Archive for May, 2009

Is heart muscle or leg muscle the limiting factor?

May 31, 2009

Both heart muscle and leg muscles play a crucial role in running. The function of both of these types of muscle can be enhanced by training. This raises two major questions:

1) When is the function of the heart the factor that limits our performance and when is skeletal muscle the limiting factor?

2) Are different training regimes required for optimal development of heart and skeletal muscle?

In my next few postings I intend to examine what evidence there is that might help answer these questions, but first is of interest to consider a few similarities and differences between the roles of these two types of muscles.

The heart must beat for life

One of the crucial differences is that the heart must continue to beat throughout life, whereas skeletal muscle is called upon to act for relatively limited periods of time, ranging from a few minutes in middle distance races to a few hours in long distance events such as the marathon. This difference in function necessitates some differences in the options for use of fuel, though during long distance races, both types of muscle rely largely on aerobic metabolism and therefore on an adequate supply of oxygen. From the point of view of the runner, the crucial issue is that a torn skeletal muscle is a frustrating inconvenience whereas serious disruption of the heart is potentially fatal. While the evidence suggests that regular exercise decreases risk of heart attack, unfortunately, there is also clear evidence that very demanding exercise, such as running a marathon, is associated with an increased risk of heart attack within the following 24 hours (Journal of the American College of Cardiology, vol 28, pp 428-431, 1996). In most cases, post mortem examination reveals that such deaths are due to pre-existing abnormality of the heart, especially abnormalities of the coronary vessels that deliver blood to the heart muscle .

The heart is a complex pump

Another crucial difference is in the complexity of the function and therefore on the susceptibility to disruption of that function. In general a skeletal muscle is simply required to either to shorten to achieve the required movement of the bones to which it is attached and thereby flex or extend a joint (i.e concentric contraction), or to resist a forcible extension of the muscle and thereby limit or slow flexion or extension of a joint (eccentric contraction). In fact the amount of tension generated within the muscle must be controlled quite exquisitely if the action of the muscle is to be efficient. Nonetheless the essential requirement is simply to exert the required amount of force along the long axis of the muscle.

In the case of the heart, the required action is much more complex. The heart is a four chambered pump: there are two atria and two ventricles. The right atrium collects the blood that is returned from the tissues of the body (via the two large draining veins known as the inferior and superior vena cava) and transfers it via a valve into the right ventricle. The right ventricle pumps the blood to the lungs to replenish its supply of oxygen and dispose of its burden of carbon dioxide. The freshly oxygenated blood from lungs is collected in the left atrium and transferred into the left ventricle from whence it is pumped into aorta, and thence distributed to the body tissues. This pumping action requires a well coordinated contraction of the four chambers with very precise timing. The timing is controlled by a wave of electrical activity that spreads through the muscular walls of the chambers, from a starting point known as the sinoatrial (SA) node in the wall of the right atrium. The spreading electrical signal is transmitted from the atrial walls to the ventricles via the atrio-ventricular (AV) node.

Left to its own devices, the SA node would fire regularly at a certain base frequency. However various influences including levels of circulating adrenaline and also input from the autonomic nervous system, adjust the rate of firing of the SA node according to the body’s needs.


While the SA node is the usual site from which the spreading electrical impulse that produces contraction is initiated, any heart muscle cell can fire spontaneously, though usually at a rate lower than that of the SA node. If for some reason, such as irritation of the muscle cells by toxins released following damage arising from inadequate blood supply via the coronary arteries, muscle cells other than the SA node fire prematurely and the orderly spread of contraction is disrupted. The wall of the relevant chamber now flaps ineffectually (fibrillation). Provided this fibrillation is confined to the atria, enough blood to fulfill the body’s basic needs is usually drawn into the ventricles as they relax following the previous contraction. Thus the ventricles fill sufficiently to allow ejection of enough blood to meet essential needs provided a ventricular contraction is initiated. In most instances of atrial fibrillation, the AV node takes over the role of initiating an orderly ventricular contraction. Perhaps the person might feel a bit dizzy, but the outcome is not catastrophic. However, if the fibrillation spreads to the ventricles, effective pumping to the tissues of the body cannot occur and the outcome is fatal unless rhythmic contraction is restored very rapidly. Thus ventricular fibrillation is a type of ‘heart attack’ that results in sudden death

Benefits of training

Training might potentially have several benefits to the heart. First of all, there is clear evidence that in heart muscle, as in skeletal muscle, exercise results in increased density of capillaries distributing blood from the coronary arteries to the heart muscle. This would be expected to improve oxygen supply and reduce the risk of heart attack However, as in the case of skeletal muscle, the benefits of training are achieved via compensation for microscopic damage due to the stress of vigorous exercise.

