world championship. That win was the first of four consecutive world championship gold medals and two Olympic golds in the 10,000m. In 2002 he turned his attention to the marathon, finishing 3rd in the London marathon. In Berlin in 2006, he took 29 seconds off Paul Tergat’s world marathon record and then a year later, another 27 seconds off his own record, recording 2:03:59.

However evidence of serious injury had first emerged in 2004, when an inflamed Achilles tendon confounded his attempt to win a third successive Olympic 10,000m gold.  He also suffers from asthma and in 2008 he withdrew from the Beijing Olympics on account of concerns about the effect of poor air quality on his breathing.  In 2010, back pain disrupted his intended assault on his own world record in the Dubai marathon, though he nonetheless won in a time of 2:06:09. Later that year, he made a premature announcement that he would retire after dropping out of the New York marathon.  However he returned to international competition but never quite achieved the dominance of earlier years.  He missed the 2011 Tokyo marathon on account of injury. Nonetheless in April of that year he won the Vienna City half marathon. In 2012 he returned to Vienna to run the half marathon, pitted against Paula Radcliffe, who was given a 7:52-minute head-start reflecting the difference in their half marathon records.  He easily overtook Paula, to win in 1:00:52.  In 2013 he again won the Vienna Half marathon,  in 1:01:14, and later that year set an over-40 world 10 mile age-group record of 46:59.  In May 2015 he retired from competition after a 25 year career in which he set 27 world records, won two Olympic gold medals and eight World Championship gold medals.  However, for the final 5 of those 25 years, his performances were substantially disrupted by musculo-skeletal injuries.  Although not unexpected, in those five years the level of his performances declined gradually even when he was not overtly injured. Nonetheless, contrary to the expectations of many, after his initial world masters title at age 40, he did not proceed to take the masters distance record book by storm in subsequent years.

Paula Radcliffe

Paula Radcliffe was born in December 1973, and began running with her distance-running father, at age 6.  Like Hailie Gebreselassie, she achieved international prominence in 1992 when she won the World Cross Country junior championship in Boston.  At senior level she continued to be successful at the World Cross Country Championships. On the track she was successful at European level but did not match Gebreselassie’s dominance at the highest international level.  Her best performance at the track World Championships was a silver medal in Seville in 1999. She finished fifth in the 5000m in the Atlanta Olympic s in 1996 and 4th in the 10,000m in Sydney in 2000.  The first of many significant injuries had emerged in 1994 when she was forced to miss the World Cross Country championship due to a foot injury.

After several strong half-marathons, she turned her attention to the marathon in 2002 with immediate success, winning the London marathon in 2:18:55, a world best time for a woman’s only race. Then in Chicago in October 2002 she set a world record time of 2:17:18. In my mind, that was her greatest race. The determination with which she pushed-on alone in the final miles was awe-inspiring.    Perhaps she will be best remembered for her astounding time of 2:15:25 in London the following year. However, despite her claims to the contrary, in that race she was clearly paced virtually all the way by two male runners, with one of them beside her as they rounded the final turn into the Mall.    The pacer was unceremoniously shunted aside by a marshal as Paula ran the final 200 metres to the tape.  Unfortunately injury blighted her chances in the 2004 and 2008 Olympics. The sight of her sitting disconsolately at the roadside after dropping out of the Athens marathon in 2004 was a striking contrast to her powerful performance in Chicago two years earlier and her triumphant run to the finish line cheered on by her home crowd in London in 2003.

She had a good year in 2005, setting a new world best for a woman’s only marathon with a time of 2:17:42, and won gold in the marathon at the World Championships held in Helsinki.  In 2006 she took a break from running due to injury, and then to have her first child, Isla.  A stress fracture of her spine delayed her return to running in 2007, though in November 2007 she won the New York marathon in a time of 2:23:09. She withdrew from the London marathon in 2008 due to a foot injury. She was also experiencing hip pain which was subsequently shown to be a stress fracture of her femur.   These injuries disrupted her preparation for the 2008 Olympic marathon in Beijing, where she struggled with cramp and eventually finished in 23rd place.  Again in November 2008 she won the New York marathon, recording 2:23:56, but soon after was plagued once again by injuries, including knee problems. She took another extended break due to injury and also to have her second child.

She set her sights on a 2012 Olympic qualifying time in the 2011 Berlin Marathon.  She came third with a time of 2:23:46, which was adequate for Olympic qualification, but not up to the standard she was aiming for.  She ran a disappointing half marathon in Vienna in 2012, where she was left trailing well behind Gebreselassie despite her 7:52 head-start.   She withdrew from the 2012 Olympics due to a foot injury and eventually retired from competitive running in 2015, after a farewell run in the London marathon surrounded by a pack of club runners. Her 25 year career had included flashes of glory that justify regarding her as the greatest female marathoner of all time, but also a sad trail of opportunities blighted by injury.

Comparing the training of Haile Gebrselassie and Paula Radcliffe.

Anecdotal evidence based on selected individuals proves very little.   Perhaps we could have selected other athletes: Emil Zatopek and Grete Waitz from earlier times or Eliud Kipchoge, the current dominant figure in the marathon.  However, to provide context for a discussion of the impact of training on longevity, Radcliffe and Gebrselassie stand out as exemplars.  They both pushed training near to the limit feasible with our current understanding of what the human body can stand and both were competitive at the highest level of distance running for more than two decades.  It should also be borne in mind that many factors: genes, early life experiences, subsequent training and mental approach contributed to their successes.   Nonetheless, by illustrating what is humanly possible, exceptional individuals do provide a valuable test of the credibility of any conclusions we might draw from more scientific examination of evidence drawn from samples more representative of typical humanity.  I have reviewed both Paula’s and Haile’s training in greater detail in previous posts, and will highlight what I consider to be the key features here.

The characteristic feature of Paula’s training was a high volume (typically between 120 and 160 miles a week when in full marathon training) with a large proportion at a place near to lactate threshold.  We can make informed guesses about the relative contributions of genes and training to her performances on account of Andrew Jones’ detailed report of physiological tests performed over many years.  At age 19, Paula already had an exceptionally high VO2max of 70 ml/min/Kg.   She had been a runner since age 6 and in her late teens had trained up to 30 miles per week. Beyond age 19 she built up to the high volume training characteristic of her later training yet over the subsequent years her VO2 max remained approximately constant. Thus it is reasonable to conclude that her high aerobic capacity was largely due to genes and early development, rather than her subsequent high volume training.

While her VO2 max did not increase after age 19, her pace at lactate threshold, the crucial determinant of marathon performance, did increase markedly.  In part this was due to an increase in leg muscle power which produced an increase in speed at VO2max (described in greater detail below).  However, measurement of her capacity to metabolize lactate demonstrated that the major contribution to her enhanced pace at Lactate Threshold came from an increased ability to metabolize lactate, thereby delaying the onset of lactate accumulation until she was nearer to VO2max.  It is probable that the high proportion of her training near to lactate threshold helped promote her ability to metabolise lactate.  However there are less stressful ways to achieve this effect, as I will discuss in my next post.

