Creating the Zone

April 3, 2018

The Zone is that magical state in which running seems almost effortless. When it descends upon you, it feels like a state of grace bestowed by Hermes, the swift-footed messenger who could effortlessly outrun all other Olympian gods.   Hermes was also a cunning trickster, and his gift cannot be taken for granted.  The exact nature of the state of mind and brain that facilitates this magical experience remains unknown. Nonetheless as outlined in my previous post, neuroscience has revealed many factors that play a part.

These include the endocannabinoids that are released during exercise. Endocannabinoids are analgesic and create a sense of euphoria. They interact in a complex manner with the neurotransmitter, dopamine, which mediates the experience of reward, and plays a key role in the learning of patterns of behaviour.  The relevant neural circuits connect the frontal cortex, limbic system and basal ganglia.   While the interactions within these circuits that mediate the experience of the Zone appear to be subtle and complex, there is little doubt that these circuits can be trained.

 

Neurons that fire together

In recent years it has become clear that in general brain circuits are far more adaptable, even in adult life, than had hitherto been recognised.  One of the earliest indicators of this plasticity of the adult human brain was provided by Eleanor Maguire’s demonstration that London taxi drivers have an increased amount of grey matter in the posterior hippocampus, a part of the limbic system that is engaged during spatial navigation.    For our present purpose, it is crucial to note that in those days, London taxi drivers spent several years learning the layout of the streets of London to qualify for a cab-driver’s licence.  Subsequent brain imaging studies have confirmed that intense practice of various motor skills (such as juggling) and cognitive skills (such utilizing material maintained in short term memory) leads to an increase in the amount of grey matter in the brain regions engaged during those activities.

Many details of the molecular mechanism by which neural pathways are strengthened are known. It is a process known as long term potentiation (figure 1).  When a signal is transmitted across the synapse connecting one nerve cell with the next one in the circuit, it not only results in the onward transmission of the electrical signal, but also sets in train a series of chemical events in the receiving nerve cell. Those chemical events lead to an immediate increase in the efficiency with which the synapse can transmit signals and also to the transcription of DNA to produce proteins that produce long-lasting changes in the strength of the connection. The delineation of this process in recent years has confirmed the speculation of the Canadian psychologist, Donald Hebb, in his book, the Organization of Behaviour, written in 1949.  Hebb proposed that ‘neurons that fire together wire together’.

LTP

Figure 1. Neurons that fire together wire together. An incoming electrical signal releases a transmitter molecule (glutamate) into the space between the nerve endings. The glutamate binds to an AMPA receptor on the surface of the receiving neuron, changing its shape allowing the flow of ions. The electrical a potential changes, thereby transmitting the electrical signal to the receiving neuron. The change of potential also expels the blocking magnesium ion from the NMDA receptor. Calcium ions flow inwards and initiate a series of chemical events that make the synapse more efficient in both the short term and also the long term. 

 

The implication is that if we wish to strengthen a particular skill we need to practice that skill persistently. The converse is also true: if we practice the relevant activity in a counter-productive  manner we will strengthen the counter-productive pattern of brain activity.  What is the right way to develop the circuit that facilitates the experience of the Zone, and what is the wrong way?

 

The Central Governor

Tim Noakes concept to the central governor provides a clue to the right way and the wrong way.    According to Noakes, our brain creates a sense of fatigue that causes us to restrict our involvement in a demanding exercise when the cumulative signals for the body about our metabolic state, indicate that we are approaching our limit.  But as anyone who has sprinted at the end of a marathon despite feeling almost overwhelming fatigue with a mile to go knows, the governor is far too conservative.   Perhaps in prehistoric times, when food supply was uncertain and our forebears needed conserve reserve fuel to escape from an unpredictable predator, their glucose-dependent brains learned to set the governor conservatively.  Our forebears did of course have an over-ride mechanism: the adrenaline system could dramatically reset the governor’s limits in case of emergency.  We too can utilise adrenaline to reset the governor during a race, but in a long race, too much reliance on adrenaline is damaging.  A better strategy is to train the brain in manner that resets the governor, and delays the onset of fatigue.  We need to reframe the experience of effort when running: rather than perceiving effort as fatiguing or painful, we need to perceive effort as satisfying, even perhaps exhilarating.

Confidence

How do we do this?  The first thing is to develop thought patterns that engender confidence.   Grandmothers’ wisdom tells us that nothing succeeds like success. In more recent times, the psychologist Martin Seligman has developed an approach to building resilience based on Positive Psychology.   His Mental Resilience Program is currently employed by the US military to produce mental toughness in soldiers. Modern neuroscience confirms that during challenging tasks, confident individuals who engage areas of the medial frontal cortex more effectively outperform individuals who do so less effectively.  If two athletes have identical aerobic capacity and efficiency, the one who believes he/she will win will almost certainly be the winner.

Perception is more important than reality.   In fact pessimistic people generally tend to see the world as it really is.  Freud famously remarked that only depressed people see the world as it really is, and much subsequent evidence has proven him correct.  But we function better with a self-reinforcing positive bias.  Nonetheless Positive Psychology is not merely about telling yourself you will win.  We are not so easily fooled.  We need to acquire the habits of optimistic thinking.  Optimistic thinking focuses on the specific details of the experience rather than overgeneralization and self-defeating prediction.  We need to train hard and give ourselves due credit for success in achieving our training goals, while identifying the specific problem when we fail to reach the target we set.

In particular, we need to frame challenges in terms of Albert Ellis’s ABC model: C (emotional consequences) stem not directly from A (adversity – e.g, the sensation of shortness of breath) but from B (one’s beliefs about adversity).   In dealing with the A’s  we need to learn to separate B’s—heat-of-the-moment over-generalised reaction to the situation (“I’m a failure”)—from C’s, the emotional consequences generated by those thoughts (“I cannot maintain this pace” is replaced by “I am breathing intensely; I’m running powerfully”). Then move on to D; dispel the fear of failing.  There is no need to abolish negative thoughts and emotions entirely.  Identify their source. Once you have given a negative thought a name, your brain can cope with it more successfully.  We need to build the sense that we are in control of ourselves; our thoughts and emotions.

 

Breathing

I find that it is very helpful to focus specifically on breathing, during both training and racing.  Start with awareness of breathing; then relate breathing to footfall as this promotes controlled breathing.  I find focus on arm swing is also useful: the brain programs whole movements rather than single muscle contractions. The brain nonetheless devotes more processing resources to arm and hand than to leg and foot.  Our brain readily links arm movement to leg movement; we can enhance this link in our brain by practicing the focus on arm swing while being aware of footfall. I think a firm down/back stroke of the arm promotes a strong drive in the second half of stance that is associated with rhythmic breathing.

However do not expect to be able to focus on all of these things at once without practice. It took several years before I could focus on these things in a relaxed confident manner. Do not get tense if you cannot focus on everything.  Find what you can focus on comfortably and aim for a relaxed focus on this.  When you are in the appropriate confident relaxed state time seems to expand to accommodate the events you are attending to.

I learned these aspects of mental focus long before mindfulness became popular.  However when the technique of mindfulness emerged into popular culture in recent years, I found the key aspects of mindfulness came easily – probably because I had developed those skills when running. Conversely, it is likely that acquiring mindfulness skills will help you to apply these techniques when running.  Brain imaging studies demonstrate that mindfulness produces changes in functioning of the insula (figure 2), plausibly promoting constructive awareness of internal reactions ‘in-the-moment’.

 

Insula and Limbic system

Figure 2: The insula and limbic system. The insula lies in a fold of cortex hidden between the medial temporal lobe, containing the amygdala and hippocampus, and the deep grey nuclei. The insula mediates the interaction between sensory perception, thought and emotion.

 

Repetition

Whatever specific strategies work for you, you need to practice them repeatedly in every training session. You will build brain circuits that can sustain a mental state that is confident and in control in all circumstances.  When Hermes smiles upon you, you will find yourself in that transcendental state in which you are running powerfully with minimal effort and no sense of fatigue.