When skeletal muscle is damaged various proteins, including the enzyme creatinine kinase, are released into the blood stream. Following prolonged vigorous exercise, such as running a marathon, blood levels of creatinine kinase rise markedly, indicating appreciable muscle damage. Similarly, when heart muscle is damaged various proteins are released into the blood stream. One characteristic marker of heart muscle damage is a high level of the protein troponin. Elevated troponin levels are observed after prolonged vigorous exercise.

Thus, the mechanism by which the density of capillaries supplying heart muscle is increased, thereby reducing long term risks of a heart attack, appears to involve at least some degree of microscopic damage. Unaccustomed strenuous exercise potentially creates an appreciable short term risk. Hence it is necessary to build up training volume gradually so that the heart gradually accommodates to the demands placed upon it.

As discussed above, in contrast to the risks of damage to skeletal muscle when the athlete might suffer a frustrating but temporary interruption of training, the risks associated with damage to heart muscle are potentially more catastrophic. On the other hand, because the normal demands of an active life style ensure that the heart is continually exercised, it is usually safe for an individual who has been leading an active lifestyle to build up training volume and intensity at a moderate rate. In very rare instances, congenital abnormalities might result in the development of abnormal electrical conducting pathways in the heart, creating the risk of sudden and tragic heart attack in an otherwise fit young person.


Development of capillaries that improve the distribution of blood from the coronary arteries to the heart muscle is not the only beneficial effect of training. It is also possible to increase the size of the heart. There are two principle types of hypertrophy: an increase in the diameter of the ventricles which leads to increased stroke volume; and an increase in the thickness of the walls of the ventricles, which can produce more powerful contraction. Increase in ventricular diameter and stroke volume will result in an increase in aerobic capacity – the ability to deliver oxygen to body tissues, including skeletal muscle, and hence is likely to improve distance running performance.

Various different training strategies have been proposed to maximize the enhancement of stroke volume. I will discuss these training strategies in a future post.

Re-examining the components of base building

May 25, 2009

Spring has become summer.  By mid-morning yesterday, the overnight clouds had given way to blue sky and bright sunshine, and I was eager to be running.  However I was tired after a heavy week at work, with late nights and relatively little sleep, so I opted for a relaxed lower aerobic run though the woods and along the river bank.  It was a delight to be out of doors.  In the woods the prominent flowers are now red campion and buttercups where only a few weeks ago celandines and bluebells were dominant. I felt comfortable focussing on maintaining relaxed good form, but whenever I tried to increase pace, I my legs felt heavy.  I covered 18.5 Km at a pace of 5 min 56 sec per Km, and a mean heart rate of 112.  Despite enjoying the run, the question nagging me at the end was whether or not my sluggishness could be accounted for entirely by a heavy week at work.

This morning it was even more tempting to be out running.  The sun was again shining brightly, while the woods and riverside were still fresh, green and inviting.  I decided to repeat yesterdays run, expecting that I could improve on yesterday’s sluggish pace without strain.  But again my legs were reluctant to cooperate.  I concentrated on keeping my hips forward attempting to conjure a brisk lift off from stance, while aiming for a feeling of fluency rather than effort. But there was little spring in my legs, I was still sluggish in getting airborne, and my stride remained short.  Checking my heart rate monitor revealed that my pulse was a little higher than yesterday, but my pace over the first 15 km was virtually identical.  In the final few Km, in an effort to break out of the state of torpor, I focussed on the downwards thrust of my arm as my foot lifted from stance.  This shift in focus was more successful in bringing my foot up briskly, and I built up pace so that  the final 3 Km was about 2 minutes faster than yesterday, with little increase in subjective effect.  Nonetheless my average pace for the entire run (5:50 per Km) was only 6 seconds per Km faster than yesterday, and my mean heart rate 118, compared with 112 yesterday.  In terms of heart beats per Km, today’s run was even less efficient than yesterday’s.