Paula also adopted measures to give herself the benefits of high altitude training . Not only did she frequently train at Font Romeu in the Pyrennees and occasionally in Kenya, but she also slept in a low oxygen pressure tent to stimulate the production of red blood cells.   The high altitude training would have added to the stimulus for lactate metabolism, though the lack of increase in her VO2max makes me dubious that sleeping in the low pressure tent was worthwhile.

Another potentially crucial aspect of Paula’s training arose from an assessment of her leg muscle power during a physiological assessment by physiotherapist, Gerald Hartmann, after her disappointing performance in the 10,000m at the Sydney Olympics in 2000.   To remedy the observed lack of power, Hartmann recommended a programme of plyometric jumping and hopping.  I suspect that this played a crucial in the development of her speed at VO2max and in the transformation of her performances over the following 2 years, though it was not without risk of injury.   Although her first seriously disruptive injury had been in 1994, it was in the period 2004 to 2015 than injury became a dominant theme shaping her career.  While no definite conclusion can be drawn, her story is a salutary reminder that plyometrics are effective in promoting leg muscle power but also risky.

Haile’s training was also characterized by a high volume. He typically covered a total of 190 Km (approximately 120 miles) per week.  Almost 60% was at 6:15 min/mile or slower (substantially slower than his marathon pace of 4:48 /mile). About 8 % was at paces near marathon pace, and 6% faster than marathon pace.  He trained at Addis Ababa at an altitude above 8000 feet. Thus the training performed near to marathon pace would have been more demanding than marathon pace at sea level.   However, it is noteworthy that he was careful to avoid too much stress. In a Q&A session with the BBC in 2002 he stated: ‘I generally have 13 training sessions a week. On Sunday I only run once. Each week, I try to do 3 speed sessions, one long run (1½/2 hours) and one or two Fartlek sessions. The rest of the sessions are endurance runs that I try not to run too fast. They help my muscles to recover from the hard training’. Thus 7 or 8 of his 13 weekly sessions were intended to facilitate recovery.  He stated that one of the best pieces of advice about running he ever received was from his agent Jos Hermens. He states: ‘Jos taught me not to run too many races and to train and rest well. When I started to do this, my performances got even better’.

In summary, both Haile and Paula employed high volume training, but whereas Paula’s training emphasized paces near to lactate threshold, Haile’s approach was more polarised, including a substantial proportion at a comfortable pace, consistent with his emphasis on recovery. While it is probable that Paula has a greater initial predisposition to injury, reflected in the onset of injury problems early in her career, it is tempting to  speculate that if she had adopted a training program that included a higher proportion of recovery runs she might have suffered fewer frustrating injuries.

Ed Whitlock and Gene Dykes

I have discussed Ed Whitlock and Gene Dykes in detail in recent posts.  Here I will summarise the key points relevant to our present discussion.  Ed was a talented school-boy athlete but gave up running while at university following a persistent Achilles problem.  Almost two decades later, after moving from the UK to Canada, he recommenced running almost incidentally in response to his wife’s suggestion that he might coach local youngsters.  He achieved world class as a masters middle distance runner, winning a world masters M45-49 title for 1500m.  Although his main focus was on the track, he ran the Ottawa marathon in 2:31:23 at age 48. He continued to run competitively as a masters distance runner, training fairly intensely including intervals.  When he turned to focus on the marathon in his late 60’s he introduced a major change in his training, phasing out the speed work and replacing it with multiple long runs up to 3 hours duration each week. He ran with a slow shuffling gait designed to minimise the stress on his legs.  His only high intensity running was in frequent races over 5K or 10K, run with a powerful, fluent stride that contrasted markedly with the shuffling gait of his long runs.  As I have described previously, he took great care to minimise risk of injury. He became the first 70 year old to break 3 hours for the marathon.  Subsequently, at age 73 he set an astounding M70-74 world record of 2:54:48.

In the following years he continued his programme of multiple long slow runs each week, actually increasing the duration up to 4 hours   On several occasions he was forced to stop running for up to a year due to arthritis.  On each occasion, as the arthritis settled he recommenced his training, building up slowly and using his performance in 5K or 10K races to assess his fitness.   In many of the years from age 70 to 85 he utterly smashed the single year age record for the marathon, while also setting world records at many other distances.  However at age 83 he complained of persisting pain in his groin which he assumed was an injury. Unfortunately, in retrospect it appears that it was pain from prostate cancer.  Nonetheless he took 38 minutes off the M85-89 marathon world record only a few months before his death shortly after his 86th birthday.  Although he modestly maintained that he could only claim that his approach worked for him, his response to his training suggests that an extremely polarised program with a large proportion of very low intensity running is a good strategy for achieving longevity.

Gene Dykes’ story is different.  He too had been a schoolboy athlete but found himself out of his depth on the track in college.  He continued to run but described himself in mid-adult years as a ‘some-time jogger’.  At age 49 he ran a marathon in his adopted home town, Philadelphia, but finished injured and did not run again for 6 years.   After recommencing, he made a determined effort to improve his marathon time, achieving a best of 3:16 at age 65. When he failed to improve at his next attempt in Toronto in 2013, he was afraid that age might be overtaking him.  To forestall that fate, he engaged a coach, John Goldthorp, who recommended a demanding program that included a substantial number of tempo sessions.  Gene continued to run a massive volume of slower paced running, including ultras of up to 200 miles.   The combination of tempo sessions with long slow ultras worked. In the Rotterdam marathon in April 2018 he became the 2nd 70 year old to break 3 hours, with a time of 2:57:43.  In contrast to Ed, Gene was still improving in absolute terms.  Six months later in Toronto he recorded 2:55:17 and then at the Jacksonville Marathon in December he recorded 2:54:23, 25 seconds faster than Ed’s M70-74 world record.  However, the race was not sanctioned by USA Track and Field, and hence Gene’s performance was not recognised as a world record.  Gene’s ability to respond well to such demanding training is truly phenomenal.  His Strava page states: ‘I run races from 1 mile to 240 miles. I run on roads, trails, track, and cross country. I run in all kinds of weather. I run a lot.’  In contrast to the usual pattern of deterioration with age beyond 40, his continued improvement into his 70’s is extraordinary.

Speculation and Conclusions

In light of the fact that both Ed’s and Gene’s training included large volumes of very slow running, it is interesting to speculate on how very slow running might enhance marathon performance.  The three main requirements for a marathoner are the ability to maintain a good pace in vicinity of lactate threshold, efficient use of stored fuel and resilience of the leg muscles.   It is likely that large volumes of relatively low impact running serve to enhance muscle resilience. It is also possible that very low intensity running is an effective way to enhance fuel efficiency by promoting shuttling of lactate from fast to slow twitch fibres where it augments the fuel supply. I will return to this issue in my next post.  However the question of whether or not Gene’s very demanding schedule will result in longevity similar to the phenomenal longevity of Ed remains to be established.