Advertisements

The runner’s high, the ‘zone’, and ‘second-wind’

February 7, 2018

This post will explore what modern neuroscience has to say about some of the mental phenomena that occupy a tantalising place in runners’ folk-lore: the runner’s high, the zone, and ‘second-wind’.   On the one hand, popular folk-lore accepts that the mind is just as important as the heart and skeletal muscles in athletic performance.  We accept the grain of truth in Yogi Berra’s incongruous quip:  “Baseball is 90 per cent mental. The other half is physical.”  In recent years the topic of sports psychology has taken up an increasing amount of space in running magazines.  On the other hand, most of us devote more attention to the question of the best way to train heart and skeletal muscles, than to the training of our minds.   Perhaps this neglect of the mind is a pragmatic response to the scant evidence that is available to guide the training of the mind.  Many of the recommendations of sport psychologists, such as the need for positive self-talk, are quite plausible in themselves but appear too simplistic to account for the runner’s high; or the transcendental experience of being that mystical zone where power is achieved effortlessly; or the second wind that inexplicably revitalises us when we are struggling to maintain our pace.

However in recent years psychology has been transformed by the advances of neuroscience. This does not mean that describing mental processes in terms of brain processes replaces the value of understanding mental processes in terms of more traditional psychological concepts: concepts such as confidence, motivation and will-power. Mind and brain are two equally valuable sides of one coin.  We now understand a lot about the ways in which the mind can shape the brain just we understand how the brain can shape the mind.  But in contrast to the less tangible tools of traditional psychological science, neuroscience provides tools for objective measurement.  It adds a new dimension to our understanding of the mind, and holds promise of a solid foundation for developing effective ways of training our minds.

But despite the potential power of neuroscience to provide reliable answers to our questions, the sheer complexity of the human brain should warn us to be careful to avoiding invest too much faith in the preliminary findings in our investigations.   With that word of warning, let us begin our exploration of this field (though perhaps ‘forest’ would be a more realistic term) with an illustration of the power of the mind from the 2017 London marathon.

Kenensa Bekele, who had started as one of the pre-race favourites, appeared to be a spent force with 7 miles still to run, and then staged an awe-inspiring resurgence that got him almost within touching distance of the break-away leader Daniel Wanjiru as they ran along the Embankment with less than 2 miles to run.  Surely something powerful happened in his mind to generate Bekele’s dramatic ’second-wind’.   Perhaps equally importantly, what mental force sustained Wanjiru while he maintained the punishing average pace of 4:43 min per mile in the 12th to 16th miles that shattered the morale of the elite field.  Then as Bekele closed the gap along the Embankment, Wanjiru was able to step up the pace again.   This was an epic battle between two runners with superlative physical fitness, but also with immense mental strength.

BekeleWanjiruLondon2017

A re-vitalised Kenenesa Bekele (right) pursuing Daniel Wanjiru along the Embankment in the London marathon, 2017

It is tempting to equate mental strength with the ability to persist despite pain.  However, this simplistic description is misleading. Pain is a protective signal indicating the need to take avoiding action to prevent damage to the body.  But this definition fails to address the fact that the experience of pain depends on many aspects of the situation including past experiences, current circumstances and future expectations.   Developing mental strength is not merely a matter of gritting ones teeth.

What insights might neuroscience offer?    Multiple brain circuits are likely to be involved, most especially the circuits making up the limbic system deep in the brain, and paralimbic cingulate gyrus lying on the brain’s medial surface, and the insula cortex, buried in a deep fold hidden by the temporal lobe (see figure 2). These circuits play key roles emotion, motivation, and in the evaluation of the signals from within the body.  The neurotransmitter, glutamate, mediates long-range communication in these circuits, while various other neurotransmitters play a modulatory role, adjusting the tone and intensity of signal transmission.  Three groups of the modulatory transmitters play an especially important role in the response to stress and pain: catecholamines, endorphins and endocannabinoids.

Insula and Limbic system

Figure 2: The insula and limbic system. The insula lies in a fold of cortex hidden between the medial temporal lobe, containing the amygdala and hippocampus, and the deep grey nuclei, which include the basal ganglia (not shown) and the thalamus.

 

Catecholamines: noradrenaline and dopamine

The two principle catecholamines in the human brain are noradrenaline and dopamine. Noradrenaline is similar to adrenaline, the hormone that acts rapidly to mobilise the body’s resources when we face any form of acute stress.  In the brain, noradrenaline  mediates arousal by increasing the overall tone of brain activity.   Dopamine plays a specific role in mediating motivation to act.  It mediates the experience of reward for beneficial actions. It plays a key role in the learning of beneficial patterns of activity.   If dopamine is depleted we become listless and lethargic.  Illicit stimulant drugs such as cocaine and amphetamine promote excessive release of dopamine, generating an unnatural surge of energy.

Endorphins

Endorphins have attracted the popular imagination because they are the brain’s natural opiates.  The concentration of endorphins in the blood increase during exercise.  However this observation provides only limited evidence for the hypothesis that endorphins play an appreciable role in the brain during exercise.  First of all, endorphins are large molecules that cannot pass across the barrier that exists between blood and brain and therefore, observed increases in blood levels do not necessarily correspond to brain levels.   Secondly, the two main side effects of opiates: respiratory depression and constipation are not observed during running.    Thus there is little direct evidence that endorphins play a substantial role during running.

Endocannabinoids

Endocannabinoids are produced naturally in the body, and bind to the cannabinoid receptors that bind the cannabinoid chemicals such as tetrahydrocannabinol (THC)  derived from marijuana. The binding of endocannabinoids to these receptors in diverse tissues of the body produces a wide diversity of effects.  In the lungs, endocannabinoids produce bronchodilation, opening the airways to allow easier flow of air into the lungs.  They also exert anti-inflammatory effects.  Endocannabinoids are fat soluble and can easily pass across the membranes that separate blood from brain.   In the brain they produce a mental state characterised by euphoria, a sense of well-being and distortion of the passage of time.  These effects are similar to the mental experience described as being in ‘the zone’.  Furthermore endocannabinoids interact with the dopaminergic system in a complex manner.  In particular they can enhance the release of dopamine in the basal ganglia thereby enhancing the experience of reward.  It is noteworthy that laboratory animals lacking the gene for the endocannabinoid, anandamide, exhibit profound under-activity.

The central governor revisited

The evidence regarding the role of endocannabiniods during exercise adds intriguing subtlety to Tim Noakes’ concept of the central governor that sets the limit on how hard we can push ourselves during exercise.   This new evidence suggests that the brain does not merely passively accumulate warning signals from the body, and dictate a shutdown when we reach a pre-set threshold at some fixed ‘safe’ percentage of our maximum physical capacity.   Instead the evidence suggests that the decision whether or not to persist with an action depends on a more complex balancing of information.

The role of dopamine in facilitating reward seeking behaviour suggests that the conservative influences that promote the avoidance of harm are balanced by adventurous impulses that encourage us to seek excitement or exhilaration.   Perhaps during our evolutionary past our forebears developed a conservative tendency to discourage them from wasting energy pointlessly when food was hard-earned and metabolic energy was a resource to be husbanded prudently.  On the other hand, the need to acquire skills and keep them well-honed demands engagement in activity for its own sake: prudence should be leavened with playfulness.

When energy resources were at a premium, in ordinary circumstances the threshold at which the balance tipped against continuing activity was likely to have been far below the level at which activity was immediately dangerous.   At times of danger, when our forebears were at risk of becoming prey, or perhaps during a hunt, when they became the predators, the threshold could be re-set.  The sympathetic nervous system, which releases adrenaline to stimulate heart and lungs, and noradrenaline to arouse the brain, provides a rapidly acting mechanism capable of the required rapid mobilisation when danger is acute; in contrast, it appears that the endocannabinoid symptom is well suited to promote sustained increases in work output during a prolonged hunt.   For many of us nowadays, energy resources are plentiful and it is plausible that our brains which had evolved in more stringent circumstances, tend to set the threshold for equipoise between benefit and harm at an unnecessarily low level.

While this reformulation of the central governor hypothesis is speculative, it does offer a plausible explanation of why evolution has provided us with several distinguishable though interacting systems for mobilising our bodies.  Whatever the details of the roles of the various components of these overlapping systems, the crucial point is that to achieve maximum athletic performance, we must not only train to develop our peak physical capacity (for example by maximizing VO2max) we also need to develop the capacity to re-set our naturally conservative threshold for shutting down the system.