In several respects the two runs this weekend have been a success. I have enjoyed being out of doors in delightful surroundings and I managed to cultivate a relaxed and fairly fluent style despite sluggish legs.  But apart from the final few Km today, in which I managed a pace of around 5 min per Km, my pace was unimpressive.  Am I making progress or have I become stuck in a rut?  Is there any point in drawing conclusions from runs in the lower aerobic zone?  In fact I think there is much to be learned from back-to-back easy long runs, and the conclusions I would draw from this weekend are in fact positive though tentative.  But in order to appreciate this, it is necessary to review the essential elements of fitness for distance running.


Building a base involves more than increasing aerobic capacity

Since the very influential work of Jack Daniels in which he delineated various training zones extending from lower aerobic to anaerobic based on the proportion of energy derived from the different energy generating metabolic pathways, much emphasis has been placed on the development of aerobic capacity – the amount of energy that can be generated by oxidative metabolism of glucose or fat.  As races over distances ranging from 10Km to the marathon are fuelled largely by oxidative metabolism, this is doubtlessly a key concept, but there is a danger that focus on aerobic capacity distracts from the fact that base-building has several additional components. 

Each individual has a range of strengths and weaknesses depending on genes and life experiences, and each individual runner needs to establish what are the limiting factors for him or herself.  In contrast to my younger self, I now find that getting fit is a slow process.  What is so different in my mid-sixties compared with my teens and twenties?  The most obvious fact is that four or five decades ago I was still in a phase of natural development, whereas now my strength is declining as anabolic hormone production decreases and body tissues lose their resilience.  However, the inevitable decline with age is only part of the story.


What was the foundation of my fitness 40 years ago?

Another part of the story is the nature of my fitness base.  As an 8 year old, I simply regarded running as the natural way to get from one place to another. I ran to school; I ran to the shops; I ran everywhere.  As a teenager, I played football for many hours each week and I still preferred to run than to walk.  In my twenties, I loved being in the mountains, walking or climbing.  As a result I never trained for running with the single mindedness that is necessary for peak performance, but in retrospect, I suspect the range of my activities created a fitness base that allowed me to make the most of the limited training that I did.   I have not kept a diary of my running and my memories are sketchy.  I won the South Australian state marathon championship sometime in the late 1960’s.  The only recorded time I have been able to find by internet search is 2:33:07 in the Australian national championships in 1970, but that was far from my best marathon.  As far as I remember my best time was around 2:25.

When training regularly I followed a Lydiard-style training program, though I rarely ran the 100 miles per week recommended by Lydiard.  I mainly skipped the low intensity sessions (the enigmatic ‘1/4 effort’ runs).  Almost all of my training runs were in the mid or upper aerobic zone.  With the self-assurance based on youth and ignorance, I regarded running at any pace less than 6 minutes per mile as a waste of time.  With hind-sight I can see that my various other activities provided the essential base that might otherwise have been achieved by slower running.  I took a sound base level of fitness for granted at the time.


The essential fitness base for distance running

In those days I certainly never troubled myself with the question of what makes up the essential fitness base for distance running.  Distance running depends on many of the body’s systems, including brain, heart, blood vessels, muscles, skeleton, lungs, liver, kidneys and the endocrine system.  While it might be argued that of these brain is the most important, in terms of measurable functions, there are three that are paramount for performance at distances from 10K to the marathon:

1) aerobic capacity;

2) the ability to metabolise lactate;

3) the ability of muscle fibres to withstand repeated eccentric contraction.


Building a base is a long term undertaking

Aerobic capacity is determined by three variables: maximum heart rate, cardiac stroke volume and capacity of muscles to extract oxygen from blood.  Maximum heart rate responds little to training.  Stroke volume increases with increased blood volume, and hence increases rapidly in the early stages of training, but also increases steadily over a period of several years of vigorous exercise.  The ability of muscles to extract oxygen from blood is determined by the density of capillaries, and by mitochondrial enzyme capacity, both of which increase steadily over a period of years.  Thus, training for distance running is a long term undertaking.  To maximise potential, the five year plan is probably more important that the strategy for the current season.