Overall, the four exceptional athletes we have discussed in this post illustrate that high volume training together with at least some intense sessions is required for world record breaking distance running performance.  The lessons regarding longevity are less clear, but the comparison of Haile Gebrsalessie with Paula Radcliffe suggests that high volume training tempered with a substantial proportion of relatively easy recovery runs is a safer route to longevity; Ed Whitlock’s training adds more evidence supporting this conclusion. The future performance of Gene Dykes will be an interesting test of the degree to which intense training is consistent with longevity

However, anecdotes about elite athletes only tell us about the limits of what is humanly possible. My next post will examine what the scientific evidence suggests for enhancing longevity in less extraordinary distance runners.

Interpreting messages from the body to the brain

May 27, 2019

My hopes of blogging more frequently in 2019 have so far been frustrated by a heavy schedule at work.   But even more frustrating has been the fact that during the past few months various things have made it difficult to find time even to run. These things have included preparing our house for sale and attending academic conferences.  Potentially more promising with regard to opportunities for running was the task of bringing our newly purchased canal boat from the south of England to the Midlands. Canal boats travel slowly and the journey took more than two weeks.  During journeys in our previous boat, I usually made the most of opportunities to run along the canal tow path, circling back as required to assist with the task of opening lock gates. However our new boat is much longer and has a deeper draught than our previous boat. Our route to the Midlands included the River Thames from London to Oxford and thence northwards on the Oxford canal. The wide river offers relatively few opportunities to disembark to run along  the riverside path. The Oxford canal meanders through delightful countryside but is notoriously shallow. With the deeper draught of the new boat we faced the risk of running aground. It was best for me to remain on board, prepared to use a pole to lift the bow slightly and nudge the boat towards deeper water, while at the stern my wife put the engine into reverse at appropriate moments to enable the propeller to force water beneath the flat bottom of the boat.  It was a journey with delightful memories, but sadly I did not run along the canal tow path at any point.  As a result, I am now at a lower ebb of fitness than at any time in the past 15 years.


Three days ago I set off for a run across the Lakeland Fells. I had no intention of running at even a moderate pace.  My intention was to begin to rebuild some fitness while enjoying the spectacular mountain scenery.  On the steep ascents I clambered upwards maintaining at least three points of contact with the rock over craggy outcrops; on the descents my main goal was to remain upright.   However, on the grassy level ridge-top, I was dismayed by how uncomfortable I felt.  Although my pace was slow, the depth and rate of my breathing told me I was near the upper limit of the aerobic zone. To my dismay, I felt a strong urge to stop and walk.  It is very rare that I ever feel the urge to stop when running. When pushing hard I often need to dig into my reserves of determination to sustain the pace, but I am rarely tempted to slow to a walk.  At first I was inclined to acquiesce to my body’s clamour for respite and simply enjoy the scenery. But before acquiescing I wondered about the nature of the signals my body was sending to my brain.

I was definitely short of breath. No doubt the accumulation of carbon dioxide and acidity in my blood was triggering a barrage of moderately insistent messages from the chemoreceptors in the large blood vessels to my brain. But I usually interpret this level of breathlessness as exhilaration rather than distress.  In addition, my leg muscles felt a little sluggish.   However, there was none of the sharp pain that arises from the transient accumulation of lactic acid when running at speed, nor the dull ache that arises from microscopic damage to muscles after an hour or more of running.  In reality, none of the signals to my brain could be interpreted as pain; they were merely markers of effort.

Possibly on account of the need to avoid wasting precious energy reserves faced by our distant forebears living on the African savannah 2 million years ago, our brains are predisposed to minimise unnecessary effort.  However, in a world where we are no longer prey nor predators in everyday life, this natural predisposition to minimise effort tends to be far too over-protective.   While it is necessary to be a little cautious when returning from a lay-off from running, at this stage of my run, with only a few miles behind me, there was little need for caution.

It was time to reinterpret these signals from body to brain.  The sensation of effort was cause for satisfaction rather a signal of need for rest. However, my legs felt unpleasantly clunky.  At this point I shifted my focus from the clunkiness of my legs and engaged a few of the tricks than promote fluent form.  In particular I focussed on the rhythmic swing of my arms, allowing the down-swing of each arm to pace the lift-off of the opposite foot from stance.   The sensation of clunkiness disappeared.  Despite my slow pace I began to feel like a runner once again, running freely along a mountain ridge with the central Cumbrian Fells defining the skyline ahead of me and the intricate facade of the distant Howgill Fells away to my left, across the valley of the river Lune that marks the natural border between Cumbria and Yorkshire.    I am still far from fit, but it is good to once again feel that I am a runner.

Ed and Gene’s genes? How do genes contribute to the longevity of a distance runner?

January 4, 2019

It is very likely that genes played an important part in the phenomenal performances of Ed Whitlock and of Gene Dykes, the only two individuals who have run a marathon in less than 3 hours at age 70 or more.  In my recent posts I have outlined their athletic careers (here and here).   What can we learn from them?  There is nothing we can do to change our own genetic endowment.  However, it is almost certain that Ed and Gene’s successes were heavily dependent on the way in which their training shaped the way in which their genes were expressed. Similarly, we can alter the way our own genes are expressed.  Even though we can only make informed guesses about what it was that transformed Gene and Ed into great marathoners, the available scientific evidence about the way in which the expression of genes can be modified by training allows us to draw some potentially useful conclusions.

The combined effects of multiple genes

The first noteworthy point is that it is unlikely that Ed and Gene’s longevity as distance runners was due to an advantageous version of a single influential gene. They were almost certainly each blessed in separate ways by a combination of many genes that each contributed to their success.   In a review of the evidence available a decade ago, Bray and colleagues concluded that over 200 genetic variations contribute to physical fitness and athletic performance.   Subsequent evidence has confirmed that multiple advantageous genetic variants contribute to various aspects of fitness, including the ability to benefit from training.    Of particular interest, Bouchard  and colleagues identified 39 sites in the human genome at which DNA variations are associated with the magnitude of increase in VO2max in response to a 20 week cycle ergometer training program  (3 times/week with sessions increasing in duration and intensity up to 50 minutes at  75% HRmax).   In that study, Bouchard examined only about 300,000 sites of DNA variation. It is important to note that they merely demonstrated an association between variation at 39 of these sites and the  response of VO2 max to training. Because genes that are located nearby on a chromosome tend to be inherited together, it is only possible to conclude that the genetic variation that was actually responsible for the increased training response was in the vicinity of one of the 39 sites.

With regard to the question of longevity as a runner, it is probable that genes associated with the  maintenance and repair of multiple body tissues play a crucial role.  These genes are likely to contribute also to overall life expectancy.  Therefore it is relevant to consider genetic variations that are associated with long life expectancy.  Again, the evidence suggests that many genes are involved.   In a study that compared 801 centenarians with a matched control group, Sebanstiani and colleagues identified 281 locations in the genome where variation is associated with the exceptional longevity.

