Archive for the ‘Physiology’ Category

Interpreting messages from the body to the brain

May 27, 2019

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

 

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

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

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

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

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

January 4, 2019

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

The combined effects of multiple genes

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

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

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

 

Relevant genetic variations influence the effectiveness of common bodily functions

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

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

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

The expression of genes is modified by training

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

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

Free radical generation during running: the Nf2 system.

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

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

Protein synthesis:  the mTOR complex

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

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

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

Myokines

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

DNA repair and protection of telomeres

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

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

exercise_geneexpression

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

 

The development of resilience

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

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

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

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

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

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

Enhancing VO2max and pace at lactate threshold

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

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

The balance between protection and harm

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

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

Implications for less gifted athletes: assessing the balance.

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

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

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

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.

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.

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.

Cross Training

June 19, 2016

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

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

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

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

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

 

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

Heart

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

Skeletal muscle

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

Systemic metabolism and hormones

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

Enhanced recovery

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

 

Conclusion

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

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

Achieving longevity as a distance runner: twelve principles.

April 27, 2016

In the past seven posts I have addressed the challenge of maximising longevity as a distance runner.  For many of us, age appears to offer the prospect of inexorable decline.  In contrast, a few individuals achieve performances in their 70’s or 80’s that would be a source of great satisfaction for many runners 30 years younger.  Ed Whitlock recorded a time of 2:54:48 in the 2004 Toronto Waterfront Marathon at age 73 and as recently as a week ago, set an M85 half-marathon world record of 1:50:47 in the Waterloo half-marathon.  Even Ed is slowing as the years pass, but he has transformed our understanding of what an elderly distance runner can achieve.

In a previous blog post I attempted to tease out the secrets of Ed’s phenomenal longevity.  I concluded that his remarkably high maximum heart rate, determined largely by his genes, was one of the key elements that made him truly phenomenal, but his life-style and training allowed him to realise the potential offered by his genes. A central feature of his training has been frequent long, slow runs of up to 3 hours duration, often up to four or five times in a week.  This high volume of low intensity running is augmented by moderately frequent races, typically over distances of 5-10Km.

For most of us, merely attempting to emulate Ed’s training would be impractical, either on the grounds of lack of time, or because our bodies could not cope with the volume of training.   However, I believe that if we examine the anecdotal evidence provided by the training of Ed Whitlock and augment this with evidence that is emerging from current scientific studies of aging itself and of the way in which the aging body reacts to training, we can begin to formulate some general principles that will help maximise the chance of achieving the potential longevity offered by our genes.   It is also encouraging that the rapid accumulation of scientific knowledge offers the prospect of even better guidance in the future.

Meanwhile I have assembled a set of 12 principles that encapsulate much of the material presented in the past seven posts.  In this summary, I will not present the evidence justifying these principles. That evidence is presented in the preceding articles. Here are the 12 principles:

  1. Continue to run regularly. The evidence indicates that continuing to run, at least into the seventh and eight decades decreases risk of disability and death. However, by virtue the stressful effect of the impact at foot-strike, and also because running tends to exacerbate the age-related shift of hormonal balance away from anabolism (building up of tissues) towards catabolism (break down of tissues), the risks associated with running are greater in the elderly than in young adults.  Greater care is required to minimise these risks.

 

  1. Increase training volume gradually. Gradual increase minimises the stress of training and decreases the risk of excessive rise in the stress hormone cortisol, and allows gradual building of resilient less injury-prone tissues.

 

  1. Recover thoroughly after strenuous training and racing. The major reason is to ensure that acute inflammation resolves rather than becoming potentially destructive chronic inflammation.  However to prevent the development of constrictive adhesions due to the deposition of collagen fibres, it is important to maintain mobility during recovery. This might be achieved by easy exercise – walking, jogging, or elliptical cross training. Perhaps stretching has a role to play though there is little compelling evidence in favour of stretching. There is substantial evidence in favour of massage.

 

  1. Do a substantial amount of low intensity training. Low intensity training promotes both mitochondrial biogenesis and fat metabolism, while also building the resilience of muscles, tendons, ligaments and bones.  Low intensity training enhances the ability to handle lactic acid by developing the ability to transfer lactate from fast twitch fibres into slow twitch fibres where it is consumed as fuel.