Approaching middle-age

Returning to the account of my own running, prior to re-commencing training regularly a little over two years ago, I had made one previous attempt to get fit.  In 2000, as I approached my mid-fifties, I started running occasionally with the intention of running a marathon six years later, at age 60.  I slowly built up training volume during the period 2000-2002 and in the summer of 2003 introduced occasional interval sessions.  Then after a winter in which I trained only sporadically, I decided at the end of May 2004 that I would enter a marathon in September of that year as a trial run.  I knew I did not have time to get fully fit, but thought it would be a useful trial before my planned ‘serious’ attempt two years later.  I followed a program similar in general outline to that I had followed 35 years previously, but somewhat lower in both intensity and volume.  In the three months from June to August I covered an average of 56 Km per week.  The majority of my runs were in the mid-aerobic zone (around 5 min per Km) together with a few upper aerobic runs.

In mid-August I reviewed progress. I had done several runs of 32 Km without significant DOMS, which I took as evidence that my leg muscles could probably cope with the mechanical trauma of the marathon adequately. However, in mid-August I did an easy 37 Km run with the intention of pushing the pace to about 5 min/km in the final 8Km, and was disappointed to find that I simply did no have the resilience my legs to allow me to increase pace with 8Km to go.  This was perhaps a warning sign, but I assumed that it was due to inadequate carbohydrate loading – in retrospect, I think this was a mis-interpretation – and I concluded it was feasible to press on with my plan to run a marathon in September.

However, as I had not raced for over three decades, I had very little idea of how fast I should run.  In the few remaining weeks there was not time to experiment with potential marathon paced runs.  However, I did have time to assess my aerobic capacity crudely by measuring heart beats per Km in a few medium length runs in the lower and mid-aerobic zone.  Provided one can rule out the confounding effects of stress hormones, circulating toxins arising from muscle damage, and dehydration, beats per Km when running in the lower to mid aerobic zone is determined primarily by cardiac stroke volume and the capacity of muscle to extract oxygen from blood, and can provide a fairly reliable estimate of aerobic capacity.  During three aerobic training runs performed during the taper at the end of August, my recorded beats/ Km were 599, 597 and 581.  These figures indicated that under ideal conditions I could expect to maintain a pace around 4:36 /Km at a heart rate of 130 which was well below my lactate threshold.  Of course I knew that under race circumstances, my heart rate would be higher, but nonetheless, a time in the range 3:15 to 3:20 appeared feasible.

Race day

I was totally unprepared for the melee at the start of the race.  In my previous marathons several decades earlier, the entire field was rarely more than a few hundred competitors, and here I was surrounded by more than 10,000.   In my attempt to break free of the melee, I ran far too fast.  I did not see any mile markers until I reached the third, in something under 21 minutes.   It was clear that I would pay for this misjudgement later, but nonetheless, I settled comfortably into a pace around 4:40 /Km.  I reached 16Km in 71 minutes and the half-way point in 93 minutes, with my heart rate in the low 130’s, confirming my prior estimate of my aerobic capacity.  Predictably, I hit the wall at around 33 Km and struggled with leaden legs to the finish at a pace around 6 min/Km for the final 8 Km, though paradoxically, I was able to mount an impressive sprint in the final few hundred metres.  My time was 3:27:35, which was disappointing but scarcely surprising.  Overall, the evidence indicated that my aerobic capacity was adequate for a time of 3:15 or faster, but my endurance (and pace judgement) was not.



I resumed training with the goal of building up my endurance before a more serious attempt at a marathon two years later.  However I struggled to find time to train adequately (as I often work a 60 hour week), and when my longstanding asthma worsened markedly the following year, I decided to put off my plans to run a marathon again until after I retired.  When I became even  more busy at work in 2005 I stopped training altogether.   About 15 months later, while on holiday I tried to run up a hill and was appalled to find how unfit I had become.  So at the beginning of 2007 I commenced training regularly again, though taking account of my work commitments, I set myself the target of making modest improvements in my half marathon performance, while building a base for later years.