Perhaps even more relevant to the question of our longevity as runners, Sood and colleagues examined the relationship between expression of genes and healthy aging.  Expression of genes is the translation of the DNA code into proteins that make up your body and control its function. The process of translating a strand of DNA into protein involves the production of a ‘messenger’ RNA molecule in which the sequence of coding letters (A,C,G and U) matches the sequence of coding letters (A,C,G and T) in the DNA strand.  The degree to which a gene is expressed in body tissues can be quantified by measuring the amount of the RNA corresponding to that gene. Sood and colleagues demonstrated that the amounts of each of a set of 150 different RNA messenger molecules isolated from muscle tissue provided a reliable predictor of healthy old age. The same set of RNA molecules derived from skin or brain tissue predicted healthy aging. In other words, the degree of expression of 150 genes in several different types of tissue, including muscle, is a good predictor of healthy aging.


Relevant genetic variations influence the effectiveness of common bodily functions

The second point is that it is likely that the relevant advantageous genes act by increasing the effectiveness of common bodily functions rather than providing novel functions that are unique to the individuals possessing those genes. The majority of genetic variants arise from differences in a single letter of the genetic code due to a mutation at some time in human history at a single location in the human DNA sequence.  Genetic variation due to such a mutation of a single letter in the code is known as a Single Nucleotide Polymorphism (SNP)

Not all of the DNA sequence is translate into proteins. Some stretches of DNA act to control the translation of those parts of the sequence that are translated.  The role of other regions of DNA remains unknown.  If a SNP occurs in a section of the DNA that codes for a protein, it can change the amino acid at the corresponding location in the specified protein.  This is known as a mis-sense mutation.  A mis-sense mutation is likely to produce a small change in the way that the amino acid chain that makes up the protein folds to create a three dimensional structure.  The change in the three dimensional shape of the protein is has the potential to change the effectiveness with which the protein performs its function.   However, even if disadvantageous, such changes rarely abolish the function of the protein. As we shall see there are ways in which life-style and training might compensate for the less advantageous version of gene.

If the SNP occurs in a non-translated section of DNA that nonetheless controls the translation of nearby DNA that codes for a protein, the SNP is likely to effect the amount of that protein which is produced in response to the various triggers that promote translation of DNA.  Again life-style and training might compensate for less advantageous versions of the gene.  Thus, in the case of the majority of the genetic variations that account for the differences between healthy individuals, there are ways in which we might partially or even fully compensate for a less advantageous version of the gene.

The expression of genes is modified by training

The practical issue for running longevity is that the expression of genes might be modified by training.  The key point to learn from the athletic careers of both Ed and Gene is that they each achieved greatness after a marked changes in their training.  As outlined on my previous posts, the thing that made Ed into a marathoner was the adoption of a program with multiple long slow runs each week.  Nonetheless it should also be borne in mind that his greatness was not limited to marathon: his 36 masters world records covered the distance range from 1500m to marathon.  In contrast, the turning point for Gene was the incorporation of high intensity training into his training schedule.  Nonetheless, the underlying foundation was his phenomenal ability to recover from intense training and frequent demanding racing.

It appears that there were both similarities and differences in the genetic endowments of Ed and Gene.  We do not know which specific advantageous genetic variations provided the foundation for their great performances. However, it is clear that their achievements were based not only on their genetic endowment but on their training. It is plausible, indeed probable, that their genetic endowment facilitated their response to training.  We are beginning to understand the role of several specific genes or groups of genes that mediate the body’s response to training.  It is potentially informative to examine the way in which the expression of these genes is modified by training, and to review the athletic careers of Ed and Gene in light of this.

Free radical generation during running: the Nf2 system.

During physical exercise, oxygen utilization typically increases by a factor of 10 to 20 in the active skeletal muscles.  The process of oxidation of fuel (either glucose of fats) in mitochondria, involves the transport of electrons between molecules, and inevitably results in the production of so called Reactive Oxygen Species (ROS) and other ‘free radicals’ that contain atoms of oxygen or nitrogen with unpaired electrons. By virtue of having unpaired electrons available for forming new chemical bonds, these ROS and other free radicals react strongly with nearby molecules. In particular, they are prone to attack any biological macromolecules especially DNA, amino acids, proteins and unsaturated fatty acids, in the vicinity.  This potentially damaging process is known as oxidative stress.

The body has several natural defences against oxidative stress.   The nuclear erythroid 2‑related factor 2  (Nrf2) pathway is a genetic pathway that leads to the switching-on of over 200 genes that serve a critical role in protecting against the cellular stress induced by exercise.  This defensive pathway is switched on by exercise.  For example, in a study of mice, Mei and colleagues demonstrated that eight weeks of aerobic exercise training lead to an increase in Nrf2 mRNA expression in the hind‑limb muscles. This suggests that graduated increase in aerobic exercise starting at low intensity might lead to enhanced defence against the potentially damaging effects of high intensity exercise. Furthermore an athlete with a variant of any of the many genes in this pathway that promoted more effective defence would be expected to gain especially enhanced protection against oxidative damage.

Protein synthesis:  the mTOR complex

mTORC1 is a protein complex that controls the synthesis of proteins.  mTORC1 activation plays a crucial role in the growth and repair of body tissues, including skeletal and cardiac muscle. Resistance exercise induces signaling cascades in skeletal muscle cells that result in the activation of mTORC1, and subsequently initiates muscle protein synthesis, thereby facilitating muscle hypertrophy.  Growth factors such as insulin play a key role in this anabolic process.

In healthy young people, aerobic exercise does not produce a strong activation of mTORC1.  However, in the elderly, muscle protein metabolism is resistant to insulin’s anabolic effect. This is associated with reduced insulin induced vasodilation.  Fujita and colleagues demonstrated that in a group of 70 year olds, a 45-min treadmill walk at 70% HRmax restored the anabolic response of muscle proteins to insulin during amino acid infusion 20 hours later.  It did this by improving the function of the endothelial cells lining small blood vessels, thereby promoting vasodilation and mTORC1 signalling.  This suggests that in the elderly, moderate intensity aerobic exercise may improve the muscle anabolic response during subsequent feeding.

However the overall effects of mTORC1 are complex.  It has been proposed that inhibition of mTORC1 (eg by dietary restriction) might enhance life expectancy by slowing the rate of depletion of stem cells.  But irrespective of the questionable effect of inhibiting mTORC1 on overall life expectancy, longevity as a runner almost certainly requires the minimization of age-related muscle loss, and hence mTORC1 signalling during post-exercise nutrition.