It is nonetheless necessary to bear in mind that our brain is designed to shut down the system when the risk of harm is high.  However provided we are in good health, it is likely that there is a large margin between our naturally conservative threshold and the maximum safe threshold. It should be noted that the increase in endocannabinoids during exercise is usually substantially less than the increase that is achieved by smoking forms of marijuana with high THC content, such as ‘skunk’.  We are unlikely to come to harm if we only invoke our own endogenous neuromodulators, .

How can we train  in a way that enhances our capacity to raise a naturally conservative threshold that is inclined to shut down the system prematurely?  This is the question I will address my next post in this series.

The mind and brain of the athlete

January 2, 2018

I am afraid that I did not post much on this site in 2017.

In part that was because of several health problems. One of these was a puzzling connective tissue disorder that remains a puzzle, but is now largely in remission.  Separate from that problem, I had been developing cataracts in both eyes over a period of several years. The problems from glare had reached a point where something needed to be done.  Last winter, when cycling home from work after dark, I was forced to find a homeward route on traffic- free minor roads to avoid potentially lethal dazzling by the lights of oncoming traffic on the main roads. On one occasion I cycled at speed into a 3 foot high barrier. Fortunately the outcome on that occasion was more comical than serious.  But it was a definite indication that it was time for surgery.   The operations went reasonably smoothly, though some minor complications caused temporary concern.  But now these minor problems have settled and I am enjoying a very pleasing improvement in my vision.  This winter I can cycle home from work after dark on my usual home-wards route without problems.

However health issues were only part of the reason for lack of blogging in 2017.  I had a busy and exciting year at work.  This was satisfying but unfortunately left little time for running and for blogging.  This year promises to be similarly busy at work and I hope will be similarly exciting.  Nonetheless, I am gradually re-building my running activities, and it is time to get back to regular blogging.  In this blog I want to set the scene for a series of posts about the mind and brain of the athlete.

I am a clinical academic.  My research is concerned with the function of the human mind and brain, and the mechanism and treatment of mental disorders.  In the 27 years since US President George (HW) Bush declared the Nineteen Nineties to be the decade of the brain, we have not achieved any triumphs as spectacular as landing a man on the moon, but we have nonetheless learned an incredible amount about how the brain works.   We have learned that simplistic answers based on assigning a particular function to one brain region, or to one brain chemical, fail to deal with the complexity of a brain containing 100 billion neurons with over a trillion connections between them.    We have learned instead about the mechanisms that sculpt the extensive networks of brain cells that support mental activity, perception and behaviour; we have discovered that even the adult human brain is remarkably plastic.

We have learned some useful principles that explain how various experiences, including social interactions,  and ‘life-style’ factors, such as exercise and diet impact in understandable way on how our brains work; and we have learned much about how mind and brain can influence the function of the entire body. Nonetheless, the unimaginable complexity of the web of interactions between our genes and our experiences in life ensures that each of us is unique.  In applying what we have learned about the principles of mind/brain/body interactions to ourselves as individuals, we are each an experiment with a sample size of one.

We should therefore avoid simplistic application of lessons based on the experiences of a single individual to ourselves, and be cautious in drawing general conclusions from studies of a small number of individuals.  We should be even more cautious in following a guru whose principles are based on mystical interpretation of idiosyncratic evidence, though paradoxically the role of faith in recovery from illness (where is known as the placebo effect) and in athletic performance (where it can take the form of trust in your coach) cannot be denied.  Understanding the mechanism by which faith can move mountains (or more prosaically, by which confidence breeds success) is indeed one of the most intriguing challenges for modern neuroscience. I hope to return to that question in a later blog.

But just as we need to exercise caution in drawing general conclusions from the experiences of a few individuals, we also need to be aware of the limitations of drawing conclusions from studies of very large numbers of individuals. In large studies, averaging across individuals irons out the wrinkles due to the idiosyncratic behaviour of an individual.  We can have some confidence in drawing general conclusions about how the average person will respond in a particular situation.  However, we cannot confidently apply those conclusions to ourselves: we might prove to be the idiosyncratic individual.

Thus, in dealing with things as complex as the human mind and brain we must be very circumspect in the application of science to our own situation. We need to combine evidence from detailed observation of individuals and from measurement of the average behaviour of large groups, with knowledge based on understanding the underlying mechanisms.  There is a rapidly growing body of evidence about the mechanisms of the two way interaction between brain and athletic activities: the role of the brain in athletic performance on the one hand, and the role of exercise in enhancing the function of the brain on the other.

EngagedNetworks

Brain networks engaged during running: upper left: dorsal attention network; upper right: executive control network, lower left: affect-rewards network;

There is a lot to write about, and I need to get my ideas organized – but to celebrate the beginning of what promises to be an exciting new year, I will get the ball rolling by pointing to an article that will be published next week in the journal Neuropsychologia (though it has been available on-line since Nov 2017).

http://www.sciencedirect.com/science/article/pii/S0028393217304591.

In this paper Ashna Samani and Mathew Heath from the School of Kinesiology and Graduate Program in Neuroscience at University of Western Ontario report that in a group of healthy young adults, a single 10 minute bout of moderate-to-vigorous intensity cycling on a bicycle ergometer produced a 10%  decrease in reaction time during the anti-saccade trials in an anti-saccade task.  This might seem like a rather arcane laboratory finding of uncertain relevance to everyday like. The anti-saccade task requires looking to the left when an attention demanding visual stimulus suddenly appears in your right visual field, and conversely, looking to the right when the stimulus appears on the left.   This task in itself does not correspond closely to anything we are commonly required to do in everyday life.  However, in fact it is a rather good marker for the function of the brain circuit that acts to inhibit unwanted distractions that get in the way achieving our goals.  Attentional focus is indeed a pre-requisite for effective performance in many domains of every-day activity.  At some point in the future, I will return to the specific role of this inhibitory control circuit within the larger topic of the brain control mechanisms that govern athletic performance, though there are many other topics to cover before then.  I am looking forward to getting started in a more organised manner soon.

Ed Whitlock: a tribute

March 30, 2017

The death of Ed Whitlock two weeks ago was a saddening shock.  He was undoubtedly the greatest master marathon runner that the world has seen.  When adjusted for age, his time of 2:54:48 in the Toronto Waterfront Marathon in 2004 at age 73 is one of the greatest marathon times ever recorded in any age group.  He was also a delightful, modest but playfully mischievous character who shared information about his training in a gracious manner.  However, he made no claim that what worked for him would work for others.

There is little doubt that individuals differ in the training program that works best for them.  Nonetheless, I believe that there are lessons in Ed’s approach to training that apply to most of us.  But before seeking to draw any general conclusions, it is necessary to note that it was a unique combination of his genes, training and mental approach that combined to make him the great runner he was.

What made him unique?

As discussed in my previous analysis of what made him great, the fact that he was from a long-living family, including an uncle who lived to age 107, make it likely that he was endowed with genes that predisposed him to longevity both as a runner and in overall health.  It is becoming increasingly clear from many sources of evidence that fitness for running is closely associated with fitness for a long life.   When tested at the High Performance Specialists clinic in North Toronto shortly before his 70th birthday Ed had a VO2max of 52.8 ml/min/Kg, compared with 35 ml/min/Kg for the average 70 year old.   When tested in the lab of Tanya Taivassalo and Russel Hepple at McGill University 11 years later at age 81, he was found to have a VO2max of 54 ml/min/Kg, typical of the value expected in a recreational athlete 50 years younger. But most importantly, there was no evidence of decrease over the 11 year period.  VO2max typically decreases by 12% per decade in sedentary individuals in their sixties, and at about half that rate in well trained master athletes.

The physiological testing in Toronto and 11 years later at McGill did not reveal anything freakish about his physiology, apart from his high aerobic capacity.  According to the formula derived by Jack Daniels, Ed’s measured VO2max as he approached age 70 would predict a marathon time of 3:01:00.  He ran 3:00:33 in London, Ontario, a month or so later.  Thus his extraordinary marathon performance in his early 70’s were largely attributable to his aerobic capacity.   It is noteworthy that his marathon performances in his early 80’s had deteriorated compared with his performances in his early 70’s despite a sustained aerobic capacity, indicating that he was no longer achieving the performances predicted by Jack Daniels.  I suspect that it is likely that deterioration in the resilience of his leg muscles was the main factor in the drop off of his marathon performance over that decade.