This lengthy story brings us almost up to date, and to the interpretation of my performance while running this weekend.  My long term goal is to build up a fitness base that will allow me to run creditable marathons in my post-retirement years.  Aerobic capacity is one component of the required base, but even more important is building endurance.  In races from 10K to half-marathon, the key element of endurance is the ability to sustain a pace near lactate threshold pace for the duration of the event, and for this the crucial physiological system is probably the biochemical pathway for metabolising lactate.  However, for longer races, the development of resistance to eccentric muscle damage is probably even more important. I am fairly sure that it was eccentric muslce damage rather than either accumulation of lactate or exhaustion of fuel that accounted for me hitting the wall in the marathon in 2004.  It was unlikley to have been lactate accumualtion because my heart rate had been well below lactate threshold.  It is unlikley to have been exhaustion of fuel, because I was able to muster an impressive sprint when the end was in sight.  The most plausible explanation is that my brain surreptitiously applied the brakes on account of circulating toxins arising from muscle breakdown.

Developing resistance to eccentric damage

I suspect that it was resistance to eccentric damage developed through a diverse range of sporting activities in childhood, and extensive hill walking in young adulthood that provided the foundation for my achievements in the marathon forty years ago.  However it is a challenge to know how to re-acquire this in late middle age.  The accumulating fatigue I experience if I attempt to run more than 80 Km per week indicates that increases in training volume must be done cautiously.

How should the build up of training volume be monitored? I have been intrigued to find that heart beats/Km in the lower and mid-aerobic provides not only a fairly reliable estimate of aerobic capacity, provided one avoids the confounds of stress, dehydration and muscle damage, but it might also be used as a index of the degree of accumulating fatigue.

When I recommenced training in 2007, beats/km averaged over three identical aerobic runs in January was 815.  In the past two years, this has steadily decreased and in recent months my average is around 670 beats/Km.  Perhaps by next year I will again achieve recordings below 600, comparable with my recordings in 2004.  But even more interesting is the effect of a long run on the value recorded the following day. I have noted that following runs of 15 Km or more, the recording of beats per Km during an easy run on the following days is always increased, but then returns to baseline after a rest day.  In March, I recorded 697 beats/Km during an easy 21 Km run on a Saturday and 749 beats/Km during an identical run the following day. This weekend, I recorded 665 beats/km on Saturday and 688 beats/Km during an almost identical run on Sunday.  The slightly faster pace in the final few Km would have only accounted for a slight increase in mean heart rate; the difference between the two runs was mainly due to a sustained higher rate throughout.


Over-reaching without over-training

This observation might be regarded as evidence that doing back-to-back long runs is over-reaching, but over-reaching without over-training is the ideal. The return to baseline after a rest day, and the gradual but steady improvement over a period of months, suggests that both my aerobic capacity and my endurance are improving, albeit slowly. I am inclined to think that the evidence for a modest degree of over-reaching after long runs indicates that I am pushing myself hard enough but not too hard, during these runs

The pros and cons of weight loss for runners

May 16, 2009

Both theory and practice indicate that the energy cost of running is proportional to body weight.  First the theory: the energy cost of running can be subdivided  in to three categories: energy required to do work against gravity; energy required to do work against horizontal ground reaction forces; and energy cost of internal muscle inefficiency. 

The cost of being airborne

We do work against gravity when we become airborne.  The energy required to lift the body is proportional to body weight. Some of this energy is recovered by converting the energy of impact into elastic energy at foot-fall, thereby allowing us to re-use that energy for upwards acceleration at lift-off from stance.  However only a proportion of the energy will be recovered.  Assuming that this proportion is approximately constant (an assumption that depends on not changing running style) the net energy cost of becoming airborne is proportional to body weight.

 The cost of being on stance

Although being airborne has a high energy cost, so does remaining on stance.  While the point of support is ahead of the centre of mass, we experience a braking force (due to the horizontal component of ground reaction) that reduces our momentum.  This braking force at any instant is determined by the angle of our leg and by the force transmitted along the length of the leg, which in turn in proportional to body weight.  Therefore the braking force will be proportional to body weight.  When the point of support is behind the centre of mass, the horizontal component of ground reaction  pushes us forwards.  When running at constant speed, the retarding impulse due to braking must be exactly balanced by the forward accelerating impulse in late stance.   We can capture some of the energy released by the braking force in early stance as elastic energy which helps provide the forwards impulse in the second half of stance, but due to inefficiency we cannot recover 100% of this energy.  Assuming no change in running style, an approximately fixed proportion of the energy will be lost.  So, the energy consumed in opposing horizontal ground reaction forces is also approximately proportional to body weight. 