Recent studies of messenger proteins excreted from muscle tissues have revealed a large number of proteins (approximately 250 in human muscle tissue) that exert wide-ranging, potentially beneficial effects on metabolism throughout the body.  These messenger molecules are known as myokines.  Aerobic exercise promotes the expression of the genes that code for many of these myokines.  One that has recently attracted attention as a mediator of the beneficial effects of endurance exercise on cardiovascular health is myonectin.  In a study of mice, Otaka and colleagues demonstrated that treadmill exercise increased circulating myonectin levels, and reduced cardiac damage associated with impaired coronary blood supply. This effect was not observed in mice lacking the gene for myonectin.   Furthermore they demonstrated that the beneficial effect of myonectin was abolished by blocking a metabolic pathway involved in inflammation.

DNA repair and protection of telomeres

Telomeres are RNA-protein complexes that serve as protective caps on chromosomes, protecting the DNA from damage during cell replication.  Usually telomeres become shorter with age, eventually reaching a stage where cells can no longer replicate.  Thus telomere shortening is potentially an important marker of aging.  However shortening of telomeres is not inevitable. Telomerase is an enzyme that acts to increase the length of telomeres.  Although the mechanism of telomere shortening or lengthening are only partially understood, it appears that low intensity aerobic exercise promotes the lengthening of telomeres.   In part this is probably partly due to the protection against oxidative stress (discussed above). In addition,  exercise promotes the expression of genes coding for proteins that repair DNA and protect telomeres.

Several studies reveal that endurance athletes tend to have longer telomeres.  For example, in a comparison of 67 ultra-marathoners with 56 healthy non-marathon runners,  Denham and colleagues  found that the ultra-runners had significantly longer telomeres


Effects of aerobic exercise on resilience, achieved by modifying the expression of genes involved in aging


The development of resilience

The genetic evidence we have reviewed so far demonstrates that aerobic exercise switches on the transcription of many genes that are potentially helpful in strengthening tissues and in protecting against damage due to oxidative stress. These are crucial achievements if one’s goal is not only to increase longevity as a runner, but also to achieve the resilience required to withstand the effects of impact forces generated by thousands of footfalls during a marathon.

The evidence from genetics indicating that low intensity aerobic exercise has a role to play fits well with the fact that both Ed and Gene included a lot of low intensity running in their training schedules (as described in my recent posts here and here.)   However the fact they coped so well to such training suggests that their genetic endowment included especially advantageous versions of relevant genes.  We do not know which of the genes we have discussed have multiple variants differing in the degree of benefit they confer.  However, it is very likely that there are functional important variants of at least some of these genes.

According to the report by the Ensembl genome database project, by December, 2016, more than 155 million unique variations in DNA sequence had been identified from the analysis of the DNA of more than 2,500 individuals.  It is estimated that there is on average one SNP for every 20-30 letters of the genetic code. As the number of letters of code required to specify a single protein ranges from about a thousand up to several million, there is a high probability that there are SNPs giving rise to variations in the proteins specified by many of the genes of interest.   In about 5% of SNPs the changes in the structure of the protein that have appreciable functional effects. Therefore it is plausible and indeed probable that Gene and Ed were each endowed with advantageous versions of the genes whose expression promotes enhanced resilience.

This is especially likely in the case of Gene. This would provide a plausible explanation for his phenomenal ability to recover from intense training and frequent demanding racing.   Favourable variants of genes promoting resilience would be expected to facilitate greater training volume  and in turn establish a virtuous circle promoting further expression of these genes and even greater resilience.

To paraphrase Gene’s own words, to become a better runner you must run a lot.  But perhaps on account of his genetic endowment, running a lot came relatively easily to Gene.  All that was necessary to enable him to run a lot was the determination to persist when his body cried out for rest. For those of us less well endowed, such determination would be likely to lead to disaster.   We need to be a little more shrewd in planning our training and adjusting our lifestyle.

I suspect that Ed was a little less well endowed with the genes that that promote resilience.  Nonetheless, he developed a training strategy that was optimised to build his capacity to withstand multiple training runs of three hours or more on consecutive days.  Ed’s cautious approach helped to keep him at the top of the word rankings for 18 years, from his 2:51 marathon at Columbus Ohio in 1999 at age 68, until his 3:56:38 in Toronto in 2017 at age 85, shortly before his death a few months later.

Enhancing VO2max and pace at lactate threshold

Traditionally the major focus in planning training for distance running has addressed the goals of increasing VO2max and increasing pace at lactate threshold.  The evidence we have reviewed so far has focused largely on genes that are likely to enhance resilience.  It is probable that low intensity exercise is optimal for this.  In contrast, there is abundant evidence that VO2max can be achieved more efficiently with more intense training.

As mentioned above, Bouchard identified 39 genetic variants that predict the response of VO2 max to standardized exercise training programs.   Ed’s multiple age group world records across a range of distances from 1500m to marathon suggest that Ed was more strongly endowed with favourable variants of the genes that influence trainability of VO2max. At age 70, he had a VO2max of 52.8 ml/min/Kg compared with the average of 35 for a 70 year old.   It is noteworthy that he had done a large amount of intense interval training in his 40’s and 50’s but over the 18 years when he set so many world records, his high intensity training consisted of participation in fairly frequent  5K to 10K races.  In contrast Gene only became an elite runner after he introduced a substantial volume of higher intensity running into his training schedule.  It is noteworthy that since turning 70, Gene has recorded life-time personal bests times at 1500m, 10K, HM and marathon. The questions of how long he will continue to improve and whether or not he will be breaking Ed’s records at age 85 is intriguing.

The balance between protection and harm

There is something of a paradox regarding the benefits of exercise on resilience.  In particular, the increased expression of genes associated with the Nf2 system that protects against oxidative stress (described above) is triggered by exercise that produces oxidative stress.  In other words, the increased protection against damage arising for oxidative stress is triggered by the stress itself.   You develop the protection against danger by exposing yourself to the danger.   The balance between protection and harm is likely to depend on appropriately graduated build-up of the training load.   Ed was very careful in building up his training volume via low intensity running after illness or injury.  Because high intensity exercise is associated with much greater stress, illustrated by much greater production of the stress hormones adrenaline and cortisol, getting the balance right with the higher intensity exercise employed by Gene is likely to be much more tricky.

At any point in your running career, the right balance is likely to depend not only on the genes you were endowed with at birth but also on past running history.  In Gene’s case, it is almost certain that he is endowed with favourable versions of multiple protective genes. As a result his performances are still on an upwards trajectory at age 70, based on training that would probably be damaging for many of us.  Before attempting any further speculation on Gene’s likely future trajectory, we need to look more closely at the evidence regarding both local muscle damage and repair, and whole-body processes including hormonal influences and inflammation that are likely to play a key role in longevity.  I will address those topics in future posts in this series.

Implications for less gifted athletes: assessing the balance.

Speculation about the nature of the genetic endowments of Ed and Gene is of interest because it provides some insight into possible reasons how they were able to achieve the target of running sub-3 hour marathons in their 70’s. It also helps us identify potentially important commonalities in their training, and provides some pointers to the issues to consider if we wish to emulate their training.  However, for most of us, the practically important thing about genes is not the differences between individuals in their genetic endowments, but the fact that the expression of genes varies greatly over time within an individual.  Many of the factors that influence gene expression are under our own control. Most importantly, exercise is a powerful modulator of gene expression.