Overall, the evidence indicates that the main contribution from his genetic endowment to his extraordinary longevity as a runner was a set of genes that led to a remarkable slowing of the usual deterioration of VO2max with age.

The unexpected shock

Conversely, in light of the link between fitness and longevity, it was an unexpected shock to hear that he had died at age 86, a good age but not an extraordinary one.   Unfortunately despite the encouraging fact that maintaining fitness for running increases the probability of a long and healthy life, good overall health does not rule out the possibility of unanticipated disruption of the mechanism governing cellular division in the tissues of the body, causing cells to proliferate malignantly.  In Ed’s case, he succumbed to prostate cancer.  There is moderately strong evidence that maintaining aerobic fitness increases the body’s defences against cancer via control of the processes of inflammation crucial to tissue health.  However, the cellular signalling systems by which the body maintains equilibrium between pro-and anti-inflammatory processes are in delicate balance, making it also possible that excessive exercise might weaken the body’s defences.  In an individual case it is difficult to determine just where the balance between protection and harm lies, though one of the most striking features of Ed’s approach to running was his careful attention to the impact that running was having on his body.  This made it all the more surprising that he died only a matter of months after taking 28 minutes off the previous world record for the M85+ category, setting a new mark of 3:56:33 in Toronto Waterfront Marathon last October.

In retrospect, there were pointers to the possibility that all was not well even as he completed the Toronto marathon.  When compared with the previous M85+ world 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 several injures in the preceding few years.

In an interview for the New York Times in December 2016 he expressed the hope that he would be running well at age 90.  However, that interview also revealed the first worrying indicator that all was not well.  He admitted that he had lost about 10 lbs in weight in recent months.  Over a period of many years he had usually maintained a healthy lean physique with a weight of around 120 lbs and height of 5 feet 7 inches.  The tests at the High Performance Specialist clinic in 2000 revealed a body fat proportion of 9.5%.  This is probably near ideal for a male marathon runner; but any further decrease in weight might not be healthy.  He also revealed in the New York Times interview that he was aware of an increasing loss of muscular strength.  In retrospect, the loss of 10 lbs in weight and loss of strength was probably an early sign of the cachexia of malignant disease.

Universal lessons

However I do not want to dwell unduly on the sad fact of his untimely death.   What are the lessons we can learn from his life and his running?  Despite his disarming impishness, he was very attentive to the way in which his body responded to training, and he was very thoughtful about the way in which he trained.  The first key component of his training was frequent long slow runs of duration roughly matching his target time for the full marathon: multiple three hours runs each week in his late sixties and early seventies, when he was aiming for a sub-three hour marathon, and frequent 4 hour runs in his mid-eighties as he prepared for a sub 4 hour marathon.  During these long runs he deliberately adopted a slow, shuffling gait to minimise stress on his legs. The second key component during his heyday, was fairly regular races, typically over distances of 5 Km or 10 Km, that helped maintain his lithe and powerful stride.

The care he took with his body was demonstrated by his choice of the Evergreen Cemetery, only a short distance from his house in Milton, Ontario, as his training venue.    On the short, mainly flat, looping paths of the cemetery he was able to avoid stressful sustained battles against the biting winds of an Ontario winter. In the event of injury, he was able to return to his nearby home with minimal aggravation of this injury.  He was not free from injury.  Over the years he experienced several lengthy lay-offs on account of knee problems and also other injuries.  During recovery from injury, he was patient.  He aimed to rebuild his fitness by gradually increasing the duration of this runs.  He used the races over 5 and 10 Km to gauge how well prepared he was for a marathon and set his targets appropriately.

Perhaps surprisingly, he denied enjoying running for its own sake.  His motivation was the setting of records.   He spoke of the boredom of his long training runs, though I wonder how much of this was an expression of the impish delight he took in down-playing what appears to have been a remarkable capacity to sustain his mental equilibrium through long hours of training.

In recent years I have modelled much of my own running on Ed’s training.  Perhaps unfortunately I lack the motivating effect of setting world records.  Fortunately, I do enjoy running for its own sake.  I run contently around a 1 Km loop in local woodland less than a mile from my house for long periods, though not as long as Ed’s 3 and 4 hour runs.  I find myself slipping into a relaxed meditative state and sometimes I think of Ed.  I will miss him.

Threshold training: integrating mind and body

February 5, 2017

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

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

 

Specificity v Variety

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

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

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

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

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

Brain and mind

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

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

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

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

waterfallgully

Waterfall Gully (photo: Nabo.co.au)

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

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

Polarized Training and Injury Prevention

December 29, 2016

Avoiding injury is one of the major goals of training for distance running.  On account of the impact forces experienced at footfall on every stride, runners are uniquely prone to injury.  However, effective strategies for preventing injury are elusive.  In recent years, advocates of techniques such as Pose have claimed that injuries are largely due to poor running technique, and have promised that the problem can be overcome by proper technique.  In particular, they have identified heel striking as a cardinal problem.  However, there is very little evidence to support this claim.   Others have advocated stretching during warm-up as a strategy to reduce risk of injury, though the evidence provides little support for this claim.  Advocates of barefoot running have proposed that running shoes are the problem, but again there is little evidence to support the claim that running barefoot or in minimalist shoes reduces risk of injury.  Conversely, the manufacturers of running shoes have placed blame on foot orientation problems such as over-pronation and claimed that motion control shoes can reduce this risk.  Yet again, the evidence is slight, though at least one study had found that over-pronation is associated with increased risk of injury.

It is likely that a wide variety of factors contribute to injury in different individuals.  Meta-analyses that pool the findings of many studies are only likely to identify risk factors that are common to many athletes.  Two risk factors emerge consistently: a history of previous injury; and a large weekly volume of training.   Lisa Callaghan has provided an up-to-date review of the evidence.

Prior injury

A history of previous injury might predispose to subsequent injury simply because the athlete has not corrected problems that contributed to the first injury.  It is also possible that unsatisfactory recovery from the previous injury plays a role.  Muscles, tendons and other connective tissues tear when subjected to force that exceed the limits of their resilience.  A cardinal factor in the resilience of connective tissues is the elongated spring-like structure of collagen fibres, making them resilient against forces acting along the direction of the fibre.  During the initial stages of repair following injury, collagen is laid down with random orientation providing a framework for tissue renovation, but full resilience requires remodelling such that the collagen fibres become aligned in the required direction.  Therefore effective recovery requires early mobilization to promote the laying down of appropriately aligned fibres, perhaps augmented by slow stretching.

Training volume

Observational studies report that training volumes of 65 Km (40 miles) or more per week are associated with higher rates of injury [Fields et al; van Ghent et al].   In part these observations might simply reflect the greater duration of exposure to risk of injury, though it is likely that fatigue plays an important role.   In particular fatigue impairs neuromuscular coordination increasing the likelihood of poor coordination between different types of muscles fibres within a muscle and poor coordination between muscles that act as agonists and antagonists, resulting in excessive local forces within tissues.

Polarized training

Simply limiting training volume is unlikely to be a satisfactory strategy for many runners, making it desirable to identify alternative strategies to reduce the damaging effects of fatigue.  As the forces exerted increase with increasing pace, it might be expected that injury risk would be greater at faster paces. However the observation by Van Middelkoop and colleagues that among marathon runners, those who do interval training have a lower risk of knee injury raises an intriguing question.  Could it be that interval training provides greater protection than training at   somewhat lesser paces in the vicinity of lactate threshold?   Interval training, in which short efforts at fast but sub-maximal pace are separated by recovery periods, tends to promote the development of neuromuscular coordination with relatively mild muscle fatigue.  As discussed in my recent post, interval training is likely to promote a favourable balance between anabolic and catabolic hormones, leading to strengthening of tissues. In contrast, running for a sustained period at threshold pace might produce fatigue with the associated risky deterioration of neuromuscular coordination during the session, and also tip the balance towards the catabolic effects of cortisol, promoting subsequent breakdown of tissues.