Unfortunately, it costs energy to be airborne and it also costs energy to spend time on stance.  Both of these costs are proportional to body weight.  Incidentally, as discussed in my posts on efficient running style summarized in the page on the Dance with the Devil, the best way to minimize these costs is to increase cadence, because higher cadence reduces the cost of overcoming gravity  – though there is a limit due to internal inefficiency at very high cadence

Internal muscle inefficiency

The energy costs due to internal muscle inefficiency are less easy to estimate. The process of muscle contraction involves the pumping of various ions, especially calcium, sodium and potassium, across the membranes that separate the different compartments of a muscle fibre.  The molecular pumps are fuelled by the energy molecule ATP, which is regenerated by consumption of glucose. There are also other metabolic processes and frictional processes within the muscles and joints, and as a result the energy consumed by a muscle is greater than the external work done by the muscle.  However, it is probably a fairly good approximation to assume that over the usual range of output, the efficiency of muscles is approximately constant, so the energy wasted internally will be proportional to external work done.  As we have seen the external work done (against gravity and against horizontal ground reaction forces) is proportional to body weight.  Thus the loss due to internal inefficiency will also be approximately proportional to body weight, though variation in the internal regulators of metabolism (such as anabolic and catabolic hormones) might also influence the costs.

Theory compared with practice

Thus, theory predicts that averaged across many individuals, the energy cost of running is approximaltely proportional to body weight, though differences in factors such as efficiency of running style and hormone levels might result in two individuals with the same weight nonetheless having slightly different energy costs.  In fact the energy cost of running averaged across many people, based on actual measurement rather than theory is given by the formula:

Energy cost in  Kcal/min/Kg  = ( 0.0024 * speed2 ) – ( 0.0104 * speed ) + 0.1408

where speed is measured in miles per hour ( ). 

This formula demonstrates that on average, energy cost per Kg is independent of weight (and hence total energy cost is proportional to weight) , but such formulae provide only a rough guide for the costs in each individual.

The conclusion from both theory and from practical evidence is that if you lose weight, you will require less energy per minute to maintain a given speed, so you can maintain a faster speed at any particular fraction of your total aerobic capacity.  Weight loss will lead to improved speed approximately in proportion to the weight loss – all other things being equal.


Balancing catabolism and anabolism

The crucial phrase is ‘all other things being equal’.  If the weight loss were to be so extreme that there were no fat reserves for use as fuel, this would result is reduced performance over distances for which fat is a valuable source of energy, such as the marathon and longer distances.  However, because fat is a very efficient fuel (providing lots of energy per gram of fat) it would be necessary to starve almost to death to deplete fat stores below the amount likely to be consumed in a marathon or ultra-marathon.  Nonetheless, even less severe weight loss can trigger hormonal changes (regulated by the hypothalamus) in order to conserve essential body issues, especially the brain, and it is likely that muscle protein would be sacrificed.  In other words, if the weight loss is sufficient to tip the balance from anabolism to catabolism, muscle protein will be broken down and muscle strength decreased.  Hence loss of speed would be expected.  


General conclusions

In practice, this means that an out-of-condition runner who has gained weight will almost certainly benefit from losing that weight.  However an athlete who has trained over a substantial period at a training volume just a little less than that required to produce the overtraining syndrome, has probably already reached the optimum balance between anabolism and catabolism and further weight loss would probably be harmful.    

If you want to achieve to your limit, it is probably best to monitor performance regularly while steadily increasing training volume.  When performance shows a tendency to decline despite increasing training volume, it is likely that the balance has shifted too far towards catabolism (break down of tissue), and you should drop back to a slightly lower training volume.  Pushing relentlessly onwards with increased volume despite decreasing performance will almost certainly result in a sustained period of staleness, in which your brain will not allow you to run at your best level.

Personal conclusions

It is also useful simply to monitor weight.  Experience has taught me that when I train regularly my weight stabilizes at around 62-63 Kg, irrespective of exactly how much running I do, at least while I remain below the limit where I feel perpetually tired. Thus I think my brain (and in particular, my hypothalamus) regulates hormonal function so that catabolism equals anabolism when my weight is around 62-63Kg. 