In the past, much of the emphasis on planning training for distance running has been on maximizing VO2max and increasing speed at lactate threshold.  However the evidence that training influences gene expression provides us with a clearer understanding of how low-intensity training might enhance the resilience that is crucial for withstanding the thousands of potentially damage impacts at footfall  during a marathon, and also crucial for optimizing running longevity.

Nonetheless the current level of understanding of the effects of training on gene expression is rudimentary.  While the current evidence does provide an understanding of why it is beneficial to run a lot, it also highlights the paradox that developing protection against damage requires exposing yourself to the risk of damage.  The evidence we have considered so far implies that an appropriately graduated build of training load is essential.  It provides a clear rationale for the base-building advocated by Arthur Lydiard on the basis of personal experience more than sixty years ago.  However before we can advance beyond the lessons based on Lydiard’s intuition we need a better understanding of how to achieve the balance between benefit and harm.  We will return to address this question after our more detailed examination of the mechanism of tissue damage and repair.

Plans for 2019

January 1, 2019

Happy New Year.

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

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

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

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

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

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

The similarities of two extraordinary marathon runners: Ed Whitlock and Gene Dykes

December 21, 2018

In my previous post, I emphasized the differences between Ed Whitlock and Gene Dykes, undoubtedly the two greatest elderly marathon runners ever.   Since that post, Gene has captured Ed’s M70 world marathon record, though they still stand should to shoulder in the Pantheon of distance runners.

[Edit: as noted by Ewen in the comment below, Gene’s record has not been ratified by IAAF. Gene wrote on his Facebook page on 22nd Dec 2018:  ‘although the Jacksonville Marathon is certified by the USATF, the race was not sanctioned by the USATF, and both must be valid for recognition of records by USATF/IAAF…..I am still proud of what I’ve accomplished – it just looks like it’s not going to be “official”. That said, I still have four more years to do it right, and, who knows, that might happen sooner than you think!]

In my previous post I emphasized that the two essential requirements for a marathon runner are the ability to sustain a pace in the vicinity of lactate threshold for a period of several hours, and the resilience required to withstand the damaging effects of impact forces generated by more than 30 thousand footfalls.  Examination of their early running careers and the process of transition to marathon greatness in their seventies reveals different routes to a similar outcome.  In this post, I will focus on the way in which their differing approaches to training allowed them to achieve a similar outcome in their early seventies despite differing natural endowments.


Ed Whitlock

Ed was gifted with an impressive ability to sustain pace in the vicinity of lactate threshold throughout his running career.  As a ‘young’ masters athlete he employed a periodized approach, building a base with a high volume of running in the winter and focusing of fairly intense speed work on the track in spring and summer. He won the M45 world masters 1500m championship in 4:09 at age 49. However, he only achieved greatness as a marathoner after developing a training program based on multiple long runs of several hours duration each week.  I have described his training is detail in several of my preceding posts.   He designed this program in a manner that minimised wear and tear on his body, most notably by adopting a shuffling gate that minimised the impact at foot fall.  Nonetheless, the duration of his long runs necessarily entailed many thousands of impacts, and it is reasonable to conclude the almost daily repetition of these long runs developed the resilience required for elite marathoning.  He became the first person over the age of 70 to run a sub-three hour marathon when he ran 2:59:09 in the Toronto Waterfront Marathon in 2003 at age 72.  The following year in Toronto, he utterly shattered his previous M70 marathon world record with a time of 2:54:48.   Over a period of 15 years he set 36 world records across the age range 70 to 85, including distances from 1500m to marathon.


Gene Dykes

In contrast, although Gene was a runner for most of his life since early teenage, it was not until his sixties that he exhibited any signs indicating the possibility of future greatness.  In his late fifties and through his sixties he ran long distances in training, mostly at modest pace.   At that stage, he was showing signs of noteworthy, but not extraordinary, resilience. He further developed this resilience by running ultras.  However it was the inclusion of faster sessions in his training program after engaging John Goldthorp as his coach 5 years ago, that allowed him to develop the ability to sustain a pace near lactate threshold,

In a post on the Slowtwitch thread in October 2018 Gene described a typical week as:

2 recovery runs of 6 miles (8:00-9:00 pace)

2 general aerobic runs of 10-16 miles (7:00-8:00 pace)

1 fast paced workout (some kind of intervals from 30 seconds to many miles in the 6:10 to 6:40 range)

1 Long Run (RR pace, picking it up in the last few miles)

He also races most weekends.  Earlier this year, he ran demanding long races (mainly marathons or ultras) on 12 consecutive weekends. He sometimes runs an ultra on the Saturday and a marathon on the Sunday.

He became the second 70 year old to break 3 hours for the marathon when he recorded 2:57:43 in Rotterdam in April 2018, a few days after his 70th birthday.  Subsequently, he recorded 2:55:18 in the Toronto Waterside marathon in October, 30 sec outside Ed’s M70 world record.  Gene ran the Viste Verde 50Km ultra on Saturday 1st December; the California International Marathon on 2nd December, and then less than two weeks later, he ran 2:54:23 in Jacksonville, Florida, taking 25 seconds off Ed’s M70 world record (2:54:48).   As Ed had run that time at age 73, he still holds the single year age world record for a 73 year old, but he no longer stands alone, head and shoulders above all other elderly marathoners.


Two colossi astride the running world

Ed and Gene are the only two 70 year-olds to break 3 hours for the marathon and jointly stand as colossi of the masters running world, towering above all other masters distance runners. They share both remarkable resilience and also remarkable ability to maintain near-tempo pace for several hours.  Both run/ran huge distances in training; both included/include an impressive amount of demanding racing in their annual calendar.  Their similarities are perhaps more striking than their differences.

Nonetheless, in looking towards the future, it is worth reiterating the differences in the paths they have followed.  Ed was endowed with greater natural speed. There is no reason to anticipate that Gene will ever seriously threaten Ed’s many masters world records in the shorter distance events.  Ed became great by adding long slow training to his previous intense training.  On the other hand, Gene became great by adding intense training to his previous high volume training.  Gene’s ability to recover from intense training and frequent demanding racing is phenomenal.

Gene is improving in absolute terms at age 70.   His 2:54:23 marathon in Jacksonville a week ago is his life-time fastest marathon.  In contrast Ed ran his personal best marathon of 2:31:23 at age 48.   Ed was already declining in absolute terms by the time he achieved colossal status as a masters marathoner. Nonetheless, despite declining in absolute terms, he continued to take major chunks off master’s world records until age 85, a few months before his untimely death.

The fascinating questions at this stage are:  for how much longer will Gene continue to improve in absolute terms; and will he still be breaking Ed’s records at age 85?