Even more speculatively, the viscoelastic character of the musculotendinous unit might result in a peak risk of damage to muscles and tendons at threshold paces. Viscoelastic materials offer strong resistance to brief sudden onset forces but less resistance to sustained forces.  Although force is greater at sprinting pace, time on stance decreases.  At speeds above LT there is actually a decrease in the impulse acting through the foot at each step because the increased force is more than compensated by  reduction in time on stance.  The product of forces x time on stance actually decreases, as illustrated in figure 1 based on data from the study by Weyand and colleagues.

ImpactForce&Impulse

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

Thus, it is possible that the risk of tissues tearing is actually less at sub-maximal paces substantially above LT than in the vicinity of LT.   Nonetheless, it is crucial to prime the requisite neuromuscular coordination during the warm-up (for example by moderate intensity strides) and it is generally desirable to avoid absolutely maximal effort that taxes neuromuscular coordination to the limit, during training.

The other pole of polarised training is low intensity running.  This has the potential to build resilience of the muscles, tendons and the other connective tissues engaged during running by repeated application of moderate forces.   Provided training volume is built-up gradually and excessive fatigue is avoided, the risk of injury is low.

Conclusion

While the predisposing and precipitating factors causing running injuries remain controversial, consistent evidence indicates that a high weekly training volume increases the risk.  In contrast, the observation that interval training provides some protection suggests that polarised training might diminish the risk.  Observational evidence and also speculation based on principles of biomechanics and physiology suggest that high intensity sessions have the potential to build effective neuromuscular coordination, while low intensity training would be expected to enhance the resilience of muscles, tendons and other connective tissues with relatively little risk.  Nonetheless, as with any type of training, it is important to build up the training load gradually, and to warm up for each session in a manner the primes the requisite neuromuscular coordination.

How does polarised training minimise lactate accumulation?

December 23, 2016

My previous post discussed evidence indicating that training in the vicinity of lactate threshold (LT) can lead to sustained elevation of cortisol which has the potential to damage to the neuromuscular system and suppress immune responses.  In particular, the study by Balsalobre-Fernandez indicates that frequent training at or a little above lactate threshold is more damaging than a lesser amount of training at a higher intensity.   This might be the key to understanding why a growing body of evidence favours polarized training, which includes a large volume of low intensity training, a small amount of high intensity training and a similarly small amount of threshold training,  in preference to a training program with a higher proportion of threshold training.

As distance races from 5 Km to marathon are raced in vicinity of lactate threshold, pace at LT is a crucial determinant of performance.  Enhancing the ability to delay the onset of lactic acid accumulation as pace increases is one of the key goals of training.   The effectiveness of polarised training raises the question of how a program with only a small about of threshold training might nonetheless be effective in enhancing ability to minimise lactate accumulation.

Lactate accumulation might be minimised by decreasing the rate of production and /or increasing ability to remove it.  The rate of production can best be minimised by increasing the capacity to generate energy aerobically, which in turn might be enhanced by increasing the capacity of aerobic enzymes in mitochondria and/or increasing delivery of oxygenated blood to muscles.

Developing Aerobic Capacity

While a large volume of low intensity running would be expected to increase the aerobic enzymes in slow twitch fibres, the more challenging question is how to enhance the aerobic capacity of fast twitch fibres.  Low intensity running beyond the point of exhaustion of slow twitch fibres might help achieve this, but frequent very long runs create the risk of excessive stress.   For many years followers of Arthur Lydiard’s approach to periodization, in which the base-building phase is almost exclusively devoted to relatively low intensity aerobic running, have  maintained that when you bring speed work into the program, you halt the development of aerobic enzymes. The size of the engine is now fixed; the task of speed work is to tune this engine.

This claim was associated with a widespread belief that the acidity generated above LT prevented development of aerobic enzymes, and perhaps even damaged them.   This belief is ill-founded.  Extensive research into high intensity interval training (HIIT) in recent years has demonstrated that HIIT is a very efficient way to increase the capacity of aerobic enzymes.  The available evidence indicates that HIIT achieves the enhancement of mitochondrial enzymes via the increasing the activity of the messenger molecule, PGC-1alpha, the same messenger as  appears to mediate mitochondrial development in response to lower intensity endurance training

HIIT research is largely focussed on comparing high intensity training with low intensity training and has not so far investigated the potential benefits of a polarised approach.  It would be anticipated that in a polarised approach the rate of gain in aerobic capacity would not be a rapid as with HIIT, but it is scarcely credible that diluting the high intensity session with low intensity sessions would abolish  the aerobic gains of the high intensity sessions, provided there is adequate opportunity for recovery.

Not only does HIIT produce efficient development of aerobic enzymes, but it is also effective in enhancing the development of the enzymes that metabolise fats, thereby promoting the generation of energy from fat, a processes that does not generate lactate

With regard to increasing the supply of oxygenated blood to muscle, sprint interval training is as  effective as endurance training in promoting development of capillaries.  Although the effect of HIIT on development of cardiac output has been less thoroughly studied, it is noteworthy that the Gerschler’s rationale for the introduction of interval training was the stimulation of cardiac output.  In his word interval training provides “a stimulus particularly powerful to reach the heart.”

Transport of lactate

The alternative approach to minimizing lactate accumulation is removal of lactate from muscle and blood.  With regard to the relative efficacy of polarised training compared with threshold training, the important issue is whether or not this is better promoted by brief surges of intensive lactate production or by sustaining a moderate level of lactate.   The mechanisms by which lactate is removed from muscle include the transport of lactate from fast twitch fibres, where it is produced, to slow twitch fibres, which have the capacity to metabolise the lactate; the transport to other organs such as heart muscle which are well adapted to metabolising lactate; or transport to the liver where the process of glycogenesis converts lactate to glucose and subsequent storage in the form of glycogen.

The transport of lactate across cell membranes is mediated via a set of transport molecules, the monocarboxylate transporters (MCTs) that transport lactate together with protons.  Transport by MCT’s involves diffusion and the rate is determined by the transmembrane gradient of either lactate or acidity (protons).  It is likely that under most conditions, lactate flux is determined mainly by the gradient produced by metabolism-driven uptake, while the availability of MCTs is rate-limiting only after the establishment of large transmembrane gradients.   Therefore, the first goal in enhancing the capacity to clear lactate during distance running is enhancing the ability to metabolise lactate. In heart and slow twitch fibres, this is achieved by enhancing vascularization and aerobic enzyme activity.  The evidence discussed above suggests that polarized training is an effective way to do this.  Nonetheless, it is desirable to ensure that MCT’s are maintained at an adequate level. Because  MCT-mediated transport is rate-limiting only in the presence of large transmembrane gradients, it would be expected that brief surges of lactate  will be more effective in promoting development of MCTs than sustained moderate levels.

Buffering of acidity

The role of acidity in stimulating training effects is ambiguous.  On the one hand rising acidity eventually halts metabolism in muscle, but on the other, some degree of stress is likely to be necessary to promote adaptation.   Ingestion of sodium bicarbonate (baking soda) which neutralises acid has been shown to diminish the secretion of anabolic hormones, such as growth hormone, following intense exercise. Thus rise in acidity appears to facilitate at least some of the desired effects of training.  In contrast, sodium bicarbonate ingestion augments the increase in activity of the messenger molecule PGC-1alpha in skeletal muscle during recovery from intense interval exercise in humans, and therefore might promote the development of mitochondria.

This raises the question of the role of natural buffering mechanisms in the blood.    During intense exercise there is a transient rise in the body’s natural buffers, phosphate ions and bicarbonate ions, that helps neutralise the rise in acidity despite the rise in lactate concentration.  Thus it is plausible that one of the advantages of interval training compared with threshold training is that the transient natural buffering during interval training allows more intense exercise and hence allows greater lactate production without excessive acidity.    Perhaps this would act as a greater stimulus to PGC-1 Alpha activity and perhaps MCT production as well. On the other hand, natural buffering might diminish the potentially beneficial increase growth hormone activity.  Overall, on account of the competing antagonistic effects, I doubt that buffering is an important adjunct to training.   The issue is similar to the debate about the value of cold baths to reduce inflammation after training.