 

  1. Do a modest amount of high intensity training. High intensity training helps to sustain power (the ability to deliver force rapidly) while also being an effective way to enhance the mechanism for pumping calcium back into muscles. High intensity training enhances the ability to clear lactate from muscle and transport it to other tissues such as liver where it can be utilised.

 

  1. Optimise cadence. A relatively high cadence at a given pace requires a shorter stride length, thereby reducing peak airborne height (and reducing impact forces) while also reducing braking forces.  Overall, potentially damaging forces are reduced. However high cadence does increase the energy cost of repositioning the swinging leg, so very high cadence is inefficient.  The most efficient cadence increases with increasing pace.  Most runners increase cadence with increasing pace.  Nonetheless for the elderly runner, it might be best to maintain a quite high cadence during training even at low paces because minimising impact forces is more important than maximising efficiency.

 

  1. Engage in low impact cross training. Although running itself is the most effective way of getting fit for running, running is a very stressful form of exercise on account of the impact forces.  Many of the desired benefits of training, especially cardiac fitness, can be acquired through other forms of exercise. Low impact cross training, (elliptical, cycling, walking) provides substantial benefit with minimum damage.

 

  1. Do regular resistance exercise. Resistance exercises help maintain strength and power, while promoting anabolism, thereby correcting the age-related tendency towards an excess of catabolism over anabolism. There are many different forms of resistance exercise.  I do regular barbell squats and dead-lifts with quite heavy loads (typically 100Kg) and also do hang-cleans to enhance power in the posterior chain muscles (glutes, hamstrings, gastrocnemius).  These exercises enhance the recruitment of type 2 fibres.

 

  1. Consume a well-balanced diet. The question of the healthiest diet remains controversial, but there is no doubt that elderly individuals require a higher intake of protein to maximise tissue repair; variety, including bright coloured vegetables, helps ensure adequate intake of micronutrients. At least a moderate amount of omega-3 fats is required to promote repair of cell membranes, but a balance between omega-3 and omega-6 is probably necessary to promote acute inflammation with minimal chronic inflammation.

 

  1. Get adequate sleep. Sleep is a crucial element of recovery. It promotes a naturally regulated release of growth hormone and encourages tissue repair.

 

  1. Avoid sustained stress. The body is a dynamic system that requires a degree of challenge, and hence of stress, to prevent atrophy. The body responds to stress of any kind – physical or mental – by increasing release of the stress hormones, adrenaline and cortisol. In the short term this shifts the hormonal balance towards catabolism mobilising the energy required to respond to the stress, but if sustained it damages tissues, not only via break-down of body tissues, but also by promoting more subtle damage to DNA, as discussed in my post on ‘whole body factors’.  To achieve well-being in life and optimum benefit from training, any stress, from whatever cause, should be accompanied by a commensurate amount of recovery.  Measurements such a heart rate, heart rate variability, and blood pressure can provide useful warnings of harmful imbalance.  However, our brains are very well attuned to assessing our level of stress, and sensitivity to one’s own sense of well-being also offers useful guidance.

 

  1. Develop confidence in control over one’s life.  Scientific evidence from large studies demonstrates that a sense of control over one’s life promotes longevity, while abundant anecdotal evidence illustrates that confidence is a key element in athletic performance.  Good health and optimal performance are facilitated by minimising self-defeating thoughts.  Each individual needs to develop their own strategies for achieving this.

 

I have been pleased to see from the stats provided by Word-press that many readers from many parts of the world read my blog. There are typically around 30,000 page views per year from over 100 different countries.  I started this blog nine years ago with the aim of encouraging discussion and debate about efficient running and training. Over the years there have been some vigorous debates, mainly about the more controversial issues of running technique.   The challenge of achieving longevity as a distance runner has not aroused the same passions. In part this is because the evidence is less controversial, but nonetheless, some of the evidence could be challenged, and there are many areas in which it could be expanded.  Please let me know if you disagree with these principles or alternatively consider there are other important things to be taken into account.

 

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

April 16, 2016

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

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

 

Hormones: achieving a balance between catabolism and anabolism

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

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

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

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

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

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

Growth Hormone

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

GH&IGF

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

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

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

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

 

Damage produced by chronic inflammation

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

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

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

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

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

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

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

 

Protecting our DNA

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

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

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

 

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

 

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

 

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

 

The Brain and its Mind

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

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

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

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

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

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

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

Conclusion

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

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