However, while 62-63 Kg appears to be my ‘equilibrium’ weight, is probable that my proportion of muscle to fat is not optimal at present.  Almost 40 years ago when I could run a marathon in 2 hours 25 minutes, my weight was also around 62 Kg.  Since then I have almost certainly lost muscle and increased fat. It is probable that I could improve my running performance by doing more resistance exercise.  Provided it is not excessive, resistance exercise promotes anabolic hormone release and would promote replacement of fat with muscle.  However, a large amount of resistance exercise resulting in bulking of fast twitch muscle fibres and a net gain in weight, without gain in aerobic capacity, would probably decrease my distance running performance on account of the increased energy cost of running with extra weight.

Outwitting the governor

May 9, 2009

Performance is determined by physical fitness and by mental attitude. We devote a lot of mental effort to the challenge in deciding how to maximize physical fitness. The finer points in the debates between the different schools of training theory – Lydiard v Furman; Maffetone v Lydiard and many others – remain a topic for fertile discussion, but the re-assuring fact is that there are many ways to get physically fit. The finer points of the debates about the physical aspects of training only really matter when we get stuck in a rut and fail to improve.

In contrast, in my experience, the topic of mental attitude has been a less fruitful topic of debate. When I read articles about the psychology of sport I usually get the feeling that what is on offer is a set of fairly trite and uncontroversial observations that might be dismissed merely as common sense. However, as a young Australian growing up in the era when John Landy vied with Roger Bannister for the glory of breaking the barrier of four minutes for the mile, and a few years later, when Ron Clarke broke world record after world record but never won an Olympic gold medal, it was clear to me that the right mental attitude was crucial but also elusive.

The 1954 Vancouver mile provided the most graphic illustration that self-belief is paramount. The image of Landy looking over his left shoulder as he rounded the bend into the home straight while Bannister stormed past his right shoulder has been cast in bronze by the sculptor, Jack Harman, and serves as an enduring reminder that mental preparation is as important as physical preparation.

While much that has been written about sport psychology has left me uninspired, I have found Tim Noakes concept of the central governor very thought provoking. In formulating his central governor hypothesis, Noakes has developed an idea proposed many decades earlier by the celebrated muscle physiologist, A.V. Hill: performance is limited not by our lungs or muscles but by our brain, acting on the basis of physiological signals from the body to prevent us from damaging ourselves.

One of the most frustrating experiences in distance running is hitting the wall in the final few miles of a marathon. It feels as if every last muscle fibre has been exhausted; there is simply no more fuel left and it takes immense will power even to drag the legs onwards to the finish line at a pace scarcely faster than a jog. Mental tricks appear totally inadequate to mobilize the legs, yet when the finish line comes into sight, suddenly it is possible to lift those leaden legs and perhaps even raise a sprint. So the limiting factor is not total exhaustion of every muscle fibre; it is some barrier in the mind. This scenario vividly illustrates the machinations of Tim Noakes’ central governor.

One of the most compelling items of evidence supporting the concept of the central governor is the study of power output and muscle activation during a cycling time trial, by Kay and colleagues from Tim Noakes’ lab (Eur J Appl Physiol. 2001;84(1-2):115-21). The cyclists were required perform 6 maximal one minute sprints interspersed within a one hour time trial. Despite the cyclists’ attempts to perform to their maximum ability, power output and muscle activation decreased steadily from sprints 2 to 5. The decrease in muscle activation demonstrated that neural drive from brain to muscles was decreasing, not increasing as would be expected if the brain was acting to recruit additional muscles fibrils to compensate for the effects of fatigue. In contrast, during the 6th sprint, which was performed during the last minute of the time trial, power output and muscle activation increased significantly, similar to the pattern observed during the final sprint in endurance races.

This evidence indicates that slowing down due to fatigue is not due to reaching the limits of maximally recruited muscle fibres, but rather to a decreased recruitment of muscles by the brain. It is likely that this is a protective mechanism triggered by chemical messages released into the blood stream by stressed heart or leg muscles, or by signals from sensory nerves in the walls of blood vessels. However, the increase in neural drive to the muscles in the 6th sprint reveals that the brain does not merely act on an automatic response to signals from heart, blood vessels or leg muscles. Rather there is a computation of expected future demand that depends on input of information about future expectations from the conscious mind, as much as it does on chemical or neural messages from muscles, heart or blood vessels.