Nonetheless, the possibility that buffering might increase tolerance of lactate production, together with the substantial evidence for improved endurance performance in rats and humans, reviewed  McNaughton and colleagues, has led to the proposal that bicarbonate doping might enhance race performance.  I am intrinsically opposed to the ingestion of substances in marked excess of the amounts present in a normal healthy diet for the sake of enhancing performance, but some athletes might argue that provided it is not illegal it is acceptable.   However, the dose required to produce an appreciable effect (20-30 gm) can cause vomiting or diarrhoea.  I would regard this is too great a risk to take.

Long term improvement

It is clear that many of the physiological adaptations required to minimise the rate of accumulation of lactate can be achieved very efficiently by HIIT.  This evidence undermines the principle that enhancement of the ability to handle lactate is achieved most effectively by specific training in the vicinity of LT.

Unfortunately, most of the HIIT research so far has focussed on the contrast of HIIT with lower intensity training, delivered over a time scale of several weeks.   There is some evidence  that the benefits of HIIT do plateau after a period of a few months.   The study by Stoggl and Sperlich demonstrated that for athletes who have a history of regular training, polarised training produces greater benefits than either threshold training or predominantly high intensity training.  It is plausible that the adaptations produced by HIIT can also be achieved, perhaps more gradually but with the potential for steady improvement over a prolonged period, by a polarised program.  Hitherto there have been too few studies that have examined the development of physiological capacities such as aerobic enzymes, delivery of blood to muscle and the transport of lactate, during training programs sustained over a full season or longer.

Injury prevention

Injury is an issue of perennial importance to athletes.  In general, muscle injury is likely if a large force is exerted unexpectedly, or if muscles are fatigued.  Protection against injury is minimised by the strengthening promoted by anabolic hormones on the one hand, or diminished by the breakdown of tissues promoted by sustained elevation of catabolic hormones such as cortisol.  In the next post in this series, I will address the question of whether injury is more or less likely with a polarised program than with threshold training.

Is threshold training over-rated? Stephen Seiler v Jack Daniels

December 19, 2016

In the early years of a runner’s career, almost any reasonably sensible training plan with a gradual build-up of training load will produce improvement.  However, once a runner has reached a plateau of performance, the challenge is to identify the type of training that offers the best chance of further improvement.   Races ranging from 5K to marathon are run at paces in the vicinity of lactate threshold (LT).  Race performance is largely determined by the fact that as pace rises above lactate threshold, acid accumulates in muscles and blood, eventually resulting in an enforced slow-down.  Thus, one of the major goals of training is increasing pace at lactate threshold, as this will allow increased race pace.  The principle of specificity of training suggests that the optimum training program will include a large amount of running near lactate threshold to enhance capacity to prevent accumulation of acid.  Indeed, this is the approach adopted by many recreational runners.

Polarized training

However, the evidence from examination of the training logs of elite endurance athletes, reviewed comprehensively in a lecture by Stephen Seiler in Paris in 2013, indicates that many elites adopt a polarised approach  that places emphasis on the two extremes of intensity. There is a large amount of low intensity training (comfortably below LT) and an appreciable minority of high intensity training (above LT).  Polarised training does also include some training near lactate threshold, but the amount of threshold training is modest; typically the proportions are 80% low intensity, 10% threshold and 10% high intensity.

As reviewed in my previous post on the topic, several scientific comparisons  of training programs have demonstrated that for well-trained athletes who have reached a plateau of performance, polarised training produces greater gains in fitness and performance, than other forms of training such as threshold training on the one hand, or high volume, low intensity training on the other.

The specificity principle

Nonetheless many  coaches and athletes who advocate specific training paces to achieve the various required adaptations required for distance running, maintain a firml belief that threshold training is the best way to increase the pace at lactate threshold, and should form a substantial component of a distance runner’s training program.  Jack Daniels, doyen among coaches advocating specific paces for specific adaptations, has argued that because stress level rises rapidly at paces exceeding threshold there is a sweet spot in the vicinity of lactate threshold that achieves sufficient stress to promote adaptation while avoiding the danger of excessive stress.

Evidence from laboratory studies of rats appears to provide some support for this view.  While it is necessary to be cautious in using evidence from studies of rats to inform training of humans, the basic physiology of rat muscle is similar to that of human muscle.  They share with us an aptitude for running at aerobic paces. The evidence from the well-controlled systematic studies that are feasible in rats is potentially useful in establishing principles that apply across species.  Dudley’s studies in which he measured changes in aerobic enzymes produced by a variety of different training intensities and durations in rats (all training for 5 days per week for 8 weeks) demonstrated that running beyond a certain duration produced no further increase in aerobic enzymes.   Furthermore, the duration of running beyond which there was no further improvement is shorter at higher training intensity.  This suggests that at any given intensity, training runs beyond a certain duration  will produce no further increase in aerobic capacity though there might of course be other gains, for example increase resilience of bones, muscles, ligaments, tendons and also the mind.  But there is also likely to be an increase in overall stress.  At very high intensity the duration limit is so short that the overall gain in aerobic fitness is less than can be achieved by longer session at lower intensity. The greatest overall increase in aerobic enzymes in muscles with predominantly red (aerobic) fibres, was achieved by an intensity that led to maximum gain at around 60 minutes.  Thus in Dudley’s rats, there appeared to be a sweet spot in intensity for optimum development of aerobic capacity.  Although Dudley did not measure lactate levels, it is plausible that this intensity corresponds roughly to lactate threshold in humans.

Hormones and training

However even if we accept that Dudley’s studies support Jack Daniel’s argument for a sweet spot, it is crucial to note that Dudley assessed the effects of training over a total duration of only eight weeks.  The important issue for the athlete who has reached a plateau is the likely consequences of training over a longer time-scale than 8 weeks.  It is probable that the crucial issue is the balance between catabolic and anabolic effects of training.  During a training session, the catabolic hormones cortisol and noradrenaline are released into the blood stream to mobilise body resources, especially glucose, required to meet the demands of training.  The release of catabolic hormones also triggers the subsequent release of anabolic hormones, such as growth hormone, that promote repair and strengthening of body tissues.    As training intensity rises above lactate threshold the release of catabolic hormones and the associated release of anabolic hormones increases sharply (as illustrated by Wahl and colleagues).  Thus the potential stimulus triggering the benefits of training rises sharply as intensity exceeds lactate threshold.  The accumulation of cortisol also increases with increased duration of running.  For example, Cook and colleagues report that salivary cortisol increases steadily during a marathon, typically achieving a fourfold increase at 30 minutes after completion of the race compared with the level prior to the start.

While a transient rise in cortisol tends to be beneficial, sustained elevation of cortisol is potentially harmful because cortisol promotes the breakdown of body tissues.  Cortisol levels in hair samples provide an indication of cortisol level sustained over a period of weeks or months.   Skoluda et al measured cortisol levels in hair in a group of distance runners over a season. They reported that these runners had abnormally high cortisol levels over a prolonged period, raising the possibility of adverse sustained catabolic effects, including suppression of the immune system.  Skoluda concluded that repeated physical stress of intensive training and competitive races is associated with potentially harmful sustained elevation of cortisol.  However, they did not explicitly compare different training programs.

There is no published evidence of differences in medium or long term catabolic/anabolic balance between polarised training and threshold training.  Furthermore, because gradual increase in training load leads to a blunting of the sharp rise in catabolic hormones produced by training in the vicinity of LT, a fully informative study would need to take careful account of the structure of the training program over a sustained period.  Nonetheless a study of high level distance runners by Balsalobre-Fernandez and colleagues does provide relevant information.  They recorded training, performance and salivary cortisol level in 15 high-level middle and long-distance runners from the High Performance Sports Center, Madrid, throughout a period of 10 months.  The group comprised 12 men and 3 women, mean age 26.4 years, with personal bests in 1500-metres between 3:38–3:58 (men) and 4:12–4:23 (women). They rated training in three zones: zone 1 included long-distance continuous training, or interval training with long sets (4–6 km), at relatively relaxed paces; zone 2 included of intervals with sets of 1–3 km at approximately 5 K pace , likely to be moderately above lactate threshold; zone 3 included short-distance and sprint interval training at paces ranging from around 1500m pace to full sprint. Thus zone 1 and 3 roughly correspond to low intensity and high intensity zones of a polarised program, while zone 2 sessions are a little more intense but less sustained than a typical threshold training session in the mid-zone of a typical polarised program.