My belief is that the odds are against Gene enjoying the same longevity as a record-breaking marathoner as Ed, but that is a very debateable issue. I had promised in my previous post that I would review the evidence regarding the optimum training strategy for achieving longevity.   That will definitely be the topic of my next post.

A contrast of two extraordinary marathon runners: Ed Whitlock and Gene Dykes

November 2, 2018

Gene Dyke’s 2:55:17 marathon in Toronto last week, at age 70, was only 29 seconds outside Ed Whitlock’s phenomenal 70-74 age-group world record of 2:54:48 set at age 73.  The similarities and differences in their background and training raise interesting issues about the optimum marathon training, and about the way to achieve longevity as a distance runner.

I have discussed Ed’s training and racing here on this site on a number of occasions, using material based on interviews and on his own frequent comments posted on the Let’s Run website.  In my most detailed analysis of his training and reasons for his phenomenal performance, I speculated that not only was he endowed with genes that favoured longevity, but also I considered that a large part of his success was a gradual build-up of training volume after ‘down-time’, and his care to avoid wear and tear on his body.

Insight into Gene’s training and racing can be gleaned from an interview with Erin Fitzgerald published on her blog in 2015; and more recently, from an interview with Gregg Lemos-Stein that was presented in a Cloud259 podcast in April 2018, and from an interview with Sarah Lorge Butler for Runners World shortly after his 2:55:17 marathon in Toronto last week.  One very striking feature is Gene’s amazing ability to cope with huge volumes of running.  On his Strava page he says: ‘I run races from 1 mile to 240 miles. I run on roads, trails, track, and cross country. I run in all kinds of weather. I run a lot.’

But it is informative to take a somewhat broader view of the backgrounds of these two runners and the transitions that led to each of them becoming phenomenal septuagenarians.

School days and beyond into early middle age.

Both were school-boy athletes.   Gene told Erin Fitzgerald that he became interested in running at age 13 because he fancied a girl who lived 3 miles away.  In high school, and subsequently in college, he ran track. In his interview with Greg Lemos-Stein he admitted that he was ‘blown off the track’ at college.  After leaving college he continued to run but he described himself to Erin Fitzgerald as a ‘sometime jogger’ until 1997 when, at age 49, he ran the marathon in his adopted home town, Philadelphia.   He finished injured and did not run again for 6 years. Up to that point, there was little evidence of greatness ahead.

Ed ran both on track and cross country as a school boy in England.  At that stage he was a gifted distance runner but not extraordinary. He ran a mile in 4:31 and on one occasion beat Gordon Pirie in a cross country race.   He gave up running at University due to recurrent Achilles problems.  He moved to Canada after leaving university, and returned to track running in his early forties.  Although his main focus was on the track, he ran the Ottawa marathon in 2:31:23 at age 48, 1979.  This was based on a winter of high mileage base-building in preparation for middle distance track the following summer.   After some speed work on the track, he won the M45 world masters 1500m championship in 4:09.   It was clear by then that he was not only a gifted distance runner, across the spectrum of distances from 1500m to marathon, but was also showing evidence of the ability to withstand ageing.


The transition to greatness

Gene Dyke

Gene began running again in 2003 in response to encouragement by a group of friends. In the following 10 years he raced fairly regularly and by age 65 had achieved a creditable marathon best of 3:16.  His training was predominantly high volume at a modest pace.  In 2013 he ran the Toronto marathon, hoping to improve his time but was disappointed to finish in 3:29.  He wondered if age had caught up with him, but decided to have a final attempt to see if he could find a better runner within himself.  He hired a coach, John Goldthorp, who lived in a different suburb of Philadelphia. His coach presented him with a program of mixed content, including some more intense running. A substantial number of his sessions were at a pace faster than marathon pace.  He rose to the challenge. Within 5 months of joining John Goldthorp, he ran 3:09 in Boston.

He nonetheless continued to run ultra-marathons, though these were primarily oriented towards building a base for the marathon.  He has run an amazing 2800 miles per year in the past two years. He runs several 200 mile races per year at an average pace of around 2 miles per hour (3 mph average moving pace).   Typically he runs multiple ultras and then spend eight to 12 weeks converting the fitness from that base training into the speed required for the marathon. Even during this period of sharpening-up he still runs some ultras.  Not uncommonly he runs an ultra within the week preceding a marathon.

In April 2018, a few days after his 70th birthday, he ran a 2:57:43 marathon in Rotterdam.  Eight days later, he ran 3:16:20 in Boston.  He reports that he had felt strong in the final stages in Rotterdam.  While running a creditable time in Boston only 8 days after Rotterdam is a remarkable testimony to his powers of recovery, I am nonetheless inclined to wonder whether or not running Boston so soon after Rotterdam was perhaps pushing his faith in his power of recovery a little too far.  I will return to this speculation later.  Whatever the wisdom of running Boston so soon after Rotterdam, he was clearly in fine fettle 6 months later when he took a further 2 minutes 26 seconds off his personal best with his time of 2:55:17 in Toronto.

Ed Whitlock

In his sixties, Ed developed his own training program without a coach. Whereas previously he had done a lot of speed work on the track, he increased the volume of training, mainly in the sheltered surroundings of a local cemetery. He focused on long slow runs most days of the week. He reduced the speed work, largely relying on occasional fartlek session and frequent races.  He typically ran 30 races over distances of 5k to15 K per year, and used his pace in these races to assess his marathon readiness.

In his frequent long runs, which were typically of 2 to 3 hours in duration he did not measure the distance and purposely kept the speed down.  In contrast to the powerful fluent stride he exhibited during the shorter races, his stride during these long runs was a shuffle, intended to minimise impact forces on his legs.  In 2003 at age 72, he became the first person over the age of 70 to run a sub-three hour marathon when he ran 2:59:09 in the Toronto Waterfront Marathon.  He increased the duration of his long slow runs in the following year. In the 20 weeks prior to his phenomenal performance of 2:54:48 in the 2004 Waterfront Marathon he did 67 three hour runs, including 18 on consecutive days.

During the subsequent 13 years he continued to focus on frequent long slow runs. He increased the duration of his longest runs up to 4 hours.  Nonetheless he continued to race at distances from 1500m to marathon. He set 36 five year age-group world records and in addition, a large number of single year age world records.  Those that are missing from his list largely reflect the occasional years in which he suffered accidental injury or recurrence of the arthritis in his knee.  Whenever he returned to running, he built up his mileage gradually.