Thus our brain acts to protect us, using information from the periphery together with information from those parts of the brain that support conscious mental activity. We tinker with this mechanism at our peril. Nonetheless, it is clear from the fact that power output increased during the final sprint that under at least some circumstances, the central governor reaches a conservative decision, and we might improve performance with little risk if we could recognize when this is so, and take steps to override the governor.

However before rushing to devise schemes to over-ride the governor, it is worthwhile to look more carefully at the governor’s decisions under various circumstances. The study by Kay demonstrates that the governor acts conservatively when called upon to regulate a sprint in the midst of an endurance event. My own experience indicates that as I have grown older, my central governor also tends to act increasingly conservatively during interval training sessions. However this is not merely an issue for an aging athlete. The wily coach who announces after the eighth repetition in a planned 8 x 1Km session: ‘Well today we will make it ten’ is exploiting his knowledge that the governor tends to be conservative, in order to increase the mental toughness of his protégés.

We will return to the concept of mental toughness in a moment, but first we need to consider a common situation where the governor gets the computation wrong in the opposite direction. In endurance races, there are good physiological reasons to aim for a negative split: that is, to run faster in the second half than in the first half of the race. It is desirable to minimize the release of chemicals (calcium ions, potassium ions and muscle proteins) that indicate muscle damage, into the blood stream until as late as possible in the race to reduce the risk that the governor will order a premature shutdown. Also, in longer races where it is desirable to utilize fat as fuel, it is important to avoid premature switching off of fat metabolism by rising acidity.  However, one of the key mechanisms by which the brain prepares us for maximum performance on race day is the release of extra adrenaline. For the inexperienced athlete, this is a potential trap. The heart beats more strongly, the capillaries supplying the muscles dilate more readily and unless the athlete has the experience to rein in his or her supercharged body, he or she will set off at a profligate pace and pay a high price later.

Thus the central governor is not infallible. We can improve its reliability by providing it with more data upon which to base its computations of how much the body can safely stand under different circumstances. In fact the coach who says ‘Today we will make it ten’ after the eight repetition in the planned 8x1Km session is actually training the athlete’s governor to make a better estimate of the athlete’s capacity. Much of ‘mental toughness’ consists of establishing a preparedness to accept that a more demanding limit is achievable.

This mental toughness is closely related to self-belief. Although John Landy started the Vancouver mile as the current world record holder, he was acutely aware of the legendary final kick that Bannister had honed in training with his colleagues, Chris Brasher, Chris Chataway at Iffley Road in Oxford. As an Australian who had to travel far to participate in world class competition, Landy had limited opportunity to instill the necessary self-belief into his brain.

Training is not only a matter of increasing the efficiency of heart, lungs and muscles, but also about a program that trains the central governor to hone its judgment appropriately for the event in question – whether that be the need to produce a finely judged negative split in a marathon, or a devastating sprint in the final lap of a 5000m. Tempo runs, interval sessions, and low key races or time-trials are fertile sources of the raw the material required to train the governor.

However training the governor is not only a matter of preparing for races. It also has an important part to play is sustaining the quality of training sessions during a demanding schedule. It is commonplace to experience that sinking feeling during the warm-up for a planned tempo or interval session in the midst of a demanding schedule, that the body just cannot possibly cope with the intended pace, today. It is of course essential to evaluate the body’s complaints, but provided you have not embarked upon some unrealistic increase in training volume or intensity, and have been keeping track of recent performances to rule out the insidious development of the over-training syndrome, then the body’s anguish is probably a miscalculation by the central governor.

For me the trick that outwits the governor is banishing all thought about the intended distance of the run or the number of repetitions remaining, and focussing on running style, and on the immediate sensations from the body. Almost invariably, the sensation of lethargy diminishes. Each stride becomes an event to be savored with no thought about the number of strides remaining. Sometimes the lethargy disappears entirely; other times it persists but I am able to enjoy the sensation that comes from maintaining good form. However if the governor continues to provoke anguish, I know it is time to reformulate my goal for the session.