During the winter months, the athletes did a substantial amount of low intensity (zone 1) training.  The 25 weeks of spring and summer training was dominated by zone 2 training.  For 15 weeks within this 25 week period, the average training zone was in the range 1.75-2.25, indicating a large proportion of zone 2 training; while for 3 weeks the average was above 2.25, indicating an appreciable amount of training in zone 3 in addition to zone 2.

In addition to recording race performance, Balsalobre-Fernandez and colleagues regularly assessed vertical counter-move jump height (CMJ) as a measure of neuromuscular performance.  Averaged over the entire season, the runners with higher long-term cortisol levels has significantly lower CMJ scores, confirming that sustained elevation of cortisol is associated with poor neuromuscular performance.  However, analysis of correlations between weekly average cortisol and CMJ values revealed that higher CMJ scores were recorded in weeks with higher cortisol levels, indicating that transient elevation of cortisol is associated with better neuromuscular performance.  The weeks with higher CMJ performance were weeks with lower training volume but higher training intensity (i.e. more Zone 3 sessions).  Finally, CMJ scores were significantly higher in the week before the season’s best competition performance

In summary, the evidence from the study by Balsalobre-Fernadez and colleagues confirms that sustained elevation of cortisol is harmful and favours a lower volume of higher intensity training rather than moderately large volume a little above lactate threshold.  This might be a key to understanding why polarised training might be superior to threshold training.   In my next post, I will examine the mechanisms by which the training adaptations required for distance running might be best achieved using a polarised approach.  In particular I will discuss the ability of negative ions such as phosphate and bicarbonate in the blood to provide temporary buffering of the acidity associated with lactate production.  This buffering might allow transient surges of lactate produced by brief high intensity exercise to produce beneficial enhancement of the transporter molecules that facilitate transport of lactate from type 2 to type 1 muscle fibres in which it can be used as fuel, and also the transport of lactate from muscles to liver and heart, without the potentially damaging effects of increased acid levels associated with sustained increase in level of lactate.

Hill sprints

December 3, 2016

In recent days there has been an interesting discussion on the Fetcheveryone ‘Polarised training’ thread about the value of the short intense hill sprints that Renato Canova and Brad Hudson recommend for distance runners.

Typically these take to form of 6 or more short (6-8 second) intense uphill sprints with adequate recovery between each sprint.  They can be done at either the beginning or end of a training session.   Canova recommends them up to twice a week. I have never done them more frequently than once per week.   Although 6 hill sprints do not add greatly to the training load of a ‘serious’ athlete, I have always been concerned to avoid the risk of excessive stress.   It is more important to maintain good form that promotes optimum muscle fibre recruitment

One of the immediate benefits is a feeling of speed in your legs that can make subsequent fast pace running feel relatively easy.   Some athletes do intense hill sprints in the 24 hours before a race for this purpose.  Although I have not habitually done this, I usually do  ‘bounding’ drills during the taper for a target race to achieve a similar result.  In fact hill sprints are probably safer than bounding drills as they present little risk of injury provided you warm up adequately.

I think that the feeling of ‘having speed in your legs’ is based largely on the sensation of recruiting fast twitch fibres.  However, you might wonder why this is helpful for a long distance runner, since fast twitch fibres are poorly adapted for aerobic metabolism.  I suspect the reason is that fast twitch fibres are good at capturing the energy of impact at footfall as elastic energy.  Provided you have developed the ability to recycle lactate from fast-twitch fibres to slow twitch fibres that can use the lactate as fuel, the fast twitch contractions do not lead to increase in blood acidity.

Non-weight-bearing aerobic cross training

September 11, 2016

All forms of low-impact aerobic cross training provide the opportunity to enhance some aspects of fitness while reducing risk of injury due to lack of the impact at footfall.  As described in my previous post, cross-training that entails weight-bearing enhances endurance of the postural muscles that provide a stable core to support the driving force exerted by the legs.  For this reason, most of my cross-training is weight-bearing.  However under some circumstances, non-weight bearing training is preferable.

If the main goal is recovery, non-weight-bearing cross-training minimises stress on the musculo-skeletal system.    In particular, swimming has been shown to produce more effective recovery than complete rest after heavy training.  It is probable that when swimming the increased blood circulation promotes removal of the debris resulting from the muscle damage during heavy training.   If the goal is maintaining fitness while recovering from injury, avoidance of weight bearing might be essential in the early phase of recovery, and a judicious combination of weight bearing and non-weight-bearing training cross-training subsequently introduced as the injury heals.  Emily Infeld’s log of her training after suffering a hip stress fracture three months before the US Trials for the Rio Olympics is a very informative description of judicious integration of non-weight bearing and weight-bearing cross training.  Finally, non-weight bearing cross training such as cycling or swimming might be preferable simply because these activities are enjoyable and mentally stimulating.

Let us consider several of the most popular forms of non-weight bearing cross training in greater detail:

Cycling

One of the great virtues of cycling is that with a few precautions and a gradual build up, you can cycle for many hours with minimal risk of injury.  It also offers great opportunities for an enjoyable alternative to running.  It is therefore a great way to develop cardiac output and endurance.   However, a crucial question is whether or not it is a good way to build up the leg muscles that are most important for running.   Like all other forms of low impact cross training, it does not condition the muscles to cope with the eccentric contractions at footfall.  Nonetheless, as in running, the main generators of power in cycling are the extensors of hip and knee, with a contribution form calf muscles in the final stage of the down-stroke.  At low and moderate intensities cycling has the potential for developing important features such as fat burning, capillary supply and the ability to shuttle lactate between type 2 and type 1 fibres, in these muscles, while at high intensity it can enhance their power.

However, the notorious challenge of the transition from bike to run in the triathlon raises the possibility that cycling might use these muscles in a different manner that is actually antagonistic to running.   Although I am not a triathlete, for more than sixty years the bike has been my major means of transport for local travel, including travelling home from work before an  evening training session and even more critically, for travelling to and from races. My experience leaves little doubt that in the short term, cycling does impede running.  What causes this and does it have implications for longer term influence of  cycling on running?  Unfortunately, I have never been able to get a convincing answer to this question in my discussions with triathletes, but I have developed some speculations based on my own experiences and on the anatomy of the hip and knee extensors.

The first point to note is that the range of hip extension differs between running and cycling.  When running, the hip extensors come into play in arresting the flexion of hip and knee in late swing (initially an eccentric contraction) and continue to act until late stance, by which stage the hip is extended beyond the neutral position and the leg is angled downwards and back.  During late stance, the hip extensors undergo concentric contraction, though the fact that the fact that the hamstrings cross both hip and knee complicates matters; we will return to the implications of this later.   When cycling the hip extensors are passively streched during the upstroke and contract concentrically throughout the down-stroke. The hip extension ends with the foot below the torso and the hip still slightly flexed. Thus, throughout the period of extension the hip is actually in a state of full or partial flexion.  Although the hip extensors are not subject to active stretching during the down-stroke, the extensors are nearly fully stretched at the beginning of the down-stroke and remain slightly lengthened relative to the neutral position at the end of the down-stroke.

Thus, despite the fact that cycling avoids the potentially seriously eccentric contraction that occurs during running, the hip extensors are at least somewhat lengthened relative to neutral and the flexors slightly shortened throughout the stroke, and there is a risk that protracted periods of cycling will lead to a tendency for shortening of hip flexors and stretching of hip extensors.  For a person with a desk job, this exacerbates the tendency for shortening hip flexors induced by hours of sitting.   Such a tendency for shortened hip flexors and stretched extensors might impede the extension of hip and knee in later stance that is crucial for powerful running.