However by age 84 his training was limited by pain in the vicinity of his upper thigh and groin     Nonetheless, in October 2017, at age 85 he once again returned to the Toronto Waterfront Marathon to set a world record of 3:56:33 in the 85-89 age group, taking 28 minutes off the previous world record.   When compared with the previous record, his sub-4 hour time was a spectacular achievement, though I had been anticipating he might achieve an even faster time.  He himself had expected better.  A photo taken during the race shows him somewhat more gaunt than usual.  At that time, it appeared that the likely explanation was that he had struggled to regain full fitness after the apparent injury in the preceding year.  Sadly he died of prostate cancer in March 2018, a week after his 86th birthday

In retrospect, there were pointers indicating that all was not well even as he completed the Toronto marathon.  In an interview for the New York Times in December 2016 he admitted that he had lost about 10 lbs in weight in recent months and was aware of increasing loss of muscular strength.  As discussed in greater detail in my post shortly after his death, the loss of 10 lbs in weight and loss of strength was perhaps an early sign of the cachexia of malignant disease.


Contrasting strengths

The marathon occupies a special place among distance events.  It demands the ability to sustain a pace not far from lactate threshold for several hours, while also requiring the resilience to withstand the stress on the muscles and connective tissues of the legs arising from the impact at each footfall repeated thirty-thousand fold. Ed and Gene differed in the balance of their natural abilities to handle these twin demands.

Ed’s natural gift was the ability to sustain a pace at or above the lactate threshold.  This natural ability was evident in his performance as a school boy athlete; as a ‘young’ veteran who won the M45 world masters 1500m championship at age 49; and in the multiple world age group records he set across the range of distances from 1500m to marathon in his 70’s and 80’s .  However, to become a great marathoner he needed to develop the resilience required for the marathon. For this he developed his training program with its focus largely on long slow running with a shuffling gait.  He steadily built-up his ability to run for several hours four or more times a week, in the sheltered environment the cemetery within easy reach of his home should any misadventure occur.  He nonetheless maintained his natural capacity to sustain pace at or above lactate threshold well-honed by frequently racing at distances from 5K to 15K.

In contrast, Gene’s strength appears to be remarkable resilience that allows him to run massive distances and to recover quickly.  He had described himself in a mildly disparaging way as a jogger during his young adult life. Racing a marathon at age 49 left him wrecked.   After recommencing running 6 years later, he worked on building his capacity to recover by participating in repeated long distance events.  In this respect his approach bore some similarity to Ed’s, but in contrast to Ed’s care to avoid wear and tear, he was more cavalier.  In part, this might have reflected a tough mental approach.  In his interview with Erin Fitzgerald in 2015, he responded to her question about getting through the tough times: ‘In marathons and beyond, when I have a lot of time to listen to my legs begging me to stop, I think back at them, “This is why I do this.” ‘ His extraordinary ability to recover from prodigious feats of endurance is evidenced by completion of the ‘triple crown’ of three of North America’s iconic 200 mile events in a single year.   In this, mental attitude again played a role. In response to a question from Brenn Jones posted on-line following his interview with Greg Lemos-Stein in 2018, Gene wrote:  ‘With respect to 200’s, the fatigue can get profound, and the sleep deprivation is awful, but the total immersion in stunning scenery and the journey from one point to another, a point that starts out seeming an unfathomable distance away, will haunt you forever, but only in the very best way.’   In the past two years he has not only run 2800 miles each year, but those massive mileages included 1300 miles of racing per year.  While systematic build-up and mental attitude no doubt played a role, it is almost certain that Gene was endowed with a remarkable natural gift that allowed his body to adapt to these prodigious demands.

However, to become a great marathoner he needed not only resilience, but also the capacity to sustain paces in vicinity of lactate threshold.   To address this need his coach John Goldthorp   introduced running at marathon pace or faster into his program five years ago.  Within five months he was transformed from a mid-pack marathoner to an elite.



Ed and Gene have followed different paths to achieving a sub-three hour marathon in their early 70’s.   What does the future hold for Gene?

Ed remained on the pinnacle of veteran distance running for a total of 18 years from his 2:51 marathon at Columbus Ohio in 1999 at age 68, until his 3:56:38 in Toronto in 2017 at age 85, shortly before his death a few months later. It is very likely that a combination of good genes and the care with which he avoided wear and tear on his body played a large part in this.   But it is noteworthy that in absolute terms he was not on a pinnacle in his early 70’s; in fact Ed was actually on a descending ridge rather than a peak during those years, albeit a ridge higher than any other runner had traversed.  He was merely managing to hold the inevitable age-related decline at bay much more successfully than any person before him.   He had shown a striking up-turn in performance between age 70 and 73, taking more than 5 minutes off his performance over those three years, but this was due in part to a relatively poor performance at age 70 (though nonetheless an age group world record at the time).

Gene, in contrast, is on an ascending ridge. His 2:55:17 in Toronto in October was a life-time personal best.  It remains to be seen whether in fact he has actually reached his personal summit.  However the fact that he finished so strongly in Rotterdam in March and might possibly have done better in Toronto if he had not slightly misjudged his pace in the earlier stages, indicates that he is capable of an even faster time.  I think the odds are in favour of continuing improvement over the next few years.

How Gene fares in the longer term future might tell us something important about the feats of endurance the human body can achieve with a lucky set of genes and an effective approach to training.   As I have discussed on this site over the past few years, there is quite strong evidence that in at least some individuals, extreme endurance activities are associated with long term damage to the body. There is an increased risk of heart rhythm disturbances and possibly calcification of coronary arteries.   The mechanism probably involves chronic inflammation induced by repeated stress.

However, there is some evidence that the damage can be alleviated by a careful build up.  Weakening of the right side of the heart after a marathon is less likely in those who have trained adequately.    That evidence is entirely consistent with the common-place observation that an excessive increase in training load can leave us with dramatic DOMS lasting several days, whereas if we build up gradually we can minimize DOMS.  This reflects the fact that acute inflammation is body’s natural mechanism for repairing damage; it is the mechanism by which many of the benefits of training are achieved.  But if the stress is prolonged, acute inflammation can become chronic, leading to persisting damage.  The art of training is harnessing acute inflammation without precipitating chronic inflammation.

Gene emphasizes that he has trained his body to recover well by regularly challenging it.  To my mind, the challenges to which he subjects his body go far beyond what most of us could cope with. Racing in the Boston marathon only 8 days after his herculean performance in Rotterdam at age 70 seemed to me to be risky.   It appears that the combination of his genes and his training have given him a unique capacity to recover and perhaps also to withstand the ageing process.  His progress over the past five years already challenges us to re-appraise what is possible for an elderly runner.   If indeed he continues to defy the ageing process for another decade or more, his example will justify a radical re-appraisal.

Although the genes that govern ageing are only poorly understood, it does appear that a very large number of genes each contribute a small amount to the process. Therefore whatever genetic advantage Gene has is likely to come from a combination of many favourable genetic variations that place him as the extreme of a continuous spectrum, rather than as the result of a rare single genetic variation that has placed him in a unique category.   If he is merely at the far end of a genetic spectrum along which most of us lie, one might expect that many of us might benefit to at least some extent, from more determined efforts to build up our resilience.   If however his brilliance fades quickly, his meteoric rise will carry the warning that the more cautious path of Ed Whitlock might be a better approach to maximizing longevity as a runner.