However, the situation is actually a little more complex. The major hip extensors are the gluteus maximus and the hamstrings.  The long hamstrings cross both hip and knee, acting as flexors of the knee in addition to extending the hip.  During both cycling and running, the knee and hip extend together, so the length of the hamstrings changes relatively little.  The issue of shortened hip flexors and stretched extensors appears at first sight to apply only the flexors and extensors crossing a single joint (psoas and gluteus maximus).  However, the picture is even more complex, because the hamstrings, apart from the short head of biceps femoris, take their origin from the ischial tuberosity which is below and slightly behind the hip joint, exacerbating the tendency for stretching as the hip flexes, while most of the fibres of the long head of biceps femoris and semimembranosis are inserted only a short distance below the knee joint, such that knee flexion produces little tendency towards shortening.  The net effect of the location of the origin and insertions of the various components of the hamstrings is that both semimembranosis and the long head of biceps femoris are stretched passively during the hip and knee flexion during the upstroke of cycling.

semimembranosis3

Illustration of the passive stretching of semimembranosis muscle as the hip and knee flex to approximately 90 degrees. The muscle is about 6 cm shorter than the femur in the neutral position, but only 2-3 cm shorter during flexion. In this illustration the pelvis remains neutral. When cycling, forward lean of the trunk displaces the ischial tuberosity backwards, adding to the stretch of semimembranosis.

Overall, there is a tendency for shortening of psoas, a hip flexor,  and lengthening of gluteus maximus and two major components of the hamstrings. At least in the short term this will impede the powerful extension of the hip in late stance required when running.   If cycling forms a large part of training, it might produce a sustained imbalance between hip flexion and extension, resulting in sustained impediment of the hip extension crucial for powerful running.

I think there are two ways of minimizing the risk of impeding hip extension.  First of all, it is probably useful to stretch the hip flexors after cycling. Static stretching should only be done while the muscles are warm. I rarely engage in passive stretching. However I regularly do dynamic hip swings (standing on one leg, swinging the other leg forward and back, with knee extended, emphasising on a good back-swing.  If I ever do a triathlon, I will be inclined to spend 30 seconds in the second transition mobilizing the hip.  The second strategy for reducing the problem of dominance of flexion over extension is cycling at a high cadence.  This favours the development of muscle properties such as capillary supply and fat metabolism rather than the building up of powerful type 2 fibres, thereby reducing risk of developing a strong imbalance between flexors and extensors.

Yet another potentially important factor is the type and fitting of the saddle.  On my commuter bike I have a saddle that is wide enough to support both ischial tuberosities (the ‘sit bones’).  On one of the few occasions when I have cycled vigorously for a sustained period, I was amazed to find that that on dismounting I could scarcely walk, let alone run. It appeared that my hamstrings were partially paralysed.  This was almost certainly due to pressure on the upper part of the hamstrings, which are attached to the ischial tuberosities.  The problem was only transient but emphasized to the importance of a well fitted saddle of the correct width.

In summary, cycling is a potentially valuable form of cross training. It is possible to cycle for far longer periods than feasible when running; it is good for developing cardiac endurance and also for the attributes of skeletal muscles important for running in the aerobic zone, but it is necessary to avoid developing an imbalance between hip flexors and extensors. This might be achieved by cycling at high cadence and at doing dynamic stretching of the hip flexors for least a short period afterwards.

Swimming

Over the years I have only swum sporadically, though for several months after I had injured the lateral ligaments of my left knee in a cycling accident last year, swimming became the mainstay of  my cross training.  I consider that the front crawl is the most useful stroke because the flutter kick and core strength required for a well-balanced position in the water help maintain the endurance of the gluteals and trunk muscles engaged during running.

Unless you devote some attention to swimming technique, front crawl can become an anaerobic activity (despite a relatively low heart rate). It is noteworthy that in the study led by Peter Peeling at University of Western Australia, in which a recovery session including 2 km of moderate intensity swimming produced more effective recovery than passive rest of similar duration after intense running interval sessions, the participants were triathletes.  I doubt that swimming would produce such a beneficial recovery in runners who were not technically accomplished swimmers.

For most people, and especially for male distance runners, the centre of mass of the body is near to the hips while the centre of buoyancy is in the chest.  As a result the body tends to rotate to a feet- down, head-up position in the water, increasing drag and tending to make swimming an anaerobic activity. The streamlined position necessary for a sustained aerobic front crawl requires a flutter kick and engagement of trunk muscles, actions which in themselves are directly beneficial to the distance runner.  I consider the Swim Smooth site is a very helpful source of guidance on front crawl technique.

Aqua-jogging   

Aqua jogging using a flotation belt for buoyancy, or deep water running, involve similar neuromuscular action to running, with zero or minimal impact.  However, the relative activity in the quads and hamstrings differs between different styles of deep water running, and is also likely to differ from ‘on land’ running.   For example, Mercer and colleagues demonstrated that when running at a stride frequency that the runners had self-selected during ‘on land’ running, activation of quads and hamstrings was lower during a high knees style of deep water running than a ‘cross-country’ style.  However, the high knees style produced greater activation of hamstrings that a body weight-supported treadmill with either 60 or 80% support, but similar activation of quads.  Furthermore, it is subjectively harder to achieve a given heart rate, and maximum achievable heart rate tends to be lower during aqua jogging or deep water running than when running on land.  This might be because of greater venous return of blood to the heart and consequently increased stroke volume, though I am not aware of direct evidence for this.

Overall the evidence indicates that aqua jogging or deep water running can produce useful gains in fitness in previously untrained individuals, and can help maintain fitness in injured athletes, but it should not be assumed to be very similar to ‘on land’ running  in either the relative activation of different muscle groups, or in cardiovascular responses.

In light of the greater perceived effort required to achieve a given heart rate, and also the potential for boredom, I consider that aqua jogging and deep-water running lend themselves better to interval style sessions, if the goal is to increase fitness. On the other hand, if the goal is recovery after hard training, aqua aerobics (perhaps best done in a group led by an enthusiastic leader and accompanied by lively music) might be enjoyable and relaxing.

Similar to the evidence that swimming can promote better recovery than passive rest after intense running, Takahashi and colleagues demonstrated that 30 minutes of walking, jogging and jumping in water daily for three days following a down-hill running session produced better recovery of muscle, evidenced by less soreness and stiffness, than were observed in a control group.

 

Body-weight-support treadmill

In the so-called anti-gravity treadmill, the lower body is encased in an airtight bag.  Air-pressure in the bag is increased thereby tending to lift you off the treadmill.  The principle is similar to aqua-jogging but with the advantage that the reduction in effective body weight can be set at any desired level from 0 to 80%.  In both principle and practice, this is can be an effective device for promoting recovery from injury, though accessibility is limited and the cost is probably prohibitive for use simply as a form of cross training.

Conclusion

Low impact, aerobic cross training is a useful way in which to increase volume of training, with beneficial effects on features such as capillary supply to heart and skeletal muscle, ability to metabolise fats, ability to shuttle lactate between type 2 and type 1 fibres, endurance of postural muscles and other aspects of fitness relevant to distance running.  It greatly reduces the risk of injury arising from impact at foot fall, but conversely, cannot enhance the ability to cope with the eccentric contraction of leg muscles at footfall that plays a cardinal role in getting airborne.  Furthermore different forms of cross training achieve the various physiological goals of cross-training to differing degrees.   The optimum choice between them depends on the specific training goals and on other circumstances.

In general, I favour weight-bearing cross training over non-weight-bearing on account of the benefits to postural muscles, bones and other connective tissues. In particular, I favour the elliptical cross trainer used in the hands-free mode, because it provides a very effective workout for postural muscles and upper body actions that are relevant to running.  However, many individuals find it boring and would prefer to be out-doors.

If you have a large amount of time available and enjoy being out-doors, walking, especially hill-walking is a good option for conditioning the legs.  Similarly, cycling is potentially a great form of cross training on account of the fact that, after adequate preparation, you can cycle virtually all day with minimal risk of injury.  However, as discussed in my speculative account of the differences in neuromuscular activity between running and cycling, I think prolonged cycling creates a risk of shortening of hip flexors and stretching of hip extensors, that might impede the hip extension in late stance that plays a key role in running.  This risk might be diminished by cycling with a high cadence and by regular hip-mobility exercises.

If the primary goal is promoting recovery from a hard session, or during the initial phases of mobilisation after injury, swimming, aqua jogging or aqua aerobics might be preferable.   Other devices such as the zero-runner or the anti-gravity treadmill are potentially useful because they allow a pattern of muscle recruitment that more closely resembles that of running. However limited accessibility and cost might be limitations for many